Search Results (5,361)

Rice false smut (RFS), caused by Ustilaginoidea virens (teleomorph: Villosiclava virens), is a devastating fungal disease that severely impacts global rice production by reducing both yield and grain quality. While the mating-type gene UvMAT1-1-3 is known to regulate both sexual and asexual reproduction in U. virens, its regulatory mechanism remains unclear. In this study, an interacting protein of UvMAT1-1-3, a putative O-methyltransferase (UvPomt), was identified using yeast two-hybrid screening, and its interaction was further confirmed by co-localization microscopy. A quantitative reverse transcription PCR (qRT-PCR) analysis showed a significant up-regulation of UvPomt expression during the early infection stage of U. virens. Functional characterization revealed that ΔUvPomt mutants exhibited reduced fungal pathogenicity, vegetative growth, conidial production, and stress adaptation. Furthermore, a Western blot analysis revealed that the UvMAT1-1-3 protein level was reduced in ΔUvPomt mutants, whereas the UvPomt protein level was elevated in ΔUvMAT1-1-3 mutants. Taken together, these findings suggest a potential reciprocal regulation between UvPomt and UvMAT1-1-3. Understanding UvPomt’s function could provide a potential molecular target for controlling RFS disease. Full article

MADS-box transcription factors have undergone in-depth investigations regarding their function in regulating the development of plant floral organs. Flower type mutants serve as critical biological models for investigating the regulatory mechanisms of MADS-box genes in floral organ development, while simultaneously constituting essential genetic resources for molecular breeding programs. In this work, we examined a lip-like sepal of the peloric mutant in Phalaenopsis ‘Huayang’, which exhibited changes in both the morphology and color of the sepals. Our cryo-SEM investigations revealed that the mutation type belonged to a sepal labellum-like variation in Phalaenopsis ‘Huayang’. Nine glycosylated anthocyanins were identified and their contents were significantly upregulated in the Se-red of mutant flowers. Transcriptomic analysis identified 9408 differentially expressed genes, including 4934 upregulated and 4474 downregulated genes. In addition, 57 MADS-box genes were identified and classed into five groups (Mα, Mβ, Mγ, MIKC*, and MIKC^C) according to a phylogenetic comparison with Arabidopsis homologs. Furthermore, 29 MADS genes were screened from the MIKC^C group, and these genes may play a crucial role in the regulation of floral organ development. Through real-time PCR analysis and protein interaction analysis, we identified three genes that were upregulated in the mutant, which may be involved in sepal development. The subcellular localization results demonstrated that three genes were found within the nucleus. Taken together, our results elucidated the molecular mechanism of sepal variation in Phalaenopsis ‘Huayang’. Our results could enhance our comprehension of the regulatory mechanisms underlying floral patterning and promote the molecular breeding process of Phalaenopsis. Full article

Volatile terpenoids (VTs) are key secondary metabolites that play dual roles as endogenous antioxidants and airborne signals in plants under abiotic stress. Their biosynthesis is orchestrated via the mevalonate (MVA) and 2-C-methyl-D-erythritol 4-phosphate (MEP) pathways, with metabolic plasticity regulated by transcription factors, phytohormonal crosstalk, and stress-responsive elements. Recent advances have revealed that VTs such as isoprene, monoterpenes, and sesquiterpenes help mitigate oxidative stress by scavenging reactive oxygen species (ROS) and modulating antioxidant enzyme systems. However, regulatory mechanisms of stress-induced VT emissions remain fragmented and species-dependent. This review synthesizes current knowledge of VT biosynthesis and emission under abiotic stress, highlights their antioxidant functions and regulatory architecture, and underscores their protective roles in redox homeostasis and stress signal transduction. By identifying key metabolic nodes (e.g., TPS, DXS and MYC2) and stress-responsive pathways, we propose potential molecular targets for the development of stress-resilient cultivars. The integration of VT-based traits into breeding strategies and production-oriented metabolic engineering offers promising avenues for improving crop performance, reducing oxidative damage, and supporting sustainable agricultural systems. Full article

