Multiple Signals Can Be Integrated into Pathways of Blue-Light-Mediated Floral Transition: Possible Explanations on Diverse Flowering Responses to Blue Light Manipulation

Abstract

Blue light (BL) plays a crucial role in regulating floral transition and can be precisely manipulated in controlled-environment agriculture (CEA). However, previous studies on BL-mediated flowering in CEA have produced conflicting results, likely due to species-specific responses and variations in experimental conditions (such as light spectrum and intensity) as summarized in our recent systematic review. This speculation still lacks a mechanistic explanation at the molecular level. By synthesizing recent advances in our understanding of the signaling mechanisms underlying floral transition, this review highlights how both internal signals (e.g., hormones, carbohydrates, and developmental stage) and external cues (e.g., light spectrum, temperature, nutrients, stress, and magnetic fields) are integrated into the flowering pathway mediated by BL. Key signal integration nodes have been identified, ranging from photoreceptors (e.g., cryptochromes) to downstream components such as transcription factors and central flowering regulator, FLOWERING LOCUS T (FT). This signal integration offers a potential mechanistic explanation for the previously inconsistent findings, which may arise from interspecies differences in photoreceptor composition and variation in the expression of downstream components influenced by hormonal crosstalk, environmental conditions, and developmental stage, depending on the specific context. This review provides novel molecular insights into how BL modulates floral transition through interactions with other signals. By systematically compiling and critically assessing recent research findings, we identify key research gaps and outline future directions, particularly the need for more studies in agriculturally important crops. Furthermore, this review proposes a conceptual framework for optimizing BL-based lighting strategies and exploring underexamined interaction factors in the regulation of flowering.

1. Introduction

As a critical developmental process, floral transition determines a plant’s reproductive success [1]. In horticultural crops, the regulation of floral transition—either through its promotion or inhibition—directly influences the timing of anthesis, thereby affecting harvest schedules and market availability. This transition is triggered by both intrinsic and extrinsic stimuli [2], with light being one of the most influential environmental cues.

Among the various wavelengths of light, blue light (BL; 400–500 nm) has been recognized for its significant role in regulating floral transition [3,4,5,6,7]. Like light-mediated flowering, BL influences this process through multiple pathways, including photoperiod pathway, light quality pathway (or shade pathway), and light quantity pathway (or photosynthesis pathway) [8,9,10]. The perception and transduction of BL signals to regulate floral transition in plants involve a complex and coordinated signaling network [9]. BL is detected by multiple photoreceptors, including cryptochromes (CRYs), phytochromes (PHYs), phototropins (PHOTs), and ZEITLUPE (ZTL) family proteins, and/or photosynthetic pigments such as chlorophylls and carotenoids [5,9,10,11]. This initiates signaling cascades that ultimately regulate the expression of genes and proteins responsible for floral induction [12].

In controlled environment agriculture (CEA), BL can be precisely manipulated using LED lighting systems. Blue LEDs have emerged as promising tools for adjusting flowering time. BL has been shown to promote flowering in model species such as Arabidopsis thaliana (hereafter Arabidopsis), like the effects of far-red (FR) light, partly due to its low phytochrome photostationary state (PPS) values, although BL can also act via CRY pathways, complementing FR effects [4]. Moreover, blue LEDs are generally more affordable and commercially more accessible than FR LEDs, making them a cost-effective alternative for promoting flowering [13]. In CEA, blue LEDs, either alone or in combination with other wavelengths, are increasingly employed to regulate flowering through various lighting strategies, including night interruption lighting, day extension lighting, supplemental lighting, and sole-source lighting, depending on desired flowering outcomes [6,7,13,14,15,16,17,18,19,20,21,22,23]. Despite their potential, studies investigating BL-mediated flowering time (under BL intensity of 0.5−100 µmol m⁻² s⁻¹, and duration of 4−15 h daily) have yielded inconsistent results even within the same species, such as chrysanthemum (Chrysanthemum morifolium;

Table 1. Diverse flowering response to blue light manipulation in chrysanthemum (Chrysanthemum morifolium).

Lighting Application	Lighting Spectrum	Lighting Intensity (µmol m−2 s−1)	Lighting Duration	Daytime Light (Intensity; µmol m−2 s−1)	Main Photoperiod	Flowering Response	Reference(s)
Night Interruption (NI)	B	10	4 h	White LED (180)	10 h/13 h	Did not inhibit flowering; delayed and reduced flower size	[19,24]
NI	B	0.8 or 3.3	4 h	Natural light in greenhouse	SD	Did not inhibit flowering	[25]
NI	B	39/20	4 h	White (150)/Blue or RB-LED (100)	12 h	No inhibition under white or RB-LED; strong inhibition under blue background	[26]
NI	B	10–40	4 h	White LED (300)	10 h or 13 h	40 µmol m−2 s−1 under 13 h inhibited flowering	[23]
NI	B-R, B-FR, R-B, or FR-B	10	4 h	White LED (180)	10 h	NI-R-B rather than NI-B-R induced flowering; NI-B-FR and NI-FR-B enhanced it more	[27]
NI	B	1, 15, 30	4 h	Natural light in greenhouse	9 h	30 µmol m−2 s−1 delayed flowering	[17]
NI	B	1.5	4 h	Natural light in greenhouse	9 h	Did not inhibit flowering	[16]
NI	BFR or RB	1.5	4 h	Natural light in greenhouse	9 h	Did not inhibit flowering	[16,28]
Day Extension (DE)	B	~20	Overnight or 14 h total	Natural light in shaded tunnel	Long day (LD)	Overnight DE inhibited flowering; 14 h DE did not	[29]
DE	B	10	4 h	White LED (180)	9 h	No delay in flowering	[19]
DE	B	~70	4 h	White fluorescent (70)	12 h	Did not inhibit flowering	[30]
DE	B	100	4 h or 13 h	RB-LED (100)	11 h	No inhibition of flowering	[6,31]
DE	B	40	4 h	RB-LED (100) or solar	11 h	Inhibited flowering in greenhouse, not in chamber	[21]
DE	B	60	4 h	RB, RBFR, or RBG-LED (180)	11 h	Inhibition of flowering with RBFR, not RB or RBG	[15]
Supplemental Lighting (SL)	B	10	4 h (pre-dark)	White LED (180)	13 h	Promoted flowering	[19]
SL	B	10–40	4 h (pre-dark)	White LED (300)	10 h/13 h	10–30 µmol m−2 s−1 promoted flowering under 13 h; 40 µmol m−2 s−1 inhibited flowering	[23]
SL	B	30	4 h every 1–7 d	White LED (300)	10 h/13 h	More frequent SL promoted earlier flowering under 13 h	[32]
SL	B	0.4–7.0	6 h or 15 h	Natural light in greenhouse	9 h	Higher BL (7.0 µmol m−2 s−1) delayed flowering; lower BL had no effect	[33]

Note: B = blue; R= red; FR = far-red; BL = blue light; RB = red + blue; RBG = red + blue + green; RBFR = red + blue + far-red; BFR = blue + far-red; B-R = 2-h blue followed by 2-h red; B-FR = 2-h blue followed by 2-h far-red; R-B = 2-h red followed by 2-h blue; FR-B = 2-h far-red followed by 2-h blue.

), let alone across different species, which have been summarized in a recent review by Kong and Zheng [7]. These discrepancies are likely due to variations in experimental materials and conditions, such as plant species, developmental stages, light regimes, and environmental factors. However, the speculation lacks an explanation in terms of molecular signalling mechanisms, highlighting the need for further research in this field.

