Advancing Stress-Resilient Rice: Mechanisms, Genes, and Breeding Strategies

Abstract

Rice (Oryza sativa L.) serves as a staple food for over half the global population, but its cultivation faces significant challenges from abiotic stresses such as drought, salinity, temperature extremes, and heavy metal toxicity. These stresses adversely impact rice growth, yield, and quality, posing a threat to global food security. This review comprehensively explores the physiological, biochemical, and molecular responses of rice to abiotic stresses, highlighting key functional genes and signaling pathways. Advanced breeding strategies, including molecular marker-assisted selection (MAS), genome-wide association studies (GWASs), and CRISPR/Cas9-based genome editing, offer innovative solutions for enhancing stress tolerance. Integrated approaches combining traditional breeding, modern molecular techniques, and exogenous applications such as plant hormones and beneficial microorganisms are discussed. These methods aim to develop rice varieties resilient to multiple stresses, ensuring sustainable production. Future prospects emphasize the integration of multi-omics technologies and the establishment of stress-resistant germplasm banks to accelerate breeding programs. This review provides some support for the development of stress-tolerant rice varieties to help address agricultural challenges in the context of climate change.

1. Introduction

Rice (Oryza sativa. L) is one of the most essential staple crops globally [1], serving as a primary source of calories for over half of the world’s population. However, global environmental degradation and extreme climate events are becoming increasingly frequent. Population growth, industrialization, as well as ozone layer depletion and declining soil quality have led to a significant decrease in rice yield sand quality, threatening global food security [2,3,4]. Consequently, understanding the mechanisms of stress tolerance in rice and developing new stress-resistant varieties has become a pressing scientific imperative.

During its growth and development, rice is highly susceptible to a wide range of environmental stresses, which can be broadly categorized into biotic and abiotic stresses [5]. Abiotic stresses, including temperature extremes (heat and cold stress), drought, salinity, heavy metal toxicity, and ultraviolet radiation, are particularly detrimental to rice growth, yield, and quality. Abiotic stresses have far-reaching impacts on agricultural production and food security in major rice-producing regions such as China and India. Firstly, saline and alkaline stresses significantly reduce the yield and quality of rice. In northeastern and northwestern China, saline soils cover a large area, resulting in restricted rice growth and reduced yields [6]. Secondly, drought stress is particularly severe in South Asian countries such as India, especially in years with unstable monsoons, where the growth cycle of rice is disturbed, leading to yield reductions [7]. In addition, rice production is also threatened by extreme heat events triggered by global warming, which inhibit pollination and seed filling, thereby affecting yields [8]. These abiotic stresses not only directly affect rice growth and yield, but also exacerbate the cost of agricultural production and increase the burden on farmers. To address these challenges, various breeding strategies have been employed, ranging from traditional approaches to advanced molecular breeding techniques such as MAS and genome editing tools like CRISPR/Cas9. These cutting-edge technologies offer new opportunities for enhancing rice performance under adverse environmental conditions.

This review provides a comprehensive overview of recent advances in the study of rice responses to abiotic stresses. It highlights the physiological and biochemical adaptations, underlying molecular mechanisms, key functional genes, and the latest developments in breeding strategies for stress tolerance. By synthesizing these findings, this work aims to provide a scientific foundation for future research on rice abiotic stress resistance and support the development of resilient rice varieties, thereby contributing to global food security and sustainable agricultural practices.

2. Research on the Effects of Abiotic Stress on Rice and Functional Genes

Different abiotic stresses can have both similar and distinct effects on individual rice plants. In some cases, multiple types of abiotic stresses may occur simultaneously, or one stress may trigger another during the growth and development of rice (Figure 1). These stresses interfere with the normal growth and development of rice through different mechanisms, resulting in reduced yield and quality [8]. In agricultural practice, rice tolerance to abiotic stress is typically evaluated using indicators such as the germination rate, root volume, root count, plant height, and tiller number.

2.1. Drought Stress

Water is a critical resource for plant growth and development, and rice, being a crop with high water demands, is particularly sensitive to water availability [9]. Given the increasing global temperatures and the more erratic distribution of rainfall due to climate change, the frequency, extent, and duration of drought events are on the rise, posing a significant threat to the yield and quality of rice and other staple crops.

Rice’s water requirements vary across different growth stages: minimal water is needed during germination and the seedling stages, while water demand increases during tillering, peaks at heading, and gradually declines after the grain filling stage as field water is drained. Drought stress leads to a substantial loss of water from the plant, triggering a series of physiological responses, including leaf wilting, reduced leaf area, decreased photosynthetic rate, stunted plant height, fewer tillers, and impaired spikelet development [10,11,12]. Moreover, reduced dry matter transport results in insufficient grain filling, which causes a significant decrease in panicle number, panicle length, and thousand-grain weight [13]. Interestingly, studies have shown that mild drought stress can sometimes promote rice growth and development [14].

Rice roots also respond significantly to drought stress. Under initial stress conditions, roots elongate and increase surface area and volume to absorb more water. However, as stress intensifies, this compensatory mechanism becomes ineffective, leading to restricted root growth, as evidenced by reduced root length, surface area, and volume [15].

In rice leaves, stomatal movement regulates photosynthesis and transpiration. During water stress, stomata close to reduce water loss, but this also restricts gas exchange, leading to a decline in photosynthesis [16]. To mitigate the stress, plants adjust their cellular osmotic pressure to enhance water uptake, thereby protecting cell structure and function [17].

In agricultural practices, water-saving techniques such as intermittent irrigation, controlled irrigation, and drip irrigation effectively meet the water requirements of rice while significantly reducing freshwater consumption [18].

Drought tolerance in rice is a complex, multigenic trait, and its signaling pathways are intricate (Figure 2). Under drought conditions, genes that impact rice yield include Drought-Responsive Oxidative Stress Tolerance 1 (DROT1), Root Length Estimation 1 (RoLe1), and O. sativa ZRT-IRT-Like Protein 23 (OsZIP23),and members of the Myeloblastosis (MYB), Ethylene Response Factor/Dehydration-Responsive Element-Binding (ERF/DRE), and NAM, ATAF1/2, CUC2 (NAC) gene families also play important roles [19]. Protein expression analysis has shown that the OsPR10A protein in rice is either not expressed or expressed at low levels during the seedling stage, but its expression increases during tillering and later stages. The overexpression of OsPR10A is linked to the activation of the Jasmonic Acid (JA) and abscisic acid (ABA) signaling pathways, enhancing drought tolerance in rice [20,21].

MYB family transcription factors play crucial roles in rice drought tolerance [22]. Different MYB transcription factors influence various aspects of rice, thereby affecting its drought tolerance. For example, the R2R3-type MYB transcription factor RRS1 affects rice morphology, the O. sativa F-box Protein (OsFLP) regulates stomatal development and water transpiration, and OsMYB60 participates in regulating the biosynthesis of epicuticular wax. The gene RRS1 negatively regulates root development in rice by activating the expression of the Indole-3-acetic acid (IAA3) gene, participating in the Indole-3-acetic acid (IAA) signaling pathway, and inhibiting root growth, thus negatively regulating drought tolerance. Some MYB transcription factors regulate ABA synthesis pathways through post-translational modifications, such as O. sativa MYB-related transcription factor 48-1 (OsMYB48-1), thereby adjusting drought tolerance. Additionally, certain MYB transcription factors interact with other proteins to modulate drought tolerance. For instance, O. sativa MYB-related protein 57 (OsMYBR57) interacts with the homeobox transcription factor O. sativa Homeobox protein 22 (OsHB22) to form the O. sativa FT-interacting protein 6-O. sativa Homeobox protein 22-O. sativa MYB-related protein 57 (OsFTIP6-OsHB22-OsMYBR57) module, which regulates the drought response in rice. OsMFT1 enhances the binding ability of downstream drought-regulated gene promoters by interacting with O. sativa basic Leucine Zipper protein 66 (OsbZIP66) and O. sativa MYB transcription factor 26 (OsMYB26), thus improving drought resistance. However, the FT-interacting protein (FTIP) gene O. sativa FT-interacting protein 1 (OsFTIP1) inhibits the nuclear mislocalization of O. sativa Mother of FT and TFL1 1 (OsMFT1), reversing its regulation of drought tolerance [23].

In the NAC family, many genes are closely associated with rice drought tolerance [24]. For example, knockout of the NAC120 gene results in reduced growth but increased drought tolerance. OsNAC120 promotes GA synthesis by activating the GA synthesis-related genes OsGA20ox1 and OsGA20ox3. The DELLA protein SLR interacts with NAC120 and suppresses its expression. Additionally, OsNAC120 inhibits the expression of ABA synthesis genes O. sativa 9-cis-epoxycarotenoid dioxygenase 3 (OsNCED3) and OsNCED4, interfering with ABA-mediated stomatal closure, which negatively impacts drought tolerance. However, the rice osmotic stress/ABA-activated protein kinase 9 (OsSAPK9) can interact with NAC120, phosphorylate it to inactivate it, and ABA accelerates this inactivation. Therefore, NAC120 is a gene that enhances drought tolerance in rice [25]. Through genome-wide association studies, it has been discovered that the gene RoLe1, which controls root length and drought tolerance in rice, has a promoter that interacts with OsNAC41. Furthermore, the OsAGAP gene also regulates auxin-dependent root development, and there is an interaction between RoLe1 and OsAGAP. In summary, the module formed by OsNAC41, RoLe1, and the O. sativa ADP-ribosylation factor GTPase-Activating Protein (OsAGAP) can improve drought tolerance in rice [26].

