https://orcid.org/0000-0003-2890-686X
Abstract
FAR-RED ELONGATED HYPOCOTYL3 (FHY3) and its homolog FAR-RED-IMPAIRED RESPONSE1 (FAR1) are transcription factors derived from transposases essential for phytochrome A–mediated light signaling. In addition to their essential role in light signaling, FHY3 and FAR1 also play diverse regulatory roles in plant growth and development, including clock entrainment, seed dormancy and germination, senescence, chloroplast formation, branching, flowering and meristem development. Notably, accumulating evidence indicates that the emerging role of FHY3 and FAR1 in environmental stress signaling has begun to be revealed. In this review, we summarize these recent findings in the context of FHY3 and FAR1 as integrators of light and other developmental and stressful signals. We also discuss the antagonistic action of FHY3/FAR1 and Phytochrome Interating Factors (PIFs) in various cross-talks between light, hormone and environmental cues.
Introduction
Light signals are perceived by a series of photoreceptors and transmitted to downstream transcription factors to initiate the alteration of nuclear gene expression that directs growth and developmental responses appropriate to environmental changes. To ensure plant survival and fitness under changing environments, light-regulated processes are coordinated with internal (hormones) and other external information (biotic and abiotic stresses). In the last decades, several light-signaling transcription factors have been identified and proved to possess the ability to integrate light with environmental and internal signals (Jing and Lin 2020). In this review, we focus on two light-signaling factors called FAR-RED ELONGATED HYPOCOTYL3 (FHY3) and its close homolog FAR-RED-IMPAIRED RESPONSE1 (FAR1) that are initially identified as essential components of phytochrome A (phyA)-mediated far-red light signaling in Arabidopsis thaliana (Hudson et al. 1999, Wang and Deng 2002). FHY3 and FAR1 encode Mutator-like transposase-derived transcription factors that have the ability to bind to promoters through FHY3/FAR1-binding site (FBS) element and regulate target gene transcription (Ouyang et al. 2011). In the regulation of phyA signaling, FHY3 and FAR1 directly promote the transcription of FHY1 and FHL, thereby controlling phyA nuclear accumulation and phyA responses (Lin et al. 2007). Besides their role in far-red (FR) light signaling, accumulating evidence reveals that FHY3 and FAR1 also play critical regulatory roles in other light environments such as red light, UV-B, diurnal light-dark cycles and reduced R/FR ratio conditions (Allen et al. 2006, Huang et al. 2012, Liu et al. 2019). More importantly, in addition to their primary function in light pathways, there are now extensive studies suggesting that other signaling pathways converge on FHY3 and FAR1 to regulate an increasing number of downstream processes including developmental processes like seed dormancy and germination, senescence, chloroplast development, branching, flowering and meristem development, as well as biotic and abiotic stress like defense response and nutritional deficiency.
Functional Profiling of FHY3 Target Genes
FHY3 and FAR1 are transcription factors with a conserved N-terminal C2H2 zinc-finger domain responsible for DNA binding and a C-terminal named after SWI2/SNF and MuDR transposases (SWIM) domain responsible for transcriptional activity. High-throughput sequencing approaches have identified many FHY3- and FAR1-regulated genes that control light signaling, growth, development and biotic and abiotic stress responses.
FHY3 and FAR1 play a role in the monochromatic light–signaling pathway and respond to the ambient light quality (high R/FR and low R/FR) change (Xie et al. 2020a). Comparison of differentially expressed genes in wild type and fhy3 or fhy3 far1 mutant seedlings revealed that, in high R/FR light conditions, FHY3 and FAR1 mainly regulate genes involved in circadian rhythm and photosynthesis. In contrast, in low R/FR, many phytohormone