Floral transition is governed by one of the most intricate signaling networks in plants [34]. To optimize reproductive success, plants integrate developmental and physiological cues with environmental signals to accurately determine the optimal timing for flowering [34,35]. Also, BL-mediated floral transition is influenced by a wide range of internal cues (such as hormonal signals, carbohydrate status, and plant age) and external factors (including other light wavelengths, temperature levels, nutrient availability, stress conditions, and magnetic field strengths) [36,37,38,39]. Given this complexity, a comprehensive understanding of the physiological mechanisms underlying the integration of other signals and BL into the flowering pathway is essential for the effective use of BL in regulating flowering time in CEA [40].

This review aims to provide a comprehensive overview of current knowledge regarding the molecular mechanisms underlying the integration of internal and external signals into the pathways of BL-mediated floral transition, encompassing both model species like Arabidopsis and agriculturally important crops, e.g., rice (Oryza sativa), particularly horticultural plants, such as tomato (Solanum lycopersicum) and chrysanthemum. Building upon this collection of research, we identify key signal integration nodes and propose potential explanations for the inconsistent findings reported in previous studies on BL-regulated flowering time. Additionally, we seek to provide a novel conceptual framework and establish a foundational understanding to guide the practical application of BL manipulation across diverse crop species in CEA. Finally, we highlight key knowledge gaps, explore underexamined interaction factors (e.g., magnetic field), and outline future research directions to advance the mechanistic understanding of BL-mediated floral transition.

2. Internal Signals

The internal signals affecting BL-mediated floral transition at least include phytohormones, carbohydrates, and growth stage/plant age. BL can affect these factors, or co-act with them, through shared pathway components to regulate floral transition.

2.1. Hormones

As major internal signal molecules, hormones play an important role in the control of flowering initiation, so the flowering responses mediated by light (including BL) inevitably interact with hormonal regulation networks in plants [41]. For example, in strawberries (Fragaria × ananassa), the promotional effect of the blue LED light on flowering was suggested to be related to lowered endogenous gibberellin (GA) levels and raised endogenous cytokinin (CTK) levels [42]. It is worthwhile to note that almost all hormonal signaling pathways are mediated by DELLA protein, a key floral transition regulator [38,43]. In Arabidopsis, the DELLA proteins can be considered as “balancers” that link various hormonal signals such as GA, Abscisic acid (ABA), CTK, Jasmonate (JA), and ethylene. However, the stability of DELLA proteins is mainly controlled by GA, and among hormone-controlled flowering, the GA pathway is considered a major flowering pathway [38].

2.1.1. Gibberellins (GAs)

GAs are key hormonal regulators of flowering, typically promoting floral induction, though their effects can vary by species, GA levels, and environmental conditions [38,44]. In Arabidopsis, GA is particularly important under non-inductive photoperiods, as GA-deficient mutants show delayed or abolished flowering, especially under short day (SD) conditions [38]. Differently, in chrysanthemum, SD-induced flowering is closely linked to increased GA levels and responsiveness [45]. At the molecular level, GA signaling promotes flowering primarily through the degradation of DELLA proteins (Figure 1), repressors of GA responses, via the GA receptor GA INSENSITIVE DWARF1 (GID1) [38,45,46]. DELLA proteins inhibit key flowering regulators such as CONSTANS (CO), FLOWERING LOCUS T (FT), and PHYTOCHROME INTERACTING FACTOR4 (PIF4), integrating GA signals with other flowering pathways, such as photoperiod and shade pathways [45,47,48,49].

The interaction between BL and GA to regulate flowering can first be reflected in the effect of low BL on GA biosynthesis and accumulation through shade avoidance response (SAR) (Figure 1). For example, the low- or modest-intensity BL from blue LED alone (PPS < 0.6) can promote plant flowering by deactivating phytochrome (PHY), especially PHYB (which can sense BL despite a primary photoreceptor of red or far-red light), as well as CRY1 to trigger SAR [14,50,51]. In petunia (Petunia × hybrida), sole-source lighting with blue LED light promoted flowering associated with much higher levels of GAs (especially GA1 and GA4), compared with red LED light [52,53]. However, the high level of active GAs in petunia grown under BL could be an indirect factor in the promotion of floral induction [54].

Also, BL photoreceptors interact with the DELLAs and GID1, the two crucial components of the GA pathway, and thus mediate GA signaling. In Arabidopsis, activated cryptochrome 1 (CRY1), a BL photoreceptor, physically interacts with DELLA proteins in a BL-dependent manner, leading to the inhibition of DELLA degradation [55,56,57]. Moreover, CRY1 interacts directly with GID1 in a BL-dependent but GA-independent manner, leading to the inhibition of the interaction between GID1 with DELLA proteins [55,56,57]. However, under low BL that act as a shade signal, the deactivated CRY1 cannot upregulate DELLA both directly and indirectly and thus promote flowering (Figure 1). Interestingly, another BL photoreceptor, FLAVIN-BINDING, KELCHREPEAT, F-BOX (FKF1), can negatively regulate DELLA protein stability under long day (LD) conditions in Arabidopsis and promote GA response in flowering [58]. Also, DELLA proteins can promote the expression of FKF1, and the suppression of FKF1 expression by GA relies on the presence of DELLA proteins. However, FKF1-DELLA interaction and FKF1-mediated protein degradation were not modulated by BL, but by the circadian clock. This suggests that FKF1-DELLA interaction integrates the photoperiod pathway and GA signaling to regulate flowering [58]. In chrysanthemum, instead of CRY, the atypical PHOTOLYASE/BLUE LIGHT RECEPTOR2 (PHR2), an identified BL receptor, interacted with CIB1 to form a complex in response to SD conditions, thus activating CmGID1B transcription to promote plant flowering under SD conditions [45].

Additionally, the GA and BL signals can be integrated through other components in the photoperiod pathway and the shade pathway. The CO antagonist, TEMPRANILLO1 (TEM1), has a role at the intersection of GA signaling and photoperiod pathway, since TEM1 inhibits GA production, and transgenic lines overexpressing TEM1 mimic GA-deficient mutants [59]. Also, the core circadian clock component, GIGANTEA (GI), has been reported to bind and stabilize DELLAs, resulting in a diurnally rhythmic expression of DELLAs, which contributes to the circadian clock gate of GA signaling in Arabidopsis [38]. For the shade pathway of low-BL-mediated flowering (i.e., CRY1/PHYB−PIFs−FT pathway) (Figure 1), shade conditions increase GA levels and lead to DELLA breakdown, enabling PIFs to activate downstream gene transcription to promote flowering [34,60].

2.1.2. Brassinosteroids (BRs)

BRs play a complex role in regulating flowering, acting through both promotive and inhibitory pathways depending on context and species [34,61]. In Arabidopsis, BR signaling primarily operates via the receptor BRASSINOSTEROID INSENSITIVE 1 (BRI1) and downstream transcription factors BRI1EMS-SUPPRESSOR 1 (BES1) and BZR1 BRASSINAZOLE RESISTANT 1 (BZR1), which modulate the expression of key flowering genes. BRs can promote flowering by repressing the floral repressor FLOWERING LOCUS C (FLC), thereby relieving inhibition on FT and SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1) [34,62]. Conversely, BES1/BZR1 can also activate FLC through interactions with FLOWERING LOCUS D (FLD) or recruitment of EARLY FLOWERING 6 (ELF6)/RELATIVE OF EARLY FLOWERING 6 (REF6) by BES1 to FLC chromatin, leading to delayed flowering [63,64,65]. Additionally, BR-activated BES1 can enhance FT expression through the BR ENHANCED EXPRESSION 1 (BEE1) transcription factor, further promoting floral transition [66].