Under drought stress, the O. sativa NAC Domain Containing Protein 023 (ONAC023) participates in regulating drought tolerance in rice by binding and controlling multiple downstream genes. It enhances drought resistance by regulating the balance of reactive oxygen species (ROS) and genes related to water transport, such as O. sativa Plasma membrane Intrinsic Protein 2;7 (OsPIP2;7), PGL3, and O. sativa FK506 Binding Protein 20-1b (OsFKBP20-1b) [27]. The APETALA2/ethylene response factor O. sativa Ethylene Responsive Factor 103 (OsERF103) interacts with stress-responsive NAC1 (SNAC1) to regulate the downstream drought-resistance gene OsZIP23, thereby enhancing rice’s drought tolerance [27,28].

Through genome-wide association studies, the DROT1 gene has been identified as conferring drought tolerance to rice. DROT1 is specifically expressed in rice vascular bundles and enhances drought resistance by increasing cellulose content and maintaining cellulose crystallinity, thereby strengthening the rice cell wall structure. The expression of DROT1 is inhibited by ERF3 but activated by ERF71, both of which are drought-responsive transcription factors [18].

Members of the Squamosa Promoter Binding Protein-Like (SPL) family, such as OsSPL10, influence stomatal closure by regulating ROS production, thus improving drought tolerance [29]. Recent studies have shown that members of the cytochrome P450 family, such as DDT1, enhance rice’s drought tolerance by improving antioxidant capacity and participating in the regulation of gibberellins (GAs) and ABA [30].

In summary, drought negatively affects rice growth by causing physiological responses like leaf wilting, reduced photosynthesis, and impaired grain filling. While mild drought stress may promote growth, severe stress leads to root restriction and compromised water uptake. To mitigate these effects, rice plants adjust osmotic pressure, and various genes play crucial roles in drought tolerance. These include genes associated with the MYB, NAC, and ERF families, which regulate key processes like stomatal movement, root growth, and stress-responsive signaling. Research has identified several genes, such as DROT1 [29] and RoLe1 [26], that improve drought resistance by strengthening cellular structures or regulating water transport. Additionally, water-saving agricultural practices, including controlled and drip irrigation, help conserve water while maintaining rice yield.

2.2. Salt Stress

Globally, approximately 100 million hectares of land are affected by salinity, accounting for 7% of the total land area [31]. Salt accumulation in the soil, primarily in the form of sodium chloride (NaCl) in irrigation water, results in both osmotic and ionic stress [32,33]. When the concentration of soluble salts in the soil reaches 0.3%, rice yields can decrease by over 50% [34]. With climate change and improper irrigation practices, the global extent of saline and alkaline soils is expected to further expand. A key distinction between plant and animal cells is the presence of vacuoles in plant cells, which significantly enhance their ability to cope with abiotic stresses, including cold, heat, salinity, and drought. Under salt stress, plants sequester sodium ions (Na⁺) into vacuoles to mitigate cellular damage and alleviate the adverse effects of salinity. Increased expression of sodium ion transporters, such as O. sativa Sodium/Hydrogen Exchanger 2 (OsNHX2), on vacuolar membranes has been shown to enhance salt tolerance [35].

Salt stress primarily targets the root system of rice, subsequently impairing shoot growth and development [36,37]. High salinity disrupts root structure, reduces root surface area, and decreases the number of functional roots, limiting nutrient uptake, disturbing osmotic balance, and ultimately causing stunted growth or even plant death. Rice plants exposed to high salinity exhibit a range of morphological changes, including reduced photosynthesis, thinner stems, shorter stature, curling and yellowing of leaves, smaller leaf area, reduced tillering, and lower seed-setting rates [38,39]. In response, rice roots employ compensatory strategies, such as restricting growth in salt-stressed regions while promoting growth in unaffected regions, to mitigate the localized effects of salinity [38].

The impact of salinity on rice varies across developmental stages. During seed germination, salt ions infiltrate cell wall pores, disrupting embryonic cell structure and function, which slows germination, restricts seedling growth, and reduces seed vigor, sometimes preventing germination entirely. At the seedling stage, salinity inhibits root and stem growth, diminishing water and nutrient uptake and placing plants in a state of water deficiency. Furthermore, salinity interferes with the transport of essential nutrients like nitrogen (N), phosphorus (P), potassium (K), and calcium (Ca), leading to deficiencies [40,41]. At the reproductive stage, high salinity delays or suppresses tillering, prolongs panicle emergence, reduces pollen viability, and ultimately decreases yield and grain quality [42,43].

There are some genes such as O. sativa High-Affinity K⁺ Transporter 1;5 (OsHKT1;5) and OsNHX2 that have been identified as key regulators of salt tolerance in rice (Figure 3). Rice has evolved intricate signaling pathways to counteract salt stress, which primarily manifests as osmotic stress and ion toxicity [17,44,45]. Osmotic stress arises from the high salt concentration in the soil, altering the osmotic pressure in rice cells, causing water loss, disrupting cellular metabolic processes, and impairing growth. Elevated salt levels also limit CO₂ uptake and compromise the selective permeability of cell membranes, leading to cellular homeostasis disruption, reduced chlorophyll content, and inhibited photosynthesis [39]. To counteract osmotic stress, plants accumulate small molecules such as trehalose and proline to maintain osmotic balance. For example, the trehalose biosynthesis gene O. sativa Trehalose-6-Phosphate Phosphatase 1 (OsTPP1) [46] and the proline synthesis gene O. sativa Pyrroline-5-Carboxylate Synthetase (OsP5CS) [47] play critical roles in the osmotic stress response.

The ion toxicity results from the accumulation of Na⁺ and Cl⁻ ions. Na⁺ competes with potassium ions (K⁺) for binding sites, disrupting K⁺-dependent metabolic processes and impairing physiological functions [48]. To alleviate ion toxicity, plants enhance K⁺ uptake through transporter families such as HAK/KUP/KT or reduce Na⁺ accumulation via vacuolar Na⁺/H⁺ antiporters like OsNHX2, thereby restoring ion balance [36].

Research also highlights the uneven distribution of salinity in soils, offering opportunities for rice roots to adapt by regulating growth in different regions. Under salt stress, affected roots generate large amounts of ROS, which interact with plasma membrane receptors to activate respiratory burst oxidase homologs (RBOHs), producing more ROS [49]. ROS can also modulate gene expression or regulate root growth via protein oxidation and auxin signaling, providing novel insights into rice adaptation to salinity [38].

In agricultural practices, applying exogenous substances can significantly mitigate the effects of salt stress on rice. For instance, during seed germination, the application of silicon, salicylic acid, or GA significantly improves germination rates under salt stress [50,51,52]. Silicon enhances root vitality, reduces malondialdehyde levels, and increases the concentrations of essential nutrients such as K, Fe, and magnesium (Mg), thereby alleviating salinity’s impact. Salicylic acid enhances the activities of glutamine synthetase, glutamate dehydrogenase, and antioxidant enzymes, while increasing soluble sugar content to improve salt tolerance. GA helps restore root and shoot growth under salt stress. Additionally, applying N, P, and K fertilizers can enhance rice’s salt tolerance and yield. Pre-planting soil leaching to reduce salinity concentrations is also an effective measure [53,54].

Under salt stress, rice adapts to the saline environment by regulating ion balance and the expression of related genes, thereby maintaining its growth and development. This process involves the coordinated action of multiple key ion transport channels and regulatory genes. Ca²⁺ is a key signaling molecule in rice’s cellular response to salt stress, mediating multiple regulatory pathways (Figure 4). Under salt stress, receptor proteins such as GIPC on the cell membrane are activated by external salt ions, which in turn open Ca²⁺ channels like OsCA1, leading to an increase in intracellular Ca²⁺ concentration [55]. The accumulation of Ca²⁺ activates the Salt Overly Sensitive (SOS) signaling pathway. Vacuolar Protein Sorting 23A (VPS23A) binds to SOS3, promoting the interaction between SOS3 and SOS2, and localizing them to the cell membrane. PKS5 then phosphorylates SOS2, enhancing its binding affinity to 14-3-3λ/κ, temporarily inhibiting SOS2 activity. However, during the early stages of stress, Ca²⁺ entering the cell through open channels binds with 14-3-3λ/κ, releasing PKS5’s inhibition of SOS2, activating SOS2, and promoting its interaction with SOS1. This ultimately activates SOS1, leading to the expulsion of Na⁺ from the cell, thereby enhancing rice’s salt tolerance [56,57].

In addition, Ca²⁺ interacts with SOS3-like Calcium Binding Protein 8 (SCaBP8) to inhibit the activity of the Clade D Protein phosphatase 2C D6 and Clade D Protein phosphatase 2C D7 (PP2C D6/D7) proteins. PP2C D6/D7 is a negative regulator that dephosphorylates and inhibits SOS1 activity. Therefore, SCaBP8 positively regulates the SOS signaling pathway, improving rice’s salt tolerance [58,59]. In phosphatidylinositol (PI) regulation, PI typically inhibits the activity of H⁺-ATPase 2 (AHA2). However, in response to salt signals, PI is converted to phosphatidylinositol-4-phosphate (PI4P) by PI4K, thereby relieving the inhibition of SOS1 [40,59,60].

Several quantitative trait loci (QTLs) related to rice salt tolerance have been identified, including Streptomyces lividans K⁺ Channel 1 (SKC1), SHT1, and RST1 [61]. Through GWAS, ten candidate genes related to salt tolerance have been identified, such as OsHKT1;5, which regulates Na⁺/K⁺ balance, O. sativa Heme Activator Protein 2E (OsHAP2E), which maintains osmotic homeostasis, and O. sativa Delayed Seed Germination 1 (OsDSG1), which functions in detoxification. Studies have shown that O. sativa Mitogen-Activated Protein Kinase Kinase 10.2 (OsMKK10.2) enhances rice’s salt stress adaptation by promoting Na⁺ efflux, while O. sativa WRKY Transcription Factor 53 (OsWRKY53), as an upstream negative regulator, inhibits the expression of both OsMKK10.2 and OsHKT1;5 [61,62,63,64,65].