The degeneration of germplasm is a key factor limiting the yield and quality of Gastrodia elata Blume. Sexual reproduction is a primary method to address this degeneration, while the number of flowers and capsules is directly related to sexual reproduction. However, the genetic mechanisms underlying the high flower/fruit-bearing traits in G. elata remain unclear. We first compared the quantitative and qualitative traits during the flowering to fruiting period of G. elata, including bolting height, flowering quantity, flowering time, fruiting quantity, capsule spacing, seed quality, etc. The natural materials were selected by multi-capsule and few-capsule for transcriptome analysis to screen the differentially expressed genes (DEGs); the candidate gene GePIF4 was suspected to regulate the formation of multiple flowers and fruits. It was confirmed that GePIF4 has multiple biological functions in the overexpression of transgenic lines, including increasing numbers of vegetative propagation corms (VPCs) and promoting the growth of G. elata. Through comparative transcriptomic analysis of EV and OE-GePIF4 transgenic lines, the transcriptional regulatory network of GePIF4 was identified, and transient expression of GePIF4 was demonstrated to significantly promote gastrodin accumulation. The dual-LUC assay and in vitro yeast one hybrid results showed that GePIF4 could directly bind to GeRAX2 to regulate multi-capsule formation, and GePIF4 could directly bind to GeC4H1 to promote gastrodin accumulation. Therefore, we elucidate the role of GePIF4 in multi-capsule formation and secondary metabolite accumulation, thereby laying the groundwork for the genetic improvement of G. elata germplasm resources. Full article

Testicular orphan receptors TR2 and TR4 serve as central regulators of erythropoiesis, orchestrating the entire continuum of erythroid progenitor cell proliferation, differentiation, and maturation. As core components of the direct repeat erythroid determinant (DRED) complex, they activate erythroid-specific transcriptional programs to dynamically control the spatiotemporal expression of globin genes. These nuclear receptors not only engage in functional interactions with key erythroid transcription factors GATA1 and KLF1 to coregulate erythroid differentiation and maturation but also recruit epigenetic modifier complexes such as DNMT1 and LSD1 to modulate chromatin states dynamically. Research has established that dysfunctions in TR2/TR4 are implicated in β-thalassemia and sickle cell disease (SCD): β-thalassemia is associated with the defective silencing of γ-globin genes, while in SCD, TR2/TR4 antagonizes BCL11A to reactivate fetal hemoglobin (HbF) expression. This review systematically dissects the molecular regulatory networks of TR2/TR4 in erythroid cells, interprets their dual regulatory properties across different stages of erythroid differentiation, and explores the therapeutic potential of targeting TR2/TR4 for treating erythroid-related disorders such as β-thalassemia and SCD, thereby providing novel directions for hematological disorder therapy. Full article

: Iron accumulation in the brain is widespread in Alzheimer’s disease (AD), the most common cause of dementia. According to numerous studies, too much iron triggers the development of neurofibrillary tangles (NFTs) and amyloid-β (Aβ) plaques, both of which accelerate the onset of AD. Iron sequestration and storage were disrupted by high iron, and the pattern of interaction between iron regulatory proteins (IRPs) and iron-responsive elements (IREs) was altered. The 5′-untranslated regions (5′-UTRs) of their APP mRNA transcripts have an IRE stem-loop, which is where iron influx enhances the translation of the amyloid precursor protein (APP). Iron regulated APP expression via the release of the repressor interaction of APP mRNA with IRP1 by a pathway similar to the iron control translation of the ferritin mRNA by the IREs in their 5′-UTRs. This leads to an uncontrolled buildup of redox active Fe²⁺, which exacerbates neurotoxic oxidative stress and neuronal death. Fe²⁺ overload upregulates the APP expression and increases the cleavage of APP and the accumulation of Aβ in the brain. The level of APP and Aβ, and protein aggregates, can be downregulated by IRPs, but are upregulated in the presence of iron overload. Therefore, the inhibition of the IRE-modulated expression of APP or Fe²⁺ chelation offers therapeutic significance to AD. In this article, I discuss the structural and functional features of IRE in the 5′-UTR of APP mRNA in relation to the cellular Fe²⁺ level, and the link between iron and AD through the amyloid translational mechanism. Although there are currently no treatments for AD, a progressive neurodegenerative disease, there are a number of promising RNA inhibitor and Fe²⁺ chelating agent therapeutic candidates that have been discovered and are being validated in April 2025 clinical trials. Future studies are expected to further show the therapeutic efficacy of iron-chelating medications, which target the APP 5′-UTR and have the ability to lower APP translation and, consequently, Aβ levels. As a result, these molecules have a great deal of promise for the development of small-molecule RNA inhibitors for the treatment of AD. Full article