The BEE1 is an important node in integrating BR and BL signals to regulate photoperiodic flowering [67,68]. It has been found that BEE1 is upregulated not only by BRs through BZR1, but also by BL to promote flowering in Arabidopsis [66]. Under BL, in addition to functioning as a coactivator of flowering genes, CRY2 also physically interacts with BEE1 and enhances its DNA-binding ability to further increase its transcriptional activity. Moreover, BEE1 protein is stabilized by BL independent of CRY2. The increased accumulation of BEE1 activates FT. Therefore, both BL and BRs can promote photoperiodic flowering through BEE1 [66].

The two key BR signal regulators, BES1 and BZR1, can also be mediated by BL through CRYs [41], despite the known subsequent effect on plant morphology rather than floral transition. It has been found that CRY1 interacts specifically with active BES1 and lead to both the inhibition of BES1 DNA binding activity and the repression of its target gene expression [69]. CRY1 negatively regulates the function of BZR1 through interfering with the DNA-binding ability of BZR1 and promoting the phosphorylation of BZR1 [70].

BR biosynthesis can also be affected by BL. Under shade, specifically from low BL, BRs, either alone or together with auxin, significantly contribute to shade avoidance responses (SARs) in plants [71,72], which potentially regulates plant flowering through the shade pathway (Figure 1). Upon shade light (both low BL and red/far-red ratio), transcription factors PIF4/5/7 are activated, and GA and BR levels are increased [73]. PIFs positively regulate BR biosynthesis by interacting with BES1, and the balance between BES1 and PIF4 levels defines whether BES1 acts as a repressor or an activator of BR biosynthesis genes [68,74].

2.1.3. Auxin

Auxin binds to its receptor complex, Transport Inhibitor Response 1/Auxin Signaling F-Box (TIR1/AFB) proteins, and the auxin−TIR1/AFB complex facilitates the degradation of AUX/IAA repressors and thus releases Auxin Response Factors (ARFs) to regulate the transcription of auxin-responsive genes, including the LFY gene, a positive floral integrator [75,76]. The ARFs, including ARF3, ARF4, and ARF8, are known to regulate flowering by modulating the expression of flowering time genes and interacting with microRNAs such as miR167 [76,77]

BL can interact with auxin to regulate flowering induced by shade (Figure 1). CRYs activated by BL interact with AUX/IAA repressor proteins, and this interaction inhibits the binding of AUX/IAA with the auxin receptor TIR1 and prevents the auxin signal [78]. CRYs serve as BL-dependent competitive inhibitors of auxin signaling [41]. However, the inactivation of PHYB and CRY1 by low red/far-red ratio and low BL, respectively, could lead to enhanced auxin signaling and SARs [73].

BL-mediated flowering is also related to altered expression of ARF genes through mediating microRNA levels (e.g., miR167), since ARFs have a critical role in plant growth and development, including flowering [79]. In Arabidopsis, compared to a fluorescent lamp or white LEDs, the blue LED promoted flowering, associated with increased miR167 expression, which enhanced transcription of ARF4 and ARF8 and reduced that of ARF2 [80]. Moreover, blue LED significantly induced the microRNA-mediated ARF gene silencing, which was involved in the activation of auxin-dependent genes [81]. It appears that the effects of BL on Arabidopsis are mediated by the auxin signaling pathway involving microRNA-dependent regulation of ARF gene expression [80]. A later study indicated that the alteration of microRNA activity by blue LED light is not the activation of CRYs, but the more complete inactivation of the PHYs, primarily PHYB, that can positively regulate the processing of mature miRNAs through PIFs [82]. The miR167-PHYB interaction has been also observed in other studies [83,84].

2.1.4. Jasmonate (JA)

Although the effect of JA on flowering time varies with the plant species and the JA concentration, generally, JA plays a negative role in the regulation of flowering [85]. The synthesis of the bioactive form of JA is catalyzed by the FAR-RED INSENSITIVE 219/JASMONATE RESISTANT 1 (FIN219/JAR1) [86]. The bioactive JA binds to its receptor, CORONATINE INSENSITIVE 1 (COI1), and triggers the degradation of JASMONATE ZIM-DOMAIN (JAZ) proteins, repressors of JA signaling, and thus allows transcription factors like Myelocytomatosis 2/3/4 (MYC2/3/4) to suppress FT expression [85]. Also, under stress conditions, JA promotes degradation of JAZs and enables TARGET OF EATs (TOEs), as APETALA2 (AP2)-like proteins, to repress FT expression, which in turn delays flowering [38,87]. Besides FIN219/JAR1, the COI1, MYC2/3/4, and JAZ appear to be three key components in the JA pathway to regulate flowering, since mutations in COI1 and MYC2/3/4, as well as overexpression of JAZ genes, result in an early-flowering phenotype [85,87]. Through FIN219/JAR1, the JA signaling affects activity of CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1), a downstream component of photoreceptors [86]. JA can suppress the formation of the COP1/SUPPRESSOR OF PHYA-105 (SPA) complex and can attenuate the function of nuclear COP1 [88]. In BL, FIN219-mediated export of COP1 from the nucleus acts in concert with CRY-mediated suppression of COP1/SPA complex [89]. However, JA enhances the CRY-FIN219 association in BL, thereby attenuating the CRY-mediated suppression of the COP1/SPA complex. This leads to enhanced COP1 activity and reduction of ELONGATED HYPOCOTYL 5 (HY5) levels in the nucleus, which promotes SAR in Arabidopsis seedlings [89]. Whether the interaction between JA and BL on COP1 would affect downstream genes in the flowering pathway is unknown.

The COI1, MYC2/3/4, and JAZ are also directly or indirectly involved in BL signal pathways. COI1 is required for the inhibition of SARs mediated by light, including BL [90]. MYC2 is a negative regulator of BL-mediated photomorphogenic growth [91], and MYC2 and SPA1 act redundantly in the dark and synergistically in BL to suppress photomorphogenesis [90]. JAZs can interact with DELLA proteins, which reduces JAZ-inhibition of their key target MYC2 and thus enhances the activity of AP2-like proteins (e.g., TOE1 and TOE2) [38]. JAZs can also target basic Helix-Loop-Helix 3/13/14/17 (bHLH3/13/14/17) in Arabidopsis, and these transcription factors antagonize the function of MYC2 or other JA-activated transcription factors to release JA-inhibited flowering [85,92]. Both AP2-like proteins (TOE1 and TOE2) and the bHLH proteins are involved in the BL signal pathway to regulate flowering [67,93,94,95,96].

As a regulator of PHYB-mediated SAS, PHYTOCHROME AND FLOWERING TIME 1 (PFT1) is a node of both the JA signal and light signal pathway [90]. PFT1 overexpression positively regulates JA-responsive defense gene expression and accelerates flowering. PFT1 has been shown to interact with COI1 and MYC transcription factors to positively regulate JA response [85].

2.1.5. Cytokinins (CTKs)

The effect of CTKs on flowering time varies with plant species, developmental stage, and environmental conditions. For example, in Arabidopsis, CTKs promoted flowering, especially under SD conditions [97,98], but in rice and maize (Zea mays), CTKs delayed flowering by suppressing the floral transition [99].

The processes in which CTKs are involved in floral transition processes are largely unknown. It has been found that TWIN SISTER OF FT (TSF; an FT homolog), FLOWERING LOCUS D (FD), and SOC1, instead of FT, are required for CTK-mediated flowering in Arabidopsis [97]. Also, in Arabidopsis, CTK oxidase/dehydrogenase and its suppressors ARABIDOPSIS HISTIDINE KINASES 2/3 (AHK2/3), which are also the CTK receptors, can affect flowering transition by affecting CTK content [98]. Additionally, in Arabidopsis, CTKs have been shown to upregulate the expression of APETALA 1 (AP1), a crucial gene for floral meristem identity [100]. In rice and maize, CTKs delay the expression of florigen genes by inhibiting Early heading date1 (Ehd1), an ortholog of the Arabidopsis CO [99].