Additionally, mutation and overexpression experiments have validated the positive role of the glycosyltransferase gene Uridine 5′-diphospho-glucuronosyltransferase 2 (UGT2) in salt tolerance. Further analysis revealed that the promoter of UGT2 directly binds to the transcription factor OsbZIP23, enhancing starch synthesis in the endosperm and improving salt tolerance [66].

Molecular switches within the cell also play a role in regulating rice’s salt tolerance. For example, catalase (CAT) reduces hydrogen peroxide accumulation through disproportionation, thus enhancing stress resistance. On the other hand, peroxisomal phosphatase PC1, which is induced by salt stress and hydrogen peroxide, interacts with CAT to reduce its enzyme activity, negatively regulating salt tolerance [67].

Within the rice Abscisic acid Stress and Ripening (ASR) family, several genes have been found to regulate responses to abiotic stresses. OsASR1 is activated under ABA and salt stress, promoting ABA accumulation and enhancing stress resistance in rice [68]. OsASR6 mitigates the damage caused by salt stress by activating antioxidant mechanisms and regulating the intracellular Na⁺/K⁺ balance. As a molecular chaperone, OsASR6 is also localized to chloroplasts, where it interacts with the key ABA synthesis enzyme OsNCED1 to regulate hormonal balance under salt stress [69].

Furthermore, the O. sativa Cellulose Synthase-Like D4 (OsCSLD4) plays a role in cell wall polysaccharide synthesis. While previous studies have focused on its function in growth and development, recent research suggests that OsCSLD4 indirectly regulates rice’s salt tolerance by promoting ABA synthesis [70].

Overall, salt stress negatively impacts rice growth by causing osmotic stress, ion toxicity, and root damage, leading to reduced yields. Rice adapts by sequestering sodium in vacuoles and regulating ion balance through transporters like OsNHX2 and OsHKT1;5. The key genes involved in salt tolerance include OsHKT1;5, OsMKK10.2, and OsNHX2. Additionally, external substances like silicon and salicylic acid can enhance stress resistance. Identifying salt tolerance-related genes and QTLs offers potential for improving rice resilience through breeding.

2.3. High-Temperature Stress

The optimal temperature range for rice growth is 22 degrees Celsius (°C) to 28 °C [37]. However, heat stress, exacerbated by industrialization and the accumulation of greenhouse gases, is exacerbating the effects of global warming on rice and other crops. High-temperatures result in smaller, curled seedling leaves, a decrease in photosynthetic rate and chloroplast content, and eventually leaf chlorosis or whitening.

Temperature stress during the panicle initiation stage is particularly impactful on pollination and fertilization. Studies have shown that the length of the anther correlates with heat tolerance: the longer the anther, the greater the heat tolerance [71]. Additionally, when heat stress occurs during panicle emergence, the stigma loses its ability to accept pollen due to rapid water loss, further reducing pollination efficiency and seed setting [72,73]. Overall, under extreme temperature conditions, pollen sterility during panicle initiation is manifested in three primary forms: (1) incomplete anther development leading to pollen sterility; (2) intact anther structure but a dehydrated stigma unable to accept pollen; and (3) limited pollen tube elongation, preventing fertilization [74].

High-temperature stress also has significant effects on rice during the tillering and ripening stages. During tillering, high temperatures accelerate growth, preventing the formation of sufficient tillers and panicles, leading to phenomena such as arrested panicle development, shortened panicle length, and stunted, weak plants. In severe cases, this results in white panicles and spikelet sterility. During ripening, high-temperatures stress increases seed chalkiness, reduces thousand-grain weight, and lowers the nutritional value of rice [75]. Furthermore, high-temperatures are often accompanied by low photosynthetic rates and high transpiration rates. When combined with drought stress, these factors create a synergistic effect, further exacerbating yield losses [76,77]. It is estimated that for every 1 °C increase in the global annual average temperature, rice yields will decrease by approximately 3.2% [78]. High temperatures also increase the number of misfolded proteins in the endoplasmic reticulum, leading to the deactivation of membrane proteins, disruption of membrane structures, and a cascade of metabolic disorders [79].

High-temperature stress can be mitigated through methods such as shading nets, deep-water rice cultivation, and applying plant growth regulators or increasing nitrogen fertilizers to enhance the plant’s ability to tolerate high temperatures. Exogenous ABA can improve the rooting ability of young shoots and enhance membrane stability, preventing pollen sterility [5,80,81].

Heat tolerance in rice is a quantitative trait controlled by multiple genes and is regulated by a complex interplay between the plant’s genetic factors and environmental conditions (Figure 5), often resulting in discrepancies between the genotype and phenotype [82]. As a result, compared to other stress responses, research on rice heat tolerance has progressed relatively slowly, and the number of cloned heat tolerance genes remains limited. Most of the identified heat tolerance genes are not naturally occurring variants but have been obtained through artificial intervention. Natural variation loci that have been discovered include Thermotolerance 1 (TT1), Thermotolerance 2 (TT2), Thermotolerance 3.1 (TT3.1), Thermotolerance 3.2 (TT3.2), and Slender Guy 1 (SLG1). TT1, which originates from a quantitative trait locus in African rice, plays a key role in clearing toxic proteins within the cell, thereby protecting the cell from heat stress [54]. TT2 encodes the γ-subunit of a G protein and acts as a negative regulator of heat tolerance [83]. TT3.1 positively regulates heat tolerance, while TT3.2 negatively regulates it; TT3.1 is located upstream of TT3.2. The Aux/IAA family gene OsIAA7 alleviates heat stress by reducing intracellular hydrogen peroxide levels under heat stress. It also interacts with the negative regulator O. sativa Auxin Response Factor 6 (OsARF6), suppressing its activity and regulating the transcription of OsTT1 and OsTT3.1, ultimately enhancing heat tolerance in rice [82,84,85]. SLG1 encodes a tRNA2-thiolation enzyme; the knock-out lines of this gene are sensitive to heat stress, whereas overexpression lines show stronger heat tolerance [86].

Heat stress induces the expression of heat shock proteins (HSPs) in plant cells. These proteins protect the cell by preventing protein degradation. Heat shock transcription factors (Hsfs) are classified into three categories: A, B, and C. HsfA acts as a transcriptional activator with an activation domain, while HsfB functions as a transcriptional repressor; the precise roles of HsfC are not yet fully understood [87,88]. Under heat stress, HSP70 dissociates from HsfA1, allowing HsfA1 to translocate to the nucleus, where it interacts with HsfA2 to activate the expression of downstream heat tolerance genes [89]. HSP101 is a key gene closely associated with heat tolerance, regulating the expression of multiple downstream heat tolerance genes. Its own expression is also regulated. Studies have shown that the transcription factor HSFA6a regulates heat tolerance by controlling HSP101 and its downstream gene modules, such as cHsp70-1, HSP16.9A-CI, and HSP18.0A-CII. cHsp70-1 acts as a positive regulator, while HSP16.9A-CI and HSP18.0A-CII are negative regulators. Furthermore, ubiquitin can inhibit the activity of HSFA6a, thus negatively regulating the HSFA6a-HSP101 module and its downstream genes [90].

Heat Tolerance Gene 3 (HTG3) is a member of the HsfA2 subfamily. The variation in the miniature inverted-repeat transposable elements (MITEs) in its promoter is closely associated with heat tolerance regulation. The heat-induced isoform HTG3a encodes an Hsf transcription factor that regulates the expression of HSP genes and JAZ family genes (such as JAC9 and JAC12), thereby enhancing heat tolerance in rice [91]. Additionally, phospholipase D (PLD) generates phosphatidic acid (PA) by hydrolyzing membrane lipids. The GA signaling pathway, through PA produced by PLDα6, binds to the soluble gibberellin receptor GID1 on the nuclear membrane, promoting the degradation of the DELLA protein SLENDER RICE1 (SLR1), thus increasing GA accumulation and enhancing heat tolerance [92].

Heat stress also induces the accumulation of misfolded proteins in the endoplasmic reticulum (ER), activating ER quality control (ERQC), ER-associated degradation (ERAD), and the unfolded protein response (UPR). These responses regulate the expression of genes such as OsbZIP74 and TT3, which help modulate heat tolerance in plants [66,67]. Moreover, G proteins mediate the regulation of several downstream genes through the G protein γ-subunit encoded by TT2, thereby enhancing rice heat tolerance [61]. OsMDHAR4, which encodes monodehydroascorbate reductase, plays a critical role in heat tolerance by participating in the hydrogen peroxide-induced stomatal closure pathway [93].

High-temperature stress significantly impacts rice growth, particularly during panicle initiation, tillering, and the ripening stages. It leads to pollen sterility, stunted growth, reduced seed quality, and yield loss. Heat stress triggers the expression of HSPs and involves key genes like TT1, TT2, and HSP101, which help protect cells and regulate heat tolerance. Strategies such as shading, deep-water cultivation, and applying growth regulators can help mitigate heat stress effects, but more research is needed to fully understand and enhance rice’s heat tolerance.

2.4. Low Temperature Stress

It is estimated that over 15 million hectares of rice cultivation worldwide are threatened by low temperatures. Large-scale cold damage can occur in rice crops every 4 to 5 years due to low temperatures [94]. Low temperatures cause leaf freezing and desiccation, and in severe cases, plant death [40,41,42].

Low temperatures can disrupt the early stages of microspore formation in pollen mother cells, leading to pollination failure and infertility in plants [95,96]. Temperature changes during the tetrad to early unicellular stages of anther development are particularly sensitive to pollen [97,98]. At this stage, abnormalities in the development of the pollen callose layer disrupt nutrient supply to pollen mother cells, preventing proper pollen maturation and release, which significantly reduces yield [99]. While the abnormal enlargement of the callose layer cells is a major cause of pollen sterility, the underlying mechanisms are likely more complex and involve additional factors [100]. Extreme temperatures also decrease the number of germinating pollen grains, delay fertilization, and inhibit anther elongation.

Low temperature stress significantly affects rice during seed germination, mainly by reducing the seed’s water absorption capacity and delaying germination. This exacerbates the negative effects of both biotic and abiotic stresses in the soil, leading to poor seedling emergence and reduced quality, which in turn impacts yield [101]. At the subcellular level, low temperatures cause ruptures in chloroplast membranes, swelling and deformation of thylakoids, reduced starch grain volume and number, mitochondrial expansion, widening of inner cristae, vacuolarization, and fragmentation and expansion of the endoplasmic reticulum and Golgi apparatus into small vesicles. As low temperature stress intensifies, cytoplasmic separation, cell membrane rupture, and organelle disintegration may occur [102,103]. Studies have shown that chloroplasts are the first organelles to respond to low temperatures, and their morphological changes can serve as an indicator of cold tolerance in plants [104,105].

For low temperature stress, plant hormones like ABA and ethephon can be used to enhance cold tolerance by regulating cell osmotic pressure, improving antioxidant enzyme activity and promoting the expression of stress-related genes [106].

Cold tolerance in rice is a complex genetic and physiological process regulated by multiple genes (Figure 5) [107]. These genes are unevenly distributed across the 12 chromosomes of rice and collectively enable the plant to withstand the adverse effects of low temperature environments. Genetic studies have identified 270 QTLs associated with cold tolerance in the rice genome. Approximately 80% of these cold tolerance genes are positive regulators, while 20% are negative regulators [108]. Among different growth stages, the seedling stage exhibits the highest proportion of cold tolerance-related QTLs, accounting for 40% [109].

V-type H⁺-ATPase (VHA), widely present in the cellular membrane systems of rice, is a crucial enzyme for material transport within plant cells. Under cold stress, the expression level of VHA significantly decreases, leading to reduced transport efficiency and thereby impairing growth and stress resistance [110,111].

The functional role of the cold tolerance gene O. sativa Mitogen-Activated Protein Kinase 3 (OsMPK3) has been validated, revealing its upstream phosphorylation kinase OsMKK6 as a key component of the signaling pathway [109,112]. OsMKK6 interacts with cold tolerance-related genes O. sativa Inducer of CBF Expression 1 (OsICE1) and O. sativa Ideal Plant Architecture 1 (OsIPA1), and in vitro kinase assays have confirmed its ability to phosphorylate these targets.

The CBF (C-repeat Binding Factor) family represents critical transcriptional regulators in cold stress responses, with functions well documented across various plant species. In Arabidopsis thaliana, ICE1 activates the expression of CBF genes by binding to MYC cis-elements on their promoters. Subsequently, CBF proteins bind to CRT/DRE cis-elements in the promoters of cold-responsive genes, enhancing cold tolerance [113,114,115]. In rice, the key regulator OsIPA1 (OsSPL14) binds to GTAC motifs on the OsCBF3 promoter, upregulating its expression and improving cold tolerance [116].

The AP2/ERF (APETALA2/Ethylene Response Factor) family, known for its role in multiple stress responses, is also involved in cold stress regulation in rice. For instance, OsERF096 negatively regulates cold tolerance through its interaction with miR1320 [117]. Recent studies further suggest that AP2/ERF factors play pivotal roles in the CBF-mediated cold stress pathway. The AP2/ERF transcription factor OsERF52, when phosphorylated by OsSAPK9, interacts with OsIPA1 and OsbHLH002 to enhance the transcription of OsCBF genes, thereby increasing cold tolerance in rice [118].

The functions of these genes and their regulatory pathways often extend beyond cold stress. For example, OsSAPKs not only positively regulate cold tolerance by phosphorylating the cyclic nucleotide-gated ion channel OsCNGC9 [119], but also participate in various other biological processes. Similarly, OsICE1 (OsbHLH002) exhibits multifunctionality across different stress responses.

G-proteins located on the rice cell membrane also contribute to cold stress responses. The regulator encoded by the cold tolerance QTL COLD1 interacts with the G-protein α-subunit under low-temperature conditions, transmitting signals that enhance cold tolerance [120].

The NAC transcription factor family plays a significant role in modulating cold stress tolerance in rice. Notably, OsNAC5 enhances cold tolerance by activating OsABI5 expression, which in turn regulates downstream cold-responsive genes such as OsDREB1A, OsMYB20, and OsPRX70.

Cold temperatures impair rice growth by disrupting seed germination, reducing water absorption, and causing cellular damage. In particular, low temperatures affect pollen development, leading to pollination failure and infertility. Subcellular effects include damage to chloroplasts, mitochondria, and other organelles, which disrupt cellular function. Cold tolerance in rice is governed by complex genetic and physiological mechanisms, with over 270 QTLs identified. Key genes such as OsMPK3, OsICE1, OsIPA1, and OsCBF regulate cold stress responses, while hormones like ABA and ethephon can enhance tolerance. Cold stress also activates several gene families, including AP2/ERF and NAC, that regulate cold response pathways, contributing to rice’s ability to withstand low temperature stress.

2.5. UV-B Stress

In recent years, light has emerged as a crucial environmental factor, with its intensity and duration playing an essential regulatory role in the growth and development of rice. Among various types of light, UV-B radiation is recognized as a form of abiotic stress (Table 1). High-intensity light and UV-B radiation generally have detrimental effects on rice growth and development. UV-B radiation increases the levels of ROS in rice [121], which can oxidize cellular biomolecules, damaging proteins and cell membranes, thereby compromising their integrity. This leads to alterations in the plant’s growth and developmental processes [122,123]. Furthermore, UV-B radiation negatively impacts photosynthetic pigments and the photosynthesis process [124,125], alters the synthesis of secondary metabolites [126], affects the plant’s anatomical features, and modifies wax deposition in the cuticle [127,128]. UV-B radiation also damages proteins and electron transport activities in Photosystem I and Photosystem II [129]. When rice is exposed to UV-B radiation during the vegetative stage, the growth of the coleoptile is inhibited, which in turn affects the overall growth, development, and yield of the plant [130].

However, some studies suggest that moderate UV-B exposure can enhance the stress tolerance of rice. Low doses of UV-B radiation can significantly reduce the excessive accumulation of ROS under NaCl and Polyethylene Glycol (PEG) stress, providing a protective mechanism for rice seedlings under stressful conditions. This helps maintain cellular redox balance, thereby mitigating oxidative stress and improving rice tolerance to NaCl and PEG stress [131,132,133]. Additionally, research has shown that rice perceives UV-B radiation through two UV-B receptors, OsUVR8a and OsUVR8b. Short-term UV-B exposure causes rice seedlings to become shorter and thicker, enhancing their ability to tolerate UV-B stress [134].

Overall, the effects of UV-B on rice growth and development are dualistic. High-intensity UV-B typically harms rice growth, while low doses of UV-B can induce beneficial adaptive mechanisms, thereby enhancing the plant’s tolerance to environmental stress.

When rice is subjected to UV-B radiation stress, it primarily mitigates oxidative damage by enhancing its antioxidant defense system. UV-B stress induces the accumulation of ROS in rice, leading to lipid peroxidation, as evidenced by increased MDA content. In response, rice boosts the levels of non-enzymatic antioxidants such as ascorbic acid and glutathione, alongside primary metabolites like proline, soluble sugars, and total proteins [130]. These compounds help neutralize free radicals, protect cellular structures and functions, and reduce the negative impacts of UV-B radiation. Different rice varieties exhibit varying degrees of sensitivity to UV-B stress. For instance, Mangalamahsuri, Aathira, and Kanchana display higher tolerance, while Swarnaprabha and Aiswarya are more sensitive [135].

Under NaCl and PEG-induced stress, ROS such as hydrogen peroxide and superoxide anions significantly accumulate in rice seedlings, whereas UV-B treatment effectively reduces this accumulation. Antioxidant enzymes, including superoxide dismutase (SOD; EC 1.15.1.1), catalase (CAT; EC 1.11.1.6), and ascorbate peroxidase (APX, EC 1.11.1.11) [136], show enhanced activity under NaCl and PEG stress, with UV-B treatment further amplifying their activities. While NaCl and PEG stress inhibits photosystem activity (PSI and PSII), UV-B treatment alleviates this suppression. Similarly, mitochondrial activity, which decreases under stress, is preserved by UV-B treatment. Rice plants subjected to UV-B without additional stress exhibit the highest mitochondrial activity. These findings suggest that rice employs a coordinated network of physiological and molecular mechanisms to respond to UV-B stress. These mechanisms collectively maintain redox homeostasis, protect photosynthetic and mitochondrial functions, and regulate osmotic balance, thereby improving tolerance to stresses such as NaCl and PEG [132].

Studies reveal that rice’s response to low doses of UV-B is partially mediated by the UV-B-specific receptor UV RESISTANCE LOCUS8 (UVR8), which regulates gene expression. In contrast, high-dose UV-B responses involve diverse regulatory pathways, including UVR8-independent mechanisms, cellular damage, and ROS-mediated oxidative stress [135,137].

OsUVR8a and OsUVR8b, the UV-B receptor genes in rice, are crucial for sensing and responding to UV-B radiation. The proteins encoded by these genes share structural similarities with the Arabidopsis UV-B receptor AtUVR8 [130], including conserved tryptophan residues that enable them to detect UV-B signals. Upon UV-B exposure, these receptors undergo a conformational change from dimers to monomers, a critical step in initiating UV-B signal transduction. The overexpression of OsUVR8a and OsUVR8b alters rice growth and developmental phenotypes. Under UV-B irradiation, overexpression lines exhibit traits such as reduced plant height and thicker stems, indicating their roles in morphological adjustments to UV-B stress [134].

UV-B exposure induces the expression of UDP-dependent glycosyltransferase (OsUGT706C2) in rice. In OsUGT706C2-overexpressing lines, the phenylpropanoid pathway and flavonoid biosynthesis genes (e.g., PAL1, C4H, 4CL5, CHS, F3H, and FLS) are significantly upregulated. These lines exhibit higher survival rates, lower MDA levels, and greater chlorophyll content under UV-B treatment. Reduced ROS accumulation in the overexpression lines, as shown by NBT and DAB staining, correlates with the downregulated expression of ROS-related genes. This suggests that OsUGT706C2 enhances ROS scavenging capacity, improving UV-B tolerance [138].

Further studies indicate that OsMYB44 plays a critical role in UV-B stress responses by directly binding to and activating the promoters of genes involved in tryptophan biosynthesis (e.g., OsTSα and OsTSβ), leading to tryptophan accumulation and enhanced UV-B tolerance. The overexpression of OsMYB44 results in traits such as greener leaves and higher aerial fresh weight under UV-B stress, whereas silencing this gene reduces tolerance. Exogenous tryptophan treatment also improves UV-B tolerance, highlighting the regulatory role of tryptophan in rice adaptation to UV-B stress [139].

Under UV-B irradiation, rice seedlings overexpressing OsRLCK160 show higher survival rates, reduced ROS accumulation (superoxide and H₂O₂), and lower MDA content. Similarly, OsbZIP48 overexpression and phosphomimetic mutant lines exhibit stronger UV-B tolerance, with improved survival rates and reduced oxidative damage. In contrast, OsbZIP48 phosphorylation-deficient mutants display heightened sensitivity to UV-B. Gene expression analyses suggest that OsRLCK160 interacts with OsbZIP48, enhancing its transcriptional activity through phosphorylation. This interaction regulates flavonoid accumulation, ultimately improving UV-B tolerance [140].

These findings illustrate that rice employs a sophisticated genetic regulatory network to respond to UV-B radiation stress, enhancing its resilience to environmental challenges (Figure 6).

Table 1. Genes related to UV-B resistance in rice.

Gene	Expression Site	Subcellular Localization	Function	References
OsUVR8a	Leaves and leaf sheaths	Nucleus	Enhances UV-B stress tolerance	[130,134]
OsUVR8b	Leaves and leaf sheathst	Nucleus	Enhances UV-B stress tolerance	[130,134]
OsUGT706C2	Leaves	Plasma membrane and nucleus	Enhances UV-B stress tolerance	[138]
OsMYB44	Leaves	Nucleus	Enhances UV-B stress tolerance	[139]
OsMYB110	Roots, leaves, and leaf sheaths	Nucleus	Enhances UV-B stress tolerance	[139]
OsRLCK160	Roots, leaves, veins, leaf sheaths, stems, and panicles	Cell membrane and nucleus	Enhances UV-B stress tolerance	[140]
OsbZIP48	Roots, leaf sheaths, stems, and panicles	Nucleus	Enhances UV-B stress tolerance	[140]

Table 1. Genes related to UV-B resistance in rice.

Gene	Expression Site	Subcellular Localization	Function	References
OsUVR8a	Leaves and leaf sheaths	Nucleus	Enhances UV-B stress tolerance	[130,134]
OsUVR8b	Leaves and leaf sheathst	Nucleus	Enhances UV-B stress tolerance	[130,134]
OsUGT706C2	Leaves	Plasma membrane and nucleus	Enhances UV-B stress tolerance	[138]
OsMYB44	Leaves	Nucleus	Enhances UV-B stress tolerance	[139]
OsMYB110	Roots, leaves, and leaf sheaths	Nucleus	Enhances UV-B stress tolerance	[139]
OsRLCK160	Roots, leaves, veins, leaf sheaths, stems, and panicles	Cell membrane and nucleus	Enhances UV-B stress tolerance	[140]
OsbZIP48	Roots, leaf sheaths, stems, and panicles	Nucleus	Enhances UV-B stress tolerance	[140]

2.6. Heavy Metal Stress

With the rapid development of agriculture and industry, various heavy metal elements such as arsenic (As), cadmium (Cd), mercury (Hg), and lead (Pb) have increasingly infiltrated soils through the use of pesticides, fertilizers, mining activities, and illegal wastewater discharges. These metals are becoming significant factors that affect crop quality and yield. In natural environments, the heavy metal stress on soil is often the result of the combined effect of multiple heavy metal pollutants.

Studies have shown that Cd is highly mobile in the environment, capable of diffusing through soil, water, and other media, and accumulating in organisms through the food chain, thus causing long-term damage to ecosystems (Table 2). Human activities such as urban waste disposal, metal smelting, mining, production of metal products, and the use of cadmium-containing phosphate fertilizers increase the concentration of cadmium in the environment, posing a carcinogenic risk to human health [141]. Cd disrupts the balance of essential elements in plants by replacing metal ions in cellular proteins, interfering with the normal absorption of key metals such as copper (Cu), iron (Fe), and zinc (Zn), leading to continuous damage to plant tissues [142]. Cd not only inhibits plant growth but also significantly reduces plant biomass. In rice, this manifests as reductions in root length, plant height, and leaf length, with plants being more sensitive to higher cadmium concentrations. Cd accumulation also obstructs photosynthesis and respiration, disrupts metabolic pathways, and severely impacts the plant’s growth, physiological functions, and metabolic processes [143,144].

The effects of heavy metals on rice are closely related to their concentration levels. Studies have found that high concentrations of cadmium (75–100 μmol/L) significantly inhibit rice seedling growth, reducing plant height by 14.6–21.9% and dry weight by 10.1–18.4%. Cd primarily accumulates in the roots, severely affecting rice quality [145]. Similarly, high concentrations of lead (1.2 mM) significantly inhibit plant height, tiller number, panicle number per plant, number of spikelets per panicle, and panicle length, as well as dry biomass and thousand-grain weight. Lead exposure induces oxidative stress, increasing hydrogen peroxide accumulation, activating antioxidant enzyme systems, altering the activity of CAT and SOD, and increasing superoxide anion (O₂⁻) levels. This leads to a significant reduction in total protein content, affects photosynthesis, and causes chlorophyll content to decrease, severely impacting rice growth, yield, and physiological metabolism [146].

The toxic effects of some heavy metals on rice also depend on their chemical forms. Mercury, a highly toxic heavy metal, has toxicity that is closely linked to its chemical form. The two main forms of mercury are inorganic mercury and methylmercury, with methylmercury (MeHg) being the most harmful form to plants and humans. This form of mercury is more easily absorbed by rice and accumulates in rice grains, posing a risk to human health through the food chain [147]. When rice is grown on mercury-contaminated soil, mercury accumulates in various organs, with the highest concentrations found in the roots, followed by the husk, stem, leaf, and seeds. As a result, the roots suffer the most significant toxic effects, which negatively impact rice yield [148].

The harmful effects of heavy metals on rice are multifaceted. As inhibits rice growth and development, leads to decreased biomass and yield, disrupts the photosynthesis and antioxidant systems, interferes with nutrient uptake and metabolism, and alters gene expression and proteome. These effects are interconnected and severely affect rice growth, yield, and quality [149]. Among the heavy metals, As and chromium (Cr) are particularly harmful to rice, with the most significant effect being the inhibition of growth and a substantial reduction in yield [150].

Rice responds to toxicity under heavy metal stress through a series of physiological responses, while related gene expression regulatory mechanisms play an important role in rice heavy metal tolerance, involving the regulation of multiple heavy metal ion transport and detoxification-related genes. Certain members of the Heavy Metal ATPase (HMA) family, such as OsHMA2 and OsHMA3, play pivotal roles in the transport and detoxification of Cd [151,152,153]. Natural Resistance-Associated Macrophage Protein (NRAMP) family proteins are involved in the transport of various metal cations, including Zn, Fe, Mn, Cu, Ni, Cd, and Pb [154]. Additionally, arsenate can enter cells via phosphate transporters like OsPHT1.1 and OsPHT1.8, while water channel proteins such as NIPs and Lsi1 are responsible for arsenate transport [155].

Transport proteins located on the vacuolar membrane are crucial for sequestering and detoxifying heavy metals. Members of the Cation Diffusion Facilitator (CDF) family, such as OZT1, transport Cd into vacuoles, facilitating its compartmentalization and thereby enhancing rice’s tolerance to heavy metals [156].

Under heavy metal stress, rice regulates the expression of auxin signaling-related genes (such as those in the YUCCA, PIN, and ABCB families) to promote the accumulation of auxin in key tissues, thus maintaining normal growth. For example, under copper stress, high levels of nitric oxide (NO) inhibit auxin levels in the root tip, leading to impaired root elongation [157]. Furthermore, ethylene plays a significant role in heavy metal responses. Stress often induces the upregulation of ethylene biosynthesis genes while suppressing cytokinin signaling genes. For example, mercury treatment induces the upregulation of ethylene biosynthesis genes such as OsACS2 and OsACO1 in rice [158], while chromium treatment increases the expression of EIN3 and EIN4 in roots [159]. The interplay between hormone signaling and MAPK signaling pathways regulates the activity of certain transcription factors, which are crucial for the plant’s response to heavy metal stress [160].

MicroRNAs (miRNAs) and transcription factors are also critical regulators in rice’s response to heavy metal stress [161]. Studies have shown that miR528 expression is upregulated under Cd stress, while the expression of most miRNAs decreases. Under As stress, certain miRNAs influence stress tolerance by regulating the antioxidant system [162]. Moreover, miRNAs play a role in physiological regulation by targeting and controlling the expression of key genes, such as miR395’s involvement in Cd detoxification. Transcription factors are also upregulated in response to stress signaling, enhancing rice’s adaptability through pathways like MAPK [161].

Under heavy metal stress, rice activates various mechanisms, including the activation of antioxidant enzyme systems to reduce free radical accumulation and protect cells from oxidative damage. Simultaneously, rice regulates root strategies for metal absorption and transport, limiting the accumulation of toxic elements in the plant (Figure 7). Studies have shown that the overexpression of OsHMA3 in indica rice significantly reduces Cd transport from roots to aerial parts, lowering Cd concentration in brown rice by 94–98%, near the detection limit, while also enhancing rice’s Cd tolerance [163]. Additionally, OsLCT2, a low-affinity cation transporter, limits the loading and transport of Cd into the xylem, reducing Cd accumulation in the aerial parts and seeds, while also affecting Zn transport and distribution, providing new genetic resources for reducing Cd content in rice [164].

OsZIP1, a transporter responsible for the detoxification of Zn, Cu, and Cd, is regulated by metal stress. Located on the plasma membrane and endoplasmic reticulum, OsZIP1 reduces metal accumulation by exporting metals, thus improving rice’s tolerance to metal stress [165]. Research has also shown that OsZIP5 and OsZIP9 cooperate in the absorption and homeostasis of Zn and Cd [166].

The overexpression of OsMT1e enhances rice growth under Cd stress, including the elongation of the aerial parts and roots, increased dry weight, and higher chlorophyll content, while promoting Cd accumulation in both roots and aerial parts. In contrast, RNA interference that suppresses OsMT1e expression increases plant sensitivity to Cd, reducing growth and Cd accumulation. This gene has potential applications in mitigating Cd pollution and its harmful effects on crops and human health [167].

The OsIRT1 gene encodes a protein localized to the cell membrane, primarily expressed in the roots. Studies have shown that OsIRT1, in cooperation with OsIRT2, is a major transporter for the absorption of Fe and Cd. In heterologous expression experiments, OsIRT1 exhibited Cd uptake functionality. In rice, the overexpression of OsIRT1 increases plant sensitivity to Zn and Cd, highlighting its critical role in Cd absorption [168].

Table 2. Genes related to heavy metal resistance in rice.

Gene	Expression Site	Subcellular Localization	Function	References
OsHMA3	Roots	Vacuolar membrane	Transports Cd	[163]
OsLCT2	Leaves, roots	Endoplasmic reticulum	Transports Cd	[164]
OsZIP1	Roots	Plasma membrane and endoplasmic reticulum	Transports Zn, Cu, and Cd	[165]
OsZIP5	Roots	Plasma membrane	Transports Zn and Cd	[166]
OsZIP7	Roots	Plasma membrane	Transports Cd	[169]
OsZIP9	Roots	Plasma membrane	Transports Zn and Cd	[166]
OsMT1e	Roots	Nucleus	Increases Cd tolerance	[167]
OsIRT1	Roots	Plasma membrane	Transports Fe and Cd	[168]
OsIRT2	Roots	Plasma membrane	Transports Fe and Cd	[169]
OsNramp1	Leaves, roots	Plasma membrane	Transports Cd	[170]
OsNramp2	Leaves, roots	Vacuolar membrane	Transports Cd	[171]
OsNramp5	Roots	Plasma membrane	Absorbs Cd and Mn	[172]

Table 2. Genes related to heavy metal resistance in rice.

Gene	Expression Site	Subcellular Localization	Function	References
OsHMA3	Roots	Vacuolar membrane	Transports Cd	[163]
OsLCT2	Leaves, roots	Endoplasmic reticulum	Transports Cd	[164]
OsZIP1	Roots	Plasma membrane and endoplasmic reticulum	Transports Zn, Cu, and Cd	[165]
OsZIP5	Roots	Plasma membrane	Transports Zn and Cd	[166]
OsZIP7	Roots	Plasma membrane	Transports Cd	[169]
OsZIP9	Roots	Plasma membrane	Transports Zn and Cd	[166]
OsMT1e	Roots	Nucleus	Increases Cd tolerance	[167]
OsIRT1	Roots	Plasma membrane	Transports Fe and Cd	[168]
OsIRT2	Roots	Plasma membrane	Transports Fe and Cd	[169]
OsNramp1	Leaves, roots	Plasma membrane	Transports Cd	[170]
OsNramp2	Leaves, roots	Vacuolar membrane	Transports Cd	[171]
OsNramp5	Roots	Plasma membrane	Absorbs Cd and Mn	[172]

3. Mechanisms of Rice Responses to Abiotic Stress

The response mechanisms of rice to abiotic stresses are complex and diverse. At the same time, there is a certain degree of commonality in rice’s response to various abiotic stresses, primarily involving regulation at the physiological and molecular levels. Understanding these mechanisms will enhance our ability to improve rice survival in unfavorable environments and provide strong theoretical support for agricultural production. The mechanisms by which rice responds to abiotic stress are described below.

3.1. Physiological and Biochemical Responses

Under abiotic stress conditions, rice cells activate a range of response mechanisms, resulting in significant changes in osmotic potential [39,173]. Some of these changes, such as the substantial accumulation of soluble sugars and proline, contribute to maintaining cellular homeostasis. However, other alterations, like elevated levels of MDA, disrupt osmotic equilibrium and exacerbate cellular damage. In high-salt environments, plants produce large amounts of MDA, which damages lipids in the cell membrane, leading to structural impairment and reduced membrane fluidity. When membrane integrity is compromised, the selective permeability of the cell membrane is disrupted, resulting in an imbalance in the exchange of substances between the inside and outside of the cell. Ions and small molecules within the cell may leak out abnormally, while harmful substances from the external environment can enter in large quantities. This disrupts the stable ion concentration and osmotic pressure inside the cell, ultimately destroying the osmotic balance and impairing normal cellular functions. In severe cases, this can lead to cell death.

Soluble sugars play dual roles under stress: they regulate osmotic pressure and protect macromolecular structures while aiding in the repair of cellular damage [174]. In response to stress, plant cells often exhibit a marked increase in soluble sugar content [175], which strengthens their stress tolerance. Generally, higher soluble sugar levels correlate with enhanced resistance to adverse conditions.

Proline, an essential osmotic regulator, accumulates extensively in rice cells under stress [176,177]. Not only does it help rice adapt to adverse conditions, but it also promotes plant growth and recovery and increases rice yields. Known for its high solubility and low toxicity, proline effectively mitigates water loss by increasing intracellular osmotic pressure [178]. Additionally, other amino acids also bolster stress resistance through diverse mechanisms. For instance, γ-aminobutyric acid (GABA), which accumulates under stress, interacts with aluminum-activated malate transporters and outward-rectifying K⁺ channels in guard cells, thereby enhancing drought tolerance [179]. Similarly, OsDIAT-mediated drought resistance is associated with the accumulation of branched-chain amino acids (BCAAs) [180].

MDA, a byproduct of lipid peroxidation in cellular membranes [181,182], increases with the severity of abiotic stress until it reaches a stable level [183,184,185]. When MDA levels plateau, it signifies severe oxidative damage to cellular membranes. Thus, MDA is commonly used as an indicator of membrane injury [186].

However, its accumulation can also activate certain adaptive responses that help rice mitigate stress damage and sustain growth. Abiotic stress also triggers excessive accumulation of ROS, including hydrogen peroxide (H₂O₂), superoxide anions (O₂⁻), and hydroxyl radicals (OH⁻) [187,188]. Excess ROS disrupt cellular membrane structures and react with proteins, nucleic acids, and lipids, ultimately leading to cell death. To combat ROS accumulation, plants rely on an antioxidant enzyme system, which includes SOD, CAT, peroxidase (POD), and APX. These enzymes convert ROS into less reactive substances, mitigating their toxic effects. During the initial stages of stress, antioxidant enzyme levels increase to enhance detoxification capacity. However, when the stress intensity exceeds cellular tolerance, enzyme structure and expression are inhibited, causing antioxidant enzyme levels to decline. Consequently, antioxidant enzyme activity typically follows a “rise-then-fall” pattern [181]. Higher antioxidant enzyme activity is directly associated with improved plant stress tolerance [189].

Effective functioning of antioxidant enzyme systems under different types of abiotic stresses is critical for rice’s adaptive capacity to adversity. Moreover, ascorbic acid (Asc) plays a crucial role in scavenging ROS and strengthening stress resilience. Under stress, plants accumulate large amounts of ascorbic acid, which eliminates free radicals and participates in the glutathione cycle to maintain a reductive cellular environment. This process further enhances the plant’s adaptability to adverse conditions [190,191].

Rice responds to stress by accumulating osmoregulatory substances (e.g., proline) and activating its antioxidant system. However, the elevated MDA levels indicate the risk of membrane damage. Moving forward, it is essential to analyze the dynamic balance mechanisms within the metabolic network to optimize the synergistic enhancement of stress tolerance and yield.

3.2. Molecular Mechanisms

When rice plants are exposed to external abiotic stressors, their cells initiate a range of responses to adapt and survive. These responses involve complex molecular mechanisms that regulate cellular processes such as osmoregulation, antioxidant defense, and stress signal transduction. At the molecular level, plants activate various stress-responsive genes, enzymes, and proteins to mitigate damage and maintain homeostasis. These mechanisms include the synthesis of protective molecules like proline, the activation of antioxidant enzymes to scavenge ROS, and the modulation of ion transport systems to maintain cellular integrity. Understanding these molecular pathways is essential for improving stress tolerance and enhancing rice resilience to unfavorable environmental conditions. Below is a brief overview of the key molecular mechanisms involved in rice’s response to abiotic stress.

3.2.1. Transcription Factors

Plant-specific transcription factors (TFs) play crucial roles in mediating responses to environmental stimuli and regulating hormone signaling pathways by modulating the expression of downstream target genes under stress conditions. Key transcription factor families involved in plant stress responses include NAC, bZIP, MYB, and Ethylene-responsive factor/dehydration-responsive element-binding (ERF/DREB), which enhance stress tolerance by fine-tuning the expression of stress-responsive genes [192].

NAC transcription factors are multifunctional, not only regulating plant growth and development but also responding to diverse stress conditions. These TFs are characterized by a conserved NAC domain at the N-terminus and a transcriptional activation domain at the C-terminus, enabling them to mediate endogenous hormone signaling pathways under abiotic stress [111]. For example, NAC transcription factors enhance stress resilience by modulating the synthesis and accumulation of plant hormones such as GA and ABA. OsNAC15 activates ABA biosynthesis, enhancing rice tolerance to salt and drought stress [112], while OsNAC120 improves drought resistance by harmoniously regulating the expression of GA- and ABA-related genes [113].

The bZIP transcription factor family is distinguished by two functional domains: a basic region for DNA binding and a leucine zipper domain for dimerization. For instance, OsbZIP72 binds to the promoters of downstream target genes, promoting the accumulation of soluble sugars under stress conditions and modulating hormone-related signaling pathways and endogenous hormone levels, thereby boosting stress tolerance [114].

Similarly, MYB transcription factors recognize and bind to specific sequences in downstream gene promoters through their unique repeat motifs, thereby regulating stress-responsive gene expression. ERF/DREB family members, characterized by one or more AP2/ERF domains, bind to the promoters of target genes to modulate their expression, playing pivotal roles in abiotic stress responses [13].

In summary, although the molecular mechanisms of these transcription factor families vary, they collectively enhance rice adaptability to adverse conditions by regulating phytohormone synthesis and signaling pathways. This regulation improves stress resilience, ensuring better survival and yield under challenging environmental conditions.

3.2.2. Hormone Signaling Pathways

Plant hormones are essential organic signaling molecules that play indispensable roles in plant growth, development, and stress tolerance. The hormone levels within these signaling pathways are regulated by various factors, including ROS-calcium ion (Ca²⁺) signaling, upstream transcription factors, hormone receptors, and interactions with other hormones.

Abscisic acid (ABA) is a crucial phytohormone that regulates stress tolerance [193]. ABA levels inversely correlate with plant growth rates. Acting as a signaling molecule, ABA regulates the expression of stress-responsive genes. Its transport depends on ABA transporters such as ABCG17 and ABCG18, which conjugate ABA with glucose to form an inactive form (ABA-GE) via UDP-glucosyltransferase activity [194]. Under abiotic stress, the expression of ABA transporters is suppressed, releasing free ABA to rapidly activate stress responses [195]. Prolonged or intensified stress leads to increased ABA accumulation [196]. Exogenous ABA can also enhance stress tolerance, but its effectiveness depends on concentration, application timing, and location. For example, applying ABA at 10 mg/L to the roots during the seedling stage yields optimal cold tolerance in rice [197,198].

During drought and salt stress, ABA further enhances tolerance by regulating associated signaling pathways. For instance, ABA mediates the interaction between SnRK2-type protein kinase SAPK9 and MADS-box transcription factor OsMADS23, increasing the transcriptional activity of OsMADS23. This interaction regulates the expression of downstream genes such as OsNCED2, OsNCED3, OsNCED4, and OsP5CR, which are associated with ABA biosynthesis and soluble sugar accumulation, thereby enhancing drought and salt tolerance in rice [199]. The bZIP family member OsbZIP72 also modulates ABA levels by binding to the promoter of OsHKT1, a high-affinity potassium transporter gene, activating ABA-responsive elements, and enhancing stress tolerance [200]. Moreover, OsWRKY5, through ABA activation, binds to the W-box sequence of the OsMYB2 promoter, suppressing OsMYB2 expression and downstream ABA signaling genes, thereby modulating stress responses [201].

GA are critical for rice growth and development, particularly during seed germination and shoot elongation. GA exists in two primary forms: bioactive and inactive. Only bioactive forms function as phytohormones [202]. While GA-related stress signaling pathways are well-studied in Arabidopsis, research in rice remains limited [203,204].

JA, a lipid-derived phytohormone, is primarily found in reproductive organs and flowers [205]. JA plays a role in mitigating salt, drought, heavy metal, and ultraviolet (UV) stresses. Under abiotic stress, JA enhances antioxidant enzyme activities to improve oxidative stress tolerance. Additionally, JA regulates stomatal closure, restores chlorophyll levels, and increases proline accumulation, further boosting stress tolerance [206].

Cytokinins (CKs) regulate stem cell integrity and cell proliferation in plants. CKs primarily exist in maize in the form of zeatin, which includes trans-zeatin and cis-zeatin isomers [205,207]. Mutants with CK deficiency exhibit enhanced abiotic stress tolerance. CK signaling involves histidine phosphotransfer proteins and transcription factors, which act as CK receptors.

Ethylene (ET), a gaseous phytohormone, regulates various aspects of plant growth, including fruit ripening, root growth inhibition, and cell division. It also plays essential roles under abiotic stresses such as temperature, salt, and drought [208]. ET signals are perceived by receptors like OsRTH1 and OsCTR2 on the endoplasmic reticulum membrane, activating two major pathways: the receptor-CTR2-OsEIN2-OsEIL1 pathway and the recently identified MHZ1-AHP1/2-OsRR21 phosphorylation pathway. In the absence of ethylene, receptors activate CTR2, suppressing MHZ1 and these pathways; ethylene binding inhibits CTR2, releasing the suppression and promoting pathway activation [209]. AP2/ERF family members such as OsDREB1A and OsDREB1B regulate stress-responsive gene expression under low-temperature stress [200,210]. The overexpression of AP2/ERF family genes also influences the accumulation of osmolytes like proline and soluble sugars, further enhancing stress tolerance in rice [211,212].

Under abiotic stress, phytohormones interact to modulate plant responses. For example, DELLA protein SLR1 interacts with JA signaling repressor OsJAZ9. High OsJAZ9 expression increases endogenous GA levels, suggesting antagonism between JA and GA. JA and ABA also influence CK biosynthesis, reciprocally regulating stress responses [213,214].

3.2.3. Non-Coding RNAs and Epigenetic Regulation

MicroRNAs (miRNAs) are synthesized in the nucleus, where miRNA genes are transcribed by RNA polymerase II. These transcripts bind to DICER-like 1 (DCL1) and are processed into double-stranded miRNA precursors. After cytoplasmic transport, mature miRNAs are cleaved by ARGONAUTE (AGO) proteins to form functional miRNAs, which play significant roles in rice stress tolerance [215].

miRNAs are closely linked to regulatory pathways under abiotic stress [216]. For instance, in drought stress, miRNAs modulate signaling pathways of ABA and GA, interacting with transcription factors or target genes. miR156 regulates SPL genes, miR167 modulates auxin signaling genes, and miR159 is involved in the ABA-MYB signaling pathway [51]. Additionally, miRNAs such as miR168a respond to salt stress by targeting downstream genes like OsAGO1 and OsRCI2-5 [216].

miRNAs also contribute to temperature stress responses in rice. For example, miR2871b negatively regulates cold tolerance, with its expression significantly reduced under low-temperatures [217]. In heat stress, various miRNAs regulate transcription factors, protein folding, and hormone signaling to improve thermotolerance.

For salt stress, miRNAs such as miR156 and miR396b regulate antioxidant pathways and ROS scavenging by interacting with POD and SOD [21,218,219]. Thus, miRNAs, alongside epigenetic mechanisms, play critical roles in fine-tuning rice responses to abiotic stresses.

4. Applications of Abiotic Stress Research in Rice Breeding

In addition to the field strategies mentioned earlier for mitigating the impact of stress on rice, advancements in biotechnology have made the development of superior rice varieties a key breakthrough in enhancing rice’s resistance to abiotic stresses.

4.1. Traditional Breeding Techniques

In plant breeding, traditional methods primarily rely on selecting rice varieties with desirable traits for hybridization. By screening through multiple generations, new varieties with stress-resistant characteristics are developed. This process involves identifying stress-resistant genes and crossing parent plants with the desired resistance traits, integrating these genes into the offspring. For instance, drought-resistant wild rice varieties are crossed with high-yielding but drought-sensitive cultivated varieties. Through genetic recombination, the offspring may retain high-yield traits while inheriting drought-resistant genes. Traditional breeding techniques also include family selection, recurrent selection, backcrossing, and induced mutations [220]. These methods have been used to identify rice varieties exhibiting favorable traits under abiotic stresses. However, these traditional methods are time consuming and their outcomes are not always predictable.

4.2. Molecular Breeding-Related Technologies

With the advancement of molecular biology techniques, modern plant breeding has become more efficient through molecular MAS. By identifying molecular markers closely associated with stress resistance traits, breeders can more accurately select plants with the desired genes, increasing breeding efficiency and success rates.

In-depth research on abiotic stress response genes has led to the development of molecular markers tightly linked to these genes. In rice breeding, these markers enable early screening of breeding materials for stress resistance, significantly improving breeding efficiency and shortening the breeding cycle for stress-tolerant varieties. For example, molecular markers can be used to select rice individuals carrying specific stress-resistant genes, thus reducing the workload and time costs associated with field screenings. Molecular breeding techniques, including genome-wide association studies (GWASs) and molecular MAS, offer higher accuracy compared to traditional breeding methods. GWAS has been widely used to investigate the relationship between crop phenotypes and genotypes [221,222,223].

In rice, GWAS has revealed the genetic and biochemical foundations of various traits. For instance, researchers used 184 recombinant inbred lines (RILs) and 295 Geng germplasms to perform QTL analysis and GWAS on root length during germination under alkaline stress, successfully identifying a major QTL—qAT11 [224,225]. In another study, using 428 rice materials for genome-wide association analysis and gene-based haplotype analysis, 90 loci significantly associated with alkaline tolerance were identified, and eight important candidate genes were selected. Among these, OsWRKY76 may play a negative regulatory role in rice’s alkaline tolerance during germination, providing genetic and haplotype resources for rice alkaline tolerance breeding [226].

Many important agronomic traits in rice are regulated by quantitative trait loci (QTLs), which have become key targets for molecular marker-assisted selection breeding. For example, through QTL-seq and RNA-seq analyses, OsSAP16 was identified as a candidate gene for qRSL7 under salt stress [227]. These studies provide new insights into breeding salt-tolerant rice varieties and exploring salt tolerance mechanisms [228].

Saltol, a major salt-tolerant QTL from the Indian rice variety Pokkali, was successfully transferred to the IR29 variety using MAS, resulting in the development of the salt-tolerant variety FL478. This salt-tolerant locus has also been successfully introduced into other major rice varieties such as Rassi, PB1, and PB1121, significantly enhancing their salt tolerance [229,230,231,232,233].

4.3. Gene Editing Techniques

With the maturation of CRISPR/Cas9 technology, gene editing has made significant strides in plant breeding. The CRISPR/Cas9 system, as a cutting-edge genome editing tool, plays a crucial role in crop genetic improvement and trait optimization. To improve rice’s resistance to both biotic and abiotic stresses, enhancing its tolerance to unfavorable environments has become a key breeding strategy. Gene editing technologies now make it possible to develop high-yielding rice varieties that meet consumer demands while also being more resilient.

For example, using CRISPR/Cas9 multi-gene editing technology, researchers mutated the GS3 and GL3.1 genes controlling rice grain shape. The resulting double-mutant gs3 gl3.1 rice exhibited plumper and rounder grains, with significant improvements in grain appearance, fullness, yield, and stress resistance compared to the single-mutant gs3 variety [234]. Additionally, knocking out the OsPAO5 gene resulted in significantly larger rice grains and increased yield, as well as enhanced stress tolerance and embryo elongation [235]. Knocking out the OsSNB gene led to significant increases in grain length, width, and 1000-grain weight, highlighting OsSNB’s critical role in rice grain shape formation [236].

Furthermore, CRISPR/Cas9 technology has also been applied to improve herbicide resistance in rice. By single-base editing, researchers precisely targeted the OsALS1 and OsACC genes, which are associated with herbicide sensitivity, and successfully generated herbicide-resistant rice varieties such as Nanjing 46 [237].

4.4. Integrated Breeding Approaches

By combining various breeding strategies, such as trait selection, trait tracking, and salt tolerance selection, and scientifically optimizing planting conditions, it is possible to breed rice varieties that are high-yielding, high-quality, and resistant to multiple stresses such as disease, drought, cold, and salinity. Since rice often faces multiple abiotic stresses in production, understanding rice’s response mechanisms to different combinations of stresses is crucial for breeding varieties with comprehensive stress resistance. Developing rice varieties that are both drought- and salt-alkali-tolerant can enhance land use efficiency in such regions and improve food production, which is vital for ensuring global food security and combating climate change.

With the advancement of molecular biology technologies, modern breeding techniques such as genome editing and molecular marker-assisted selection have made rice variety improvement more precise and efficient. Recently, the application of gene stacking technology has successfully improved rice’s tolerance to multiple abiotic stresses. For example, genetically modified rice AC39020, which carries genes from Pennisetum glaucum (Pg47), Pea (p68), P. glaucum Heat Shock Factor4 (PgHSF4), and Pseudomonas Aldo Keto Reductase1 (PsAKR1), exhibited superior growth characteristics under salt stress, accelerated aging, temperature fluctuations, and oxidative stress [232,238].

In addition, rhizosphere-promoting bacteria (PGPR) have been shown to effectively mitigate the impact of abiotic stresses on rice growth. These microorganisms reduce the migration of heavy metals, alleviate their toxic effects on rice, and improve rice tolerance through the production of plant hormones or by promoting nutrient absorption [239].

5. Challenges and Future Prospects

5.1. Challenges

As discussed earlier, plant responses to abiotic stresses involve complex and multifaceted mechanisms. Even under a single stress, multiple transcription factors, signaling pathways, and genes within the plant cell are intricately regulated. These signaling pathways and mechanisms vary considerably between plant species, each exhibiting distinct characteristics. Therefore, to comprehensively understand the signaling pathways and regulatory mechanisms involved in plant responses to a particular abiotic stress, significant research investment and cross-disciplinary collaboration are required. This is not a task that can be accomplished by a few individuals but rather demands collective intelligence and shared resources for exploration.

An even greater challenge lies in the complexity of natural environments, which far exceed the controlled conditions of laboratory experiments. In the field, plant growth is influenced by multiple environmental factors interacting simultaneously, and the “gardener” of nature cannot be entirely replicated in experimental settings. For instance, plants in the field may simultaneously endure salt stress and high-temperature stress, or UV stress may occur alongside heat. Additionally, the same field may experience different types of abiotic stresses at different times. These dynamic and fluctuating environmental conditions often lead to situations where rice mutants, selected for tolerance to a single stress under controlled conditions, may exhibit unexpected or even completely lost stress-resistance traits when grown in real-world field environments.

While laboratory research is invaluable, its outcomes must ultimately serve practical agricultural production, rather than remain at a theoretical level. The goal is to breed stress-resistant rice lines and superior varieties that improve stress tolerance, increase yield, and enhance rice quality, ultimately benefiting field cultivation practices.

On the other hand, integrating transgenic plants obtained through genetic transformation into everyday life still faces significant challenges. While countries such as the United States, Canada, and Australia have waived pre-market approval and labeling requirements for genetically modified (GM) crops, the situation is markedly different in places like Japan, New Zealand, and Norway, where the development of GM food crops has been exceptionally slow and, in some cases, heavily restricted. Overall, the legal acceptance of GM crops remains limited [240].

5.2. Future Prospects

Traditional breeding techniques face several limitations, such as low genetic stability, limited heritability, long breeding cycles, and high costs. To overcome these challenges and address discrepancies between gene function and field performance, optimizing breeding methods and integrating multidimensional resource data is essential. With the rapid advancement of technology, biological research has entered the multi-omics era, providing a solid foundation for stress-resistance gene studies in rice. For example, GWAS can efficiently identify genes associated with complex traits in rice, providing precise data to guide the breeding of stress-resistant varieties.

Multidisciplinary breeding strategies represent a key direction for advancing precision breeding. By combining modern techniques such as molecular MAS, GWAS, genome editing technologies (e.g., CRISPR/Cas9), and QTL mapping, the accuracy and genetic stability of rice breeding can be significantly improved. These methods also help shorten the breeding cycle for stress-resistant plants, overcoming the limitations of traditional approaches. Additionally, using gene stacking techniques, multiple stress-resistant genes can be integrated into the same genetic locus via co-transformation or re-transformation, further enhancing rice’s resistance to abiotic stresses [241].

At the same time, it is essential to promote the establishment of stress-resistant germplasm resource banks. Systematic screening and cultivation of high-quality stress-resistant rice germplasm will provide robust support for future breeding programs and sustainable agricultural development.

6. Conclusions

Plant growth and development are regulated by internal factors such as genetics and hormones, while external environmental conditions also play a crucial role. Extreme environmental conditions, such as extreme temperatures, drought, and salinization, which are forms of abiotic stress, severely impact plant growth and may even threaten plant survival. Abiotic stresses, particularly those affecting rice, have become a significant challenge to global food security. Rice growth, yield, and quality are often compromised by adverse soil and climate conditions, making research into the effects of abiotic stress on rice critical, especially for rice stress-resistance breeding.

Addressing abiotic stress issues not only helps improve crop resilience and reduce agricultural losses but also has profound implications for global food security and ecological balance. Modern breeding technologies, such as genetic breeding, genetic engineering, and biotechnology, can effectively enhance plant adaptability to stress, ensuring the sustainability of agriculture. Genetic breeding manipulations can be conducted in various rice varieties. Commonly used wild-type varieties for genetic modifications include Nipponbare, Zhonghua 11, 9311, and IR64. These varieties are favored due to their well-annotated genomes, clear genetic backgrounds, and strong tissue culture responsiveness, making them ideal for gene function studies and breeding applications. As climate change intensifies, developing rice varieties that can adapt to multiple abiotic stresses is becoming increasingly important.

In the future, research on rice stress resistance will depend on identifying key genes and utilizing modern molecular breeding techniques like CRISPR/Cas gene editing and marker-assisted selection to further improve rice resilience and yield. Integrating multi-omics technologies, such as QTL mapping, GWAS, and transcriptomics, will provide precise molecular insights for rice breeding. In summary, research on abiotic stress is crucial for improving rice resistance, stability, yield, and for mitigating the impacts of climate change, making it an indispensable component of rice breeding efforts.