The CorA/MRS2-type transporters represent a crucial family of magnesium ion transporters widely distributed in plants. Through comprehensive screening and alignment using the Phytozome database, we identified seven magnesium-related MdMRS2 Confirm the deletion of the “Chinese Province” column in the address. genes in apple (MdMRS2-1 to MdMRS2-7), which were distributed across seven distinct chromosomes. Phylogenetic analysis classified these genes into five distinct clades. Tissue-specific expression profiles revealed the differential expression patterns of MdMRS2 members in different tissues such as the apple roots, stems, leaves, seedlings, seeds, flowers, and fruits. Among them, the expression level of MdMRS2-5 was the highest in fruits, while that of MdMRS2-6 was the lowest in seeds. Analysis of cis-regulatory elements in MdMRS2 promoter regions identified numerous light-responsive elements, MYB binding sites, and hormone-responsive elements, suggesting their transcriptional regulation may be influenced by related metabolic pathways or signaling molecules. qRT-PCR results showed that the relative expression levels of all genes were significantly upregulated compared with CK under M3 treatment, while there were no significant differences in other treatments. Among them, the upregulation of MdMRS2-7 was the most significant, increasing by 142% compared with CK. Notably, all MdMRS2 genes were significantly upregulated under 4 mmol·L⁻¹ MgSO₄ treatment. Subcellular localization experiments conducted in tobacco leaves confirmed the membrane and cytoplasmic distribution of these transporters, consistent with bioinformatic predictions. These genes may become candidate genes for subsequent functional studies. This work will provide a basis for future research on the response mechanism and function of the MRS2 gene family in response to magnesium stress. Full article

The Nuclear factor erythroid 2-related factor 2 (NRF2) Neurogenic locus NOTCH homolog protein (NOTCH) crosstalk has emerged as a critical regulatory axis in the progression of solid cancers, especially lung, affecting tumor growth and resistance to therapy. NRF2 is a master transcription factor that orchestrates the cellular antioxidant response, while NOTCH signaling is involved in the cell–cell communication processes by influencing the patterns of gene expression and differentiation. Although frequently altered independently, genetic and epigenetic dysregulation of both NRF2 and NOTCH pathways often converge to deregulate oxidative stress responses and promote tumor cell survival. Recent findings reveal that the NRF2/NOTCH interplay extends beyond canonical signaling, contributing to metabolic reprogramming and reshaping the tumor microenvironment (TME) to promote cancer malignancy. Emerging scientific evidences highlight the key role of biochemical and metabolomic changes within NRF2–NOTCH crosstalk, in contributing to cancer progression and metabolic reprogramming, beyond facilitating the adaptation of cancer cells to the TME. Actually, the effects of the NRF2–NOTCH bidirectional interaction in either supporting or suppressing lung tumor phenotypes are still unclear. This review explores the molecular mechanisms underlying NRF2–NOTCH crosstalk in lung cancer, highlighting the impact of genetic and epigenetic deregulation mechanisms on neoplastic processes, modulating the TME and driving the metabolic reprogramming. Furthermore, we discuss therapeutic opportunities for targeting this regulatory network, which may open new avenues for overcoming drug resistance and improving clinical outcomes in lung cancer. Full article

Small RNAs (sRNAs) are pivotal in regulating gene expression and are involved in a diverse array of biological processes. Among these, microRNAs (miRNAs) and phased small interfering RNAs (phasiRNAs) have been extensively investigated over the past decades. We conducted an in-depth analysis of deep sequencing data from the gymnosperm Ginkgo biloba, encompassing sRNA, transcriptome, and degradome libraries. Our analysis identified a total of 746 miRNAs and 654 phasiRNA precursor (PHAS) loci, with 526 (80%) of the PHAS loci predicted to be triggered by 515 miRNAs (69%). Several miRNA-PHAS modules, particularly the miR159/miR319-PHAS module, were found to potentially regulate reproductive development by targeting GAMYB genes and triggering phasiRNA biogenesis. The miR390-PHAS module appears to be involved in flavonoid biosynthesis by targeting key enzyme genes such as chalcone synthase (CHS) and anthocyanin synthase (ANS). Through target gene identification and coexpression analysis, we uncovered two distinct models of complex regulatory networks: growth-related factors like ARF and GRF seem to be regulated exclusively by miRNAs (Model 1), while certain disease resistance-related genes are predicted to be regulated by both miRNAs and phasiRNAs (Model 2), indicating diverse regulatory mechanisms across different biological processes. Overall, our study provides a comprehensive annotation of miRNA and PHAS loci in G. biloba and elucidates a post-transcriptional regulatory network, offering novel insights into sRNA research in gymnosperms. Full article

Elephant grass (Cenchrus purpureus) is an important forage crop hindered by high lignin content. Although MYB transcription factors (TFs) regulate lignin biosynthesis, their roles in elephant grass remain unclear. In this study, we identified 247 CpMYB TFs through whole-genome bioinformatic analysis of elephant grass and classified them into 23 phylogenetic subgroups. Among them, 233 were mapped to 14 chromosomes, and 14 to unanchored contigs. Gene structure, conserved motifs, and domain analyses revealed subgroup-specific conservation and CpMYB proteins dominated by random coils and α-helices. Gene duplication and selection pressure analyses indicated that segmental duplication predominantly contributed to family expansion. Transcriptome analysis identified 48 CpMYB genes differentially expressed in internodes at least one of three developmental stages, with promoters containing various growth-, phytohormone-, and stress-related cis-elements. Additionally, nine CpMYB genes were consistently differentially expressed across all three stages, and predicted protein–DNA interaction suggested that four of them (CpMYB094, CpMYB131, CpMYB145, and CpMYB148) potentially regulate key lignin biosynthetic genes, including 4-coumarate:CoA ligase 1 (4CL1), hydroxycinnamoyl transferase (HCT), caffeoyl-CoA O-methyltransferase 1/7 (CCoAOMT1/7), and reduced epidermal fluorescence 3 (REF3). However, their regulatory functions require further experimental validation. Overall, this study characterizes the CpMYB family in elephant grass and highlights their potential roles in lignin biosynthesis. Full article

Tumor cells alter lipid metabolic pathways to meet their demands for energy and membrane biosynthesis. Despite its crucial role in tumor cell growth, survival, and metastasis, the mechanisms underlying tumor cell lipid metabolic reprogramming remain poorly understood. Pre-B-cell leukemia transcription factor 3 (PBX3), a member of the PBX family, could promote tumorigenesis; however, whether it is involved in tumor lipid metabolic reprogramming remains unknown. Herein, we found that PBX3 significantly promotes tumor growth by enhancing lipid accumulation in HCC cells. By assessing the effect of PBX3 on the expression levels of lipid metabolism-related genes, we found that PBX3 could positively regulate the expression of 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR), a rate-limiting enzyme in the cholesterol biosynthesis pathway. Mechanistically, we revealed that PBX3 could directly bind to the −167/−151 region of HMGCR promoter, thereby increasing its transcriptional activity and, subsequently, its expression level. This leads to the increase of HCC cell cholesterol biosynthesis and, eventually, to the increase of the in vivo tumorigenic potential. Collectively, our research revealed an unprecedented regulatory mechanism of cholesterol metabolism in HCC cells through PBX3 positive regulation on HMGCR expression levels. These findings provide novel insights into tumor metabolic reprogramming and uncover a previously unknown physiological function for PBX3. Moreover, these results suggest the potential of targeting PBX3 as an anti-tumor therapeutic strategy. Full article

Early B-cell factor 1 (EBF1) is a crucial transcription factor that governs the development and differentiation of B lymphocytes. Furthermore, it is essential in developing multiple organs and tissues. The functional dysregulation of EBF1 expression is intricately associated with the occurrence, recurrence, and treatment resistance of B-lineage acute lymphoblastic leukemia. In recent years, EBF1 has demonstrated a more intricate and multifaceted role in solid tumors. It does not immutably adhere to the conventional classification of tumor suppressor genes. On the contrary, EBF1 is a flexible regulatory factor that exhibits diverse functional characteristics and regulatory models according to the different types of tumors and their microenvironment differences. This review elucidates the unique function of EBF1 in various solid tumors and associated signaling pathways, offering a theoretical foundation for a thorough comprehension of EBF1’s intricate roles in solid tumor development. Full article

In plants, ferric-chelate reductase (FRO) plays a critical role in mediating extracellular iron (Fe) reduction, a process essential for cellular Fe homeostasis and abiotic stress tolerance. However, the biological functions and regulatory mechanisms of FRO proteins in fruit crops remain poorly characterized. Here, six VvFRO genes were identified in the table grape cultivar ‘Yanhong’. Transcriptional analysis revealed that root expression of these genes was mainly induced under Fe deficiency, Fe depletion, NaCl stress, and PEG-induced drought stress, respectively, but remained unchanged by low temperature (4 °C) or heat treatment (45 °C). Among them, VvFRO3 exhibited the highest constitutive expression, predominantly in leaves, and was significantly up-regulated under Fe deficiency, Fe depletion, or NaCl treatment. Functional complementation assays demonstrated that heterologous overexpression of VvFRO3 in the Arabidopsis thaliana fro2 knockout mutant rescued its growth retardation phenotype, particularly under Fe-deficient conditions. This study advances our understanding of Fe uptake, transport, and homeostasis mechanisms in perennial fruit crops. Full article

Heart failure (HF) remains a leading cause of morbidity and mortality worldwide, driven by diverse pathophysiological mechanisms. Among its major risk factors, obesity has emerged as a lobal public health concern affecting individuals across all age groups. The rising prevalence of obesity significantly increases the risk of cardiovascular complications, including the development and progression of HF. MicroRNAs (miRNAs), small non-coding RNA molecules, have garnered attention for their regulatory roles in cardiovascular disease, particularly through post-transcriptional modulation of gene expression. This review highlights the involvement of miRNAs in key pathological processes observed in the obese heart, including cardiac remodeling, apoptosis, angiogenesis, inflammation, mitochondrial dysfunction, and myocardial lipotoxicity. Understanding how specific miRNAs and their targets contribute to HF in the context of obesity may inform the development of novel RNA-based therapeutic strategies for cardiometabolic disease. Full article

The expansion of the polyglutamine tract in ATXN1 contributes to the pathogenesis of SCA1. ATXN1 functions as a transcriptional regulator that interacts with multiple transcription factors, and transcriptional dysregulation has been observed in SCA1. In addition, splicing dysregulation has been identified in cells derived from SCA1 patients and model mouse tissues. Although ATXN1 binds to RNA and splicing factors, its direct involvement in pre-mRNA splicing remains unclear. Here, we demonstrate that ATXN1 regulates the alternative splicing of several minigenes. Using an Mbnl1 minigene, we found that neither expansion nor deletion of the polyglutamine tract affected ATXN1-mediated splicing regulation. Deletion analysis revealed that its splicing regulatory activity involves a central region of ATXN1, the AXH domain, and a nuclear localization signal in the C-terminal region. The AXH domain alone failed to exhibit splicing regulatory activity, whereas the central region demonstrated weak but significant splicing regulation. Full regulatory function required at least one of these regions, suggesting their redundant role in splicing modulation. Importantly, we newly identified the central region as mediating RNA binding. These findings suggest a novel role for ATXN1 in alternative splicing, providing new insights into the mechanisms underlying SCA1 pathogenesis. Full article