HY5 is a point of convergence between BL and CTK signaling pathways in Arabidopsis. In addition to CRY1, CTKs also enhance HY5 protein stability by reducing its degradation mediated by COP1 in the presence of BL [101]. This stabilization would allow for a more robust response to BL, potentially mediating flowering through enhanced expression of flowering-related genes.

2.1.6. Ethylene

Ethylene plays a complex role in regulating flowering time, with its effects varying across different plant species and environmental conditions. For example, in many species, such as Arabidopsis and Pharbitis nil, ethylene signaling has been shown to delay flower development, but in some plants like pineapple (Ananas comosus) and urn plant (Aechmea fasciata), ethylene can promote flowering [102].

By binding to its specific receptors, ethylene reduces the activity of CONSTITUTIVE TRIPLE RESPONSE 1 (CTR1) and activates ETHYLENE INSENSITIVE 2 (EIN2), which leads to the stabilization of transcription factors like EIN3 and EIN3-LIKE 1 (EIL1) [103,104]. EIN3 and EIL1 can recruit histone modification factors to increase the expression of FLC and ultimately control ethylene-induced flowering delay in Arabidopsis [105].

There are interactions between ethylene and BL signaling pathways. For example, the ein2 mutants enhance both PHY- and CRY-dependent responses in a LONG1 (an ortholog of HY5)-dependent manner [106]. Also, ethylene shortens the circadian period through CTR1 and EIN3, conditional on the effects of sugar and requiring GI [107].

BL signaling components can also affect ethylene biosynthesis and levels. In peas (Pisum sativum), PHYA and PHYB are important in regulating ethylene levels in mature plants grown under light (including BL), and especially PHYA plays a prominent role in the downregulation of ethylene accumulation [106,108]. Also, in Arabidopsis, seedlings overexpressing PIF5 enhanced levels of the ethylene biosynthetic enzymes, 1-Aminocyclopropane-1-Carboxylic Acid Synthase 4 (ACS4) and ACS8, and produce 4-fold higher levels of ethylene, while reducing PHYB levels [109]. Additionally, the circadian clock controls the expression of ACS8 gene, and thus is probably responsible for the rhythmic changes in ethylene production [108].

2.1.7. Abscisic Acid (ABA)

ABA can promote or inhibit flowering, depending on environmental conditions and specific pathways. For example, in response to drought, ABA plays a significant role in Arabidopsis to induce early flowering by upregulating the expression of FT/TSF and SOC1 [110,111].

ABA regulates flowering time through multiple pathways. After biosynthesis, ABA binds to PYRABACTIN RESISTANCE/ PYRABACTIN RESISTANCE-LIKE/ REGULATORY COMPONENTS OF ABA RECEPTORS (PYR/PYL/RCAR) receptors, and the complex inhibits PROTEIN PHOSPHATASE 2Cs (PP2Cs) to release its suppression on SNF1-RELATED KINASE 2s (SnRK2s), which activate downstream components, including ABA-responsive TFs/ABA-responsive element binding factors (ABFs/AREB), and ABSCISIC ACID-INSENSITIVE 4/5 (ABI4/5) [110,112]. ABFs can activate SOC1 and thus promote FT expression and plant flowering, and ABI4/5 can promote FLC expression to inhibit FT expression and delay flowering.

The key node to connect ABA signaling pathways and the photoperiod pathway of BL-mediated flowering is GI, through which ABA regulates the recruitment of CO to the FT promoter, affecting FT expression, and potentially bridging the two stimuli to regulate flowering time [112,113,114]. BL can also affect GI to regulate flowering, indicating a potential interaction between ABA and BL in this response.

BL receptors, CRYs, modulate ABA signaling by repressing the expression of related genes such as ABIs [115], and this interaction may affect flowering time regulation. Also, BL and ABA signaling pathways converge at the level of transcription factors (such as bHLH48 and bHLH60), which regulate FT expression under LD conditions, and their activity is modulated by both BL and ABA-regulated DELLA proteins [68,116]. Additionally, BL treatment affects the balance of ABA and GAs [117], which plays a role in regulating flowering time.

It has been found that there is a molecular crosstalk between light signaling factors [such as HY5, COP1, PIFs, and B-box containing proteins (BBXs)] and ABA signaling components (such as the PYL receptors and ABI5), and in particular, ABI5 and PIF4 promoters are key ‘hotspots’ for integrating these two pathways [118]. However, how they integrate BL and ABA signaling to regulate floral transition is unknown.

2.2. Carbohydrates

Carbohydrates such as sucrose, fructans, starch, trehalose-6-phosphate (T6P) become abundant during floral bud development, despite varying carbohydrate types among species [111]. Also, exogenous application of sucrose at two different concentrations leads to an opposing effect on flowering, associated with different expression of floral integrator genes such as FT and SOC1 [119]. This suggests that carbohydrates are a part of the signaling mechanisms rather than only a general biochemical response of the plant to fuel reproductive growth [111].

For the light quantity pathway (or photosynthesis pathway) in BL-mediated flowering (Figure 2), carbohydrates from assimilates can act as part of a complex flowering signal [10]. The signals may differ depending on the BL amount. Starch metabolism was differentially regulated during the floral transition in response to light amount, and the distribution of sugar and starch is linked to the floral transition [68,120,121]. As important assimilates, free sugars are important signaling molecules to regulate plant flowering [122]. Exposure to different light amounts changes the sugar content in Ranunculus asiaticus, showing a positive correlation between early flowering and higher accumulation of free sugars [123]. As a signal to initiate flowering, the sugar type also varies with plant species [68]. For example, sucrose accumulation in the phloem increased during floral induction in Sinapis alba [124], but Arabidopsis has a higher demand for glucose and fructose than sucrose in the reproductive stage [125].

In addition to sucrose, glucose, and fructose, other carbohydrates may also play a role in the signalling of BL-mediated floral transition. For example, T6P accumulation is induced by sucrose, and T6P content is regulated in plants by T6P synthase (TPS) and T6P phosphatase (TPP) [126]. T6P signaling regulates flowering time in two different tissues: one is in the leaf where TPS1 is responsible for the induction of FT and TSF in response to photoperiod, and another one is in the shoot apex where the TPS1 and T6P signaling regulates the floral transition by the controlling the transcription level of SPL3/4/5 via the age pathway, independent of the photoperiod pathway [68,127]. This indicates that at least through T6P, the light quantity pathway can be integrated into other signal pathways.

Apparently, despite the early signal for flower induction, carbohydrates are strongly involved in BL-mediated flowering through the light quantity pathway, with interaction with other flowering pathways (e.g., photoperiod, hormone, and age pathway) as well [121]. For example, in the photoperiod pathway, sucrose affects the stability of circadian oscillator proteins, e.g., GI and ZEITLUPE (ZTL), and can mask the effects of ethylene on the circadian system in Arabidopsis [107]. Also, photoperiod can regulate starch metabolism differentially during the floral transition, and a disturbance in starch metabolism causes a change in flowering time [128,129]. CO may play a crucial role in the balance between free sugars and starch during floral transition by controlling the timing and the expression levels of GRANULE BOUND STARCH SYNTHASE (GBSS) [68,129,130]. Additionally, a recent study on chrysanthemum has found that plant flowering responds to the intensity of prolonged-photoperiod lighting (NI lighting) with BL, suggesting the co-regulation of carbohydrates from assimilates and differential photoreceptors in flowering [23].

Although carbohydrates from assimilates themselves are part of a complex flowering signal, a sufficient mass flow of carbohydrates can also contribute to the delivery of mobile flowering signals like FT [10]. In this case, besides sugar accumulation, carbohydrate transport may also be an important factor during the floral transition [68]. For example, chrysanthemum treated with exogenous sucrose showed a high induction of CmFTLs, FT homologs, and flowered early under both LD and SD conditions [131]. However, the precise molecular mechanisms by which light (including BL) quantity, potentially through carbohydrates from assimilates, modifies the length of the juvenile phase remain less clear.

2.3. Growth Stage/Age

Additional intrinsic signals that determine the readiness to flower are derived from the plant’s physiological outputs, such as plant age, size, or the number of leaves, which is called the age pathway [132]. Some of these signals consist of nutrient combinations and phytohormones, which move from leaves to the shoot apex to induce flowering, and other factors that can be part of the signal might be microRNA and proteins in phloem sap [132]. For example, GAs are generally considered to be plant age determination factors that confer “competence to flower”, due to their absolute requirement for flowering under non-inductive SD conditions [38]. More recently, it has been found that the miR156 expression is a more effective age-determination factor than GAs [38], given that the expression of miRNA156 decreases with age and it exerts a stronger and more direct control over the flowering network in the age pathway [44].

In the age pathway, the miR156 can regulate flowering through either the miR156−SPLs−FT pathway or the miR156−SPLs−miR172−AP2−FT pathway [44,133]. The miR172 promotes flower development, as most targets of miR172 are AP2-like proteins (e.g., TOEs), which negatively regulate FT [134]. The miR156 delays flower transition, because its targets are SPLs that directly or indirectly upregulate FT. For example, some target genes, SPL3/4/5, directly bind the FD-FT complex to activate flowering-related genes [133]. Other target genes, SPL9/10, can specifically bind to the promoter of miR172b, leading to miR172 accumulation, and thus promote flowering through the miR156−SPL−miR172−AP2−FT pathway [134]. Therefore, miR156 and miR172 are recognized as important components of the age pathway controlling flowering time in Arabidopsis [38]. In horticultural plants, miR156 and miR172 have also been identified to regulate flowering time. Over-expression of apple (Malus domestica) MdmiR156h in Arabidopsis reduced endogenous SPL9/15 expression and extended the juvenile phase, leading to later flowering [135]. Over-expression of apple MdmiR172e in Arabidopsis resulted in an early flowering phenotype [136].

The expression levels of flowering-regulatory microRNAs can be modulated by BL [137]. In Arabidopsis, BL upregulates miR172, but red light downregulates it [138]. At least four photoreceptors, PHYA, PHYB, CRY1, and CRY2, regulate miR172 levels [138,139]. In Arabidopsis, after BL stimulation, CRY1 and CRY2 mediate the expression of miR172 in a CO-independent manner to regulate photoperiodic flowering time [137,138]. In addition, BL duration can also affect miR172 abundance [139], since the miR172 abundance is regulated by photoperiod via GI-mediated miRNA processing [138,140]. Differing from miR172, after BL exposure, the expression levels of miR156/157 were moderately reduced, which correlated with an increase in their targets, SPL9 and SPL15, that encode transcription factors critical to the juvenile-to-adult transition and flowering [141,142].

The age pathway can be integrated with the shade pathway to regulate flowering. Shade signals repress miR156 genes transcription through direct binding of PIFs (e.g., PIF5), relieving SPLs, which promote flowering by directly binding FUL, LFY, and AP1 [44,143]. Also, FAR-RED ELONGATED HYPOCOTYLS 3 (FHY3) and FAR-RED IMPAIRED RESPONSE 1 (FAR1), two shade-responsive transcription factors involved in PHYA signaling, interact and regulate the DNA-binding activity of SPL3/4/5 [44,144]. However, how the integration of the two pathways affects BL-mediated flowering is still unclear.

3. Environmental Signals

BL-mediated floral transition can be influenced by various environmental signals. For example, light wavelengths other than BL, ambient temperature, mineral nutrition, and stress signals can also affect plant flowering [12,145], by sharing some pathway components with BL signals.

3.1. Other Light Wavelengths

In natural light or broad-spectrum lighting that contains BL, plants receive an integrated light signal via different photoreceptor systems from different light wavelengths rather than BL only. In this case, the flowering time of plants grown is determined, in part, by the balanced action of different photoreceptors exerting antagonistic or redundant effects on the floral transition [146].

Red light inhibits floral transition by activating PHYB under both LD and SD conditions [147], but its co-action with BL can affect flowering mediated by BL receptors [146]. For example, in Arabidopsis, the flowering-promotion function of CRY2 is dependent on the co-action of BL and red light [146]. Although BL is known to promote the flowering of Arabidopsis, the cry2 mutant flowered at the same time as the wild type in continuous BL, and flowered late in white light or blue + red light [148,149]. Possibly, PHYB mediates a red light-dependent suppression of floral initiation, whereas CRY2 mediates a BL-dependent inhibition of the PHYB function [146,148,149]. For the shade-regulated flowering pathway (Figure 3), red light can activate PHYB in suppressing low-BL-mediated SARs [73,150]. It has been found that several common components, such as PIF4 and HYPERSENSITIVE TO RED AND BLUE PROTEIN (HRB1), downstream of the photoreceptors, integrate red light and BL signals into flowering regulation [147]. However, PIF4 and HRB1 function in different flowering pathways: the shade pathway and photoperiod pathway, respectively.

FR light promotes flowering by activating PHYA, which suppresses PHYB function or promotes flowering independent of PHYB [147]. FR-promoted flowering may override BL-mediated flowering in the photoperiod pathway [18]. A moderately high-intensity BL has no apparent effect on the FR promotion of flowering in an LD plant, despite the attenuation of elongation growth by inhibiting SARs, possibly [18]. However, BL-mediated photoperiodic flowering can be affected by FR light, since the action of PHYA affects the function of CRY2 in the regulation of flowering time [146]. Although the cry2 mutant delayed flowering in blue + red light, it did not after the addition of FR light, suggesting the enrichment in FR light may stimulate PHYA activity in promoting flowering, which compensates (or overrides) the effect of the loss of the CRY2 gene [146,151]. Moreover, low-level BL can enhance low-red/far-red-induced SARs by increasing PIF5 abundance and attenuating high-level FR-induced gene expression of LONG HYPOCOTYL IN FAR-RED1 (HFR1), one of the SAR negative regulators (Figure 3), to increase expression of downstream genes such as FT [73,152].

The mechanism involved in the co-action of BL and red light or FR light includes photoreceptor interactions, direct signal convergence, indirect signal convergence, and inter-tissue signal interactions [153]. For photoreceptor interactions, CRY1 physically binds with PHYA and PHYB in vitro, and CRY2 directly binds with PHYB in plant cells [151,154]. For direct signal convergence, CRYs and PHYs both bind with the COP1/SPA complex, which targets CO for degradation [153]. For indirect signal convergence, CRYs and PHYs share common intermediates on PIFs in the regulation of SAR [153]. For the inter-tissue signal interaction, CRY2 antagonizes PHYB in the regulation of photoperiodic flowering [149]. PHYB is expressed mainly in mesophyll cells and partly in vascular tissue to regulate flowering time, but CRY2 promotes photoperiodic flowering solely in vascular tissue [155,156]. CRY2 stabilizes CO by inactivating the COP1/SPA complex, but PHYB mediates the degradation of CO independent of COP1, which regulates the accumulation of CO to promote the transcription of FT in the vascular tissue to initiate flowering [153].

Limited information is available on the interaction of light wavelengths other than red and FR light with BL to regulate flowering, except for green and UVB light. There are inconsistent reports about the interaction effect of green light and BL on flowering [157], possibly due to critique differences in experimental conditions or photoreceptor expression levels. In one experiment, green light caused inhibition of BL-induced flowering through its reversal regulation on CRY2 [158]. In another study, green light did not inhibit BL-mediated CRY2 activity and CRY2-CIB1 interaction, and thus the expression of the FT gene [159]. Also, as a shade signal, green light may reduce CRY1 activity to induce SAR and thus affect flowering [160,161,162]. UVB light causes a general delay in plant flowering, and the active UV RESISTANCE LOCUS 8 (UVR8), a UVB receptor, through interaction with COP1 and stabilization of HY5, regulates the expression of genes involved in BL signaling [34,163,164]. In addition, UVB may influence flowering indirectly via SAR pathways, though evidence remains limited. Low-level UVB can co-act with low BL to mediate SAR through modulating PIF4 and PIF5 activity [73], which may indirectly affect the floral transition.

3.2. Temperature

Temperature also affects plant flowering, and temperature for flower induction shares some regulatory networks with light signals, despite the employment of specific regulatory pathways [165]. Exposure to prolonged cold temperature (0−10 °C) induces flowering through a process called vernalization by silencing a key flowering repressor, FLC, which represses the expression of FT in the leaf and SOC1 in the shoot apex [34,145]. In addition to cold temperatures, moderately elevated temperatures (above 10 °C), which do not induce heat stress, generally promote flowering [145,165], although exceptions exist in day-neutral strawberries [166]. In Arabidopsis, flowering initiation at warm temperatures is mainly mediated by PIFs, especially PIF4 along with its orthologs (PIF5 and PIF7), through the PIFs-FT pathway [34,167,168,169]. In addition to FLC and PIFs, temperature can also affect many other pathway components in the signal network of BL-mediated flowering (Figure 4).

PIFs are key integrators of the flowering pathway mediated by both warm temperature and BL. In Arabidopsis, PIF4 is stabilized at warm temperatures under SD, and PIF4 can directly bind the FT promoter for FT induction in a temperature-dependent manner [167]. Similarly to PIF4, PIF5 can promote flowering at warm temperatures in SD, acting through the FT paralogue, TSF [170]. Also, the PIFs are regulated by PHYB and CRY1, which are involved in BL-mediated flowering through shade pathway [9]. Under shade conditions induced by low BL (i.e., BL with a low intensity and/or a low PPS), deactivated PHYB and CRY1 lift the suppression on the PIFs, which are able to promote flowering as a SAR [73,157]. PHYB, primarily a red or far-red light photoreceptor, can also sense BL [5] and change its activity under different background light conditions: PHYB is deactivated under blue LED alone (PPS < 0.6), but activated under blue + red LED (PPS > 0.8) [14,171], which deactivates and activates CRY1, respectively due to an interaction between CRY1 and PHYB [50]. Consequently, the different activities of either CRY1 or PHYB under blue LED alone and blue + red LED can affect the action of PIFs and thus the downstream pathway components to regulate flowering. For example, activated PHYB leads to the degradation of PIF4/5/7 and CO, but inactivated PHYB allows the induction of PIF4/CO and subsequently FT [167,168,170].

The function of the main BL photoreceptors, CRYs, is mediated by temperature. First, CRY-mediated flowering is influenced by ambient temperature [172,173]. It has been found that cry1 mutants flowered at a similar time to wild plants at 23 °C, but were delayed at 16 °C [174]. Also, CRY2 degradation occurs at lower temperatures (16 °C vs. 22 °C), which can be observed only under BL and not under red light or in the dark [175]. Furthermore, CRY2 directly participates in thermosensing [121,176]. It has been found that CRY2 interacts with INTERACTING SPLICING FACTOR 1 (CIS1) to regulate thermosensory flowering via FLOWERING LOCUS M (FLM) alternative splicing, which establishes a CRY2–CIS1–FLM signaling pathway that links flowering responses to both BL and ambient temperature [177]. The function of PHYs, the secondary BL photoreceptors, is also affected by temperature. For example, PHY-regulated flowering is influenced by ambient temperature. At 22 °C, phyB mutants displayed a pronounced early flowering phenotype, which correlated with elevated FT transcript levels [174], but at 16 °C, the phyB mutant phenotype is completely lost [173]. Also, it has been found that in cooler conditions, activated PHYE, and to a lesser extent, PHYD, perform a dominant role in suppressing flowering [174]. Furthermore, PHYB acts as a thermosensor by modulating its binding to promoters of temperature-responsive genes, particularly at night [34,178]. Unlike PIF4, the binding of PHYB to promoter regions of these genes was decreased at a warmer temperature [178]. Recent studies have shown that PHYs and members of the evening complex (EC), such as EARLY FLOWERING 3 (ELF3), present additive functions, making it likely that temperature information can be transmitted through the EC during flowering initiation [34,179]. PHYB is thus believed to act in both ‘light quality’ and ‘ambient temperature’ pathways, and it has been suggested that PHYB does so by regulating FT activity via an intermediate gene PFT1 [173,180].

Temperature can also interact with other BL receptors to mediate plant flowering. For example, ZTL, as a ZTL family protein and a BL receptor, is also involved in warm-temperature responses, and functions in temperature compensation of the circadian clock [176]. Intriguingly, ZTL and CRYs play opposite roles in thermo-responses; the mechanism and potential physiological significance of this remain to be explored [176]. Phototropins (PHOTs) can also sense temperature signals [181,182], but their direct role in floral induction remains unexplored, warranting further investigation.

In addition to photoreceptors, the circadian clock is mediated by the interaction between temperature and BL. In thermosensitive and photoperiodic flowering, internal rhythms established by the circadian clock must coincide with the externally imposed environmental variation of light and temperature, which is termed “external coincidence” [165]. BL and CRYs were reported to be required for ‘temperature compensation of the circadian clock’ [183]. In other words, CRY1 and CRY2 can maintain the pace of the circadian clock and circadian rhythmicity and show only small changes across a broad range of physiologically relevant temperatures [176,183]. It has been found that cry mutants displayed a longer circadian period at higher ambient temperatures (27 °C) in combined red light and BL [183]. Although both BL and temperature can regulate flowering through the circadian clock, they employ different pathways: GI is mainly involved in resetting the clock by light (including BL), while TIMING OF CAB EXPRESSION 1 (TOC1) is mainly involved in clock resetting by temperature [184]. Temperature also affects some core clock components, such as LUX ARRHYTHMO (LUX), ELF4, and ELF3, which are expressed in the evening and are members of the EC. The LUX acts as a flowering repressor [147,185], and its expression is activated by BL and red light through HY5 with a major effect for BL, and also by cold temperatures [186]. ELF4 stabilizes the EC, especially under elevated temperatures, and the ECs mediate heat-induced flowering by repressing PIF4 and thus inhibit FT [185]. ELF3 acts as a thermosensor, and during a warm night temperature, ELF3 decreases its activity and cannot stabilize the EC, thereby increasing PIF4 and PIF5 expression [169,185].

The COP1 also acts as an integrator of photoperiod and ambient temperature signaling. As a downstream component after photoreceptors in the BL signalling pathway, COP1 activity can be enhanced by elevated temperature, but this seems to be tissue-specific [86]. For example, COP1 is depleted at higher temperatures in the Arabidopsis rosettes, which stabilizes GI and accelerates flowering [187]. In other words, COP1 is more stabilized at low temperatures and accelerates GI turnover, which reduces the direct association of GI with the promoter of FT, and thus the COP1-triggered GI turnover delays flowering at low temperatures via a CO-independent pathway [187].

Temperature can also indirectly affect BL-mediated flowering through DELLA, FLM, SHORT VEGETATIVE PHASE (SVP), and microRNAs. Warm ambient temperatures can affect DELLA binding and thus the activity of PIF4, a positive regulator of FT and an important component of the shade pathway in BL-mediated flowering [38]. As negative floral integrators, FLM-β and FLM-δ are predominant at low and high temperatures, respectively, and they both interact with the floral repressor SVP to delay flowering by regulating SOC1, FT, and FLC genes [188,189]. Additionally, microRNAs such as miR156 and miR172 are induced by temperature signals [38], and they are key integrators of the flowering pathway mediated by age and BL, as mentioned in Section 2.3.

3.3. Nutrients

Generally, plants bloom faster under low mineral nutrition availability, although too poor nutrition delays blooming [190]. In Arabidopsis, nutrient scarcity promotes flowering via FT upregulation while suppressing vegetative growth [190]. Limited information is available about the effects of nutrients on BL-mediated flowering, except nitrogen (N) and phosphate (P).

3.3.1. Nitrogen (N)

N functions as a signal for modulating BL perception and the central circadian clock to interfere with photoperiodic flowering [121]. Under low N conditions, flowering is accelerated due to increased expression of genes acting in the photoperiod pathway [191]. Lower N levels induce photoperiodic flowering by at least two independent pathways (Figure 5).

N signaling can act as an input to the central circadian clock to regulate BL-mediated flowering via CRY1 [191]. Low-N conditions upregulate FERREDOXIN-NADP (+) OXIDOREDUCTASE (FNR1), enhancing CRY1 abundance, and increasing CO and FT expression [192]. In this case, CRY1 functions as an input signal to the circadian clock, promoting flowering by upregulating flowering output genes (e.g., GI and CO).

The low N conditions can also increase the expression levels of CO through FLOWERING BHLH4 (FBH4), potentially acting independently of CRY1. Low N prevents FBH4 phosphorylation, and the decreased phosphorylation promotes FBH4 nuclear localization [193]. Also, due to the decreased phosphorylation, FBH4 binds to the CO promoter and enhances the transcription of CO and its downstream gene FT to accelerate flowering. CO transcriptional regulation may be one of the crosstalk points where the information of N conditions is integrated into the flowering pathway, although the direct interaction with BL signaling is still unknown.

Additionally, N levels can regulate the flowering process by affecting the expression of FT, FLC, and SOC1 genes through other pathways [190,194,195]. For example, under high N conditions, the GA signaling pathway directly represses FT expression [193].

3.3.2. Phosphate (P)

In Arabidopsis, low P levels delay flowering, although low N levels induce flowering, due to an antagonistic relationship between P and N [190]. Transcript levels of FT, LFY, and AP1 are reduced, and FLC expression is increased in plants grown under low P conditions [121]. Because the P and GA levels are positively correlated, P starvation causes a reduction in bioactive GA levels, which causes DELLA accumulation [196]. Possibly, the delayed flowering by low P levels is at least through the GA signal pathway. The flowering response to low P levels can be affected by shade, where flowering in Trifolium subterraneum is delayed by a P deficiency, but is unaffected by that deficiency if plants are shaded [121]. Possibly, P levels can affect BL-mediated flowering through the shade pathway; however, so far, the direct interaction between BL and P levels on flowering is unknown.

3.4. Stresses

Abiotic stresses can affect plant flowering through interaction with the circadian clock [140]. The clock component, GI plays a central role in photoperiod sensing and also mediate responses to diverse stresses including drought, oxidative, osmotic, and cold stresses [140]. GI integrates environmental stress signals into the photoperiodic flowering pathway by modulating key flowering regulators like CO and FT.

Environmental stress conditions also influence flowering time by affecting the induction of CO and FT induction, partly through modifying the function of FBHs [95]. FBHs can be phosphorylated by signaling components linked to drought and pathogen responses, including ABA and mitogen-activated protein kinases, thereby upregulating CO transcription [95]. However, the direct molecular connections between these stress-induced modifications and BL-mediated flowering remain unclear.

Drought stress can lead to either accelerated flowering (drought escape) or delayed flowering (drought tolerance), depending on the species and environmental conditions [197]. Drought alters internal hormone levels, notably increasing ABA, which promotes flowering in many plants. Yet, in rice, drought suppresses florigen genes such as HEADING DATE 3a (Hd3a) and RICE FLOWERING LOCUS T 1 (RFT1), delaying flowering under both SD and LD conditions [121,198]. Moreover, drought interacts with photoperiodic flowering responses, with Arabidopsis flowering earlier under drought in LD conditions but later in SD conditions [199]. Despite these insights, there is currently no direct evidence linking drought stress to modulation of BL-mediated flowering pathways, representing a significant knowledge gap.

Salt stress generally delays flowering [200,201,202], as seen in Arabidopsis where salt stress upregulates PHOSPHATIDYLINOSITOL 4-KINASEγ3 (PI4Kγ3), which upregulates FLC and downregulates GI via stress-responsive kinases under salt stress, thereby postponing flowering [203]. Salt stress also causes rapid degradation of GI, suppressing CO and FT expression, key components of the photoperiodic flowering pathway [121,200,204]. Additionally, salt stress induces accumulation of DELLA proteins and reduces LFY transcript levels, implicating GA signaling and age-related pathways in floral repression [121]. However, the extent to which salt stress impacts BL-mediated flowering mechanisms remains to be elucidated.

3.5. Magnetic Field

CRY has been suggested to act as a magnetoreceptor [205]. After exposure to light, especially BL, CRY could form radical pairs that were involved in the magnetoreception [206]. The suppressed flowering by near-null magnetic field has also been observed in wild Arabidopsis plants under BL, especially with lower intensity (10 µmol m⁻² s⁻¹) and shorter cycle (6 h light/6 h dark), but not under red light at any intensity and cycles [39]. Also, the flowering time of cry1/cry2 mutants did not show any difference between plants grown in the near-null magnetic field and the local geomagnetic field under detected light conditions. This indicates that CRY is involved in Arabidopsis flowering mediated by the interaction between BL and a magnetic field [39].

The magnetic field can affect BL-mediated flowering by modifying the active state of CRY [205]. The 500 lT magnetic field enhanced the BL-dependent phosphorylations of CRY1 and CRY2, and the near-null magnetic field weakened the BL-dependent phosphorylation of CRY2 but not CRY1 [206]. Dephosphorylations of CRY1 and CRY2 in the darkness were slowed down in the 500 lT magnetic field but were accelerated in the near-null magnetic field. These results suggest that a magnetic field with a strength higher or lower than the local geomagnetic field affects the activated states of CRYs, which thus modifies the functions of CRYs [206].

The magnetic field can also affect BL-mediated flowering by modifying the subsequent signaling cascade, especially downstream flowering genes [205]. When the local geomagnetic field was eliminated, associated with delayed flowering time in wild Arabidopsis plants, the transcript level of PHYB was elevated, and that of CO and FT was reduced [205]. Also, transcriptions of flowering-related genes, LFY and SOC1, in wild-type plants were downregulated by the near-null magnetic field, while they were not affected by the near-null magnetic field in cry1/cry2 mutants [207].

In addition, magnetic fields can also affect BL-mediated flowering by modifying hormone levels mediated by CRY. Near-null magnetic field caused CRY-involved suppression of GA biosynthesis [207]. Moreover, near-null magnetic field affects CRY-mediated distribution of auxin, transcriptional regulation of auxin transporter genes, and expression of transcriptional repressor genes [208]. The signals of hormone changes caused by near-null magnetic fields result in a delay in flowering.

4. Future Direction

Floral transition is a vital physiological process in plants and plays a key role in determining the productivity and timing of many crops [1,209]. Although significant progress has been made in understanding the multiple signals involved in BL-mediated floral transition, further mechanistic research is necessary to deepen our knowledge in this area.

To date, much of our understanding has been derived from studies on the model plant Arabidopsis, a facultative LD plant, which may differ in BL-mediated flowering from other plant species, especially SD plants. For example, Arabidopsis plants flower earlier as day length increases, and its photoperiodic response is primarily governed by the GI–CO–FT module, with BL acting through CRYs to regulate CO stability and FT expression [210,211,212]. In contrast, SD plants such as rice and chrysanthemum exhibit strict daylength thresholds and often rely on distinct photoperiodic mechanisms, including sensitivity to the duration of darkness and the presence of night-break phenomena [21,211]. Furthermore, the molecular regulators that mediate BL responses in Arabidopsis may have divergent or even opposing functions in SD crops—for example, the rice CO homolog Hd1 represses flowering under LDs, inverting the Arabidopsis paradigm [211,212]. Additionally, the ability of BL to induce or inhibit flowering can vary dramatically among species, with SD plants often requiring precise spectral and temporal cues for floral induction that do not align with Arabidopsis responses [21,213].

While Arabidopsis has served as a valuable tool for molecular studies on flowering, it lacks agricultural relevance due to its small floral size and limited applicability. Recent findings highlight substantial differences in BL-mediated flowering responses between model and crop species: for instance, Arabidopsis shows strong sensitivity to BL, whereas tomato plants exhibit minimal response [213]. As a result, there is increasing interest in directly investigating BL-mediated floral responses in crop species, with the goal of translating this knowledge into practical applications for crop production and management. However, the relevant mechanistic research on agricultural/horticultural crops is still much less than that on the model plant, Arabidopsis, despite the differences between them (

Table 2. Comparison of some exampled aspects in blue-light-mediated floral transition between Arabidopsis and agricultural/horticultural species.

Aspect	Arabidopsis (Model Species)	Agricultural/Horticultural Species	Notes/Knowledge Gaps
Blue Light (BL) Effect on Flowering	BL promotes flowering through at least three pathways: photoperiod pathway, shade pathway, and photosynthesis pathway	Variable effects: BL can promote or delay flowering depending on species, developmental stage, and conditions	Mechanisms in crops often differ; direct links between BL and flowering regulators less characterized than in Arabidopsis
Key Photoreceptors	Cryptochromes (CRY1/2), phytochromes (PHY A/B), ZEITLUPE (ZTL) Family Members	Besides the common BL photoreceptors, species-specific photoreceptors, e.g., PHOTOLYASE/BLUE LIGHT RECEPTOR2 (PHR2) in chrysanthemum, Halotolerance protein (HAL3) in rice have been identified to regulate flowering	Functional diversity of BL photoreceptors across species requires further study
Role of GIGANTEA (GI)	Central integrator in photoperiod sensing and BL-mediated flowering; mediates stress responses affecting flowering	GI homologs are present but with potentially different roles. In chrysanthemums, CsGI can control photoperiodic flowering by shaping the gate for light induction of CsAFT, an anti-florigen	Extent of GI function conservation under BL and stress in crops is unclear
Role of CONSTANS (CO)	CO normally has a positive role in flowering induction in LD conditions by upregulating FLOWERING LOCUS T (FT) expression. However, CO also has a negative role in flowering induction in short day conditions	In rice, two key CO-LIKE transcription factors regulate flowering: HEADING DATE 1 (Hd1; an Arabidopsis CO ortholog) and EARLY HEADING DATE 1 (Ehd1; rice-specific). Ehd1 promotes florigen genes and is upregulated by BL in the morning. In contrast, Hd1 represses flowering under noninductive long-day (LD) conditions	The species-specific role of CO in BL mediated flowering is unclear
FLOWERING BHLH (FBH) Transcription Factors	Low nitrogen can mediate FBHs phosphorylation to regulate CO transcription	FBHs or homologs less studied; phosphorylation and BL regulation poorly understood	Direct evidence of BL impact on FBHs in both Arabidopsis and crops is lacking
Hormonal Interactions	Low BL influences Gibberellin (GA), auxin, and Brassinosteroid (BR) levels, and interacts with these hormones to regulate flowering through shade pathway	Hormonal responses to BL vary; e.g., blue LED promotes flowering in petunia with increased GA levels. However, in strawberries, the promotional effect of the blue LED light on flowering is related to lowered GA levels	Hormone-BL crosstalk in crops needs more detailed mechanistic insights
Stress Interaction with BL	Drought and salt stresses modulate flowering via GI, CO, FT, and DELLA; BL pathways intersect but direct links unclear	Stress effects on BL-mediated flowering poorly characterized	Significant knowledge gaps on how abiotic stresses affect BL-mediated flowering in crops
Photoperiod and BL Integration	Well-studied CRY2-CO-FT pathway integrates BL and photoperiod signals to regulate flowering in this LD plant	Diverse flowering responses to photoperiod-BL integration in crops belonging to different or similar photoperiodic groups	More comparative studies needed to clarify photoperiod-BL crosstalk in crops
Carbohydrate interaction	Arabidopsis has a higher demand for glucose and fructose than sucrose in the reproductive stage	Different carbohydrate requirements for crops. For example, sucrose accumulation in the phloem increased during floral induction in Sinapis alba	As a signal to initiate flowering, sugar type also varies with plant species. How BL light affects this variation among crop species is unknown

).

Even in model plants, further in-depth studies are required to fully elucidate the complex signaling networks regulating flowering. For instance, the molecular integration of temperature and light cues in flowering regulation has only recently been explored, leading to the discovery of novel signaling components that bridge these two environmental pathways [34]. However, the integration of BL signals with other environmental and internal cues remains poorly understood. Over the past few years, our laboratory has conducted preliminary studies on the co-action of BL with other light wavelengths and the interaction between photoreceptors involved in BL-mediated flowering, using Arabidopsis mutants and transgenic lines [50,51,214]. These investigations have helped explain some of our intriguing findings regarding BL-induced flowering and elongation responses in horticultural species under both pure and impure BL spectra [14,171,215,216,217].

In addition to photoreceptors, numerous downstream components have been identified in recent decades as key players in the integration of diverse signaling pathways to mediate floral transition. For example, bHLH transcription factors such as FBH1/2/3/4 promote early flowering by upregulating CO expression, either through the photoperiodic pathway or under low nitrogen conditions [37,67,193]. Similarly, another transcription factor, NO FLOWERING IN SHORT DAY (NFL), accelerates flowering in Arabidopsis specifically under SD conditions via a GA-dependent pathway [37,67,210]. However, whether these transcription factors are also involved in the BL-mediated flowering pathways remains unclear. Despite emerging insights, the molecular mechanisms underlying the convergence of the BL signal with other signalling pathways in floral induction remain largely elusive. A deeper understanding of signal integration and crosstalk is essential to explain the diverse flowering responses observed under BL manipulation and to optimize lighting strategies in response to microclimate factors within controlled-environment production systems.

5. Conclusions

BL-mediated floral transition is influenced by a wide array of internal and external signals, which can be integrated into the flowering pathways mediated by BL, highlighting the complexity of the underlying regulatory network. This review has identified key integration nodes in the pathway and provided novel insights into how BL regulates floral transition through interactions with other signals. This intricate interplay helps explain the previous diverse and sometimes contradictory flowering responses, which may result from differences in photoreceptor composition across species, and variation in the expression of downstream components influenced by experimental materials and conditions, depending on the specific context. This not only underscores the importance of carefully considering all interacting factors when applying BL to regulate flowering, but also proposes a conceptual framework for optimizing BL-based lighting strategies in the regulation of flowering. This review has also identified key research gaps, explored underexamined interaction factors (e.g., magnetic field), and outlined future directions. To fully harness the potential of BL in horticultural practices, further in-depth research is needed to elucidate the mechanisms involved in BL-mediated flowering not only in model species but also in agriculturally important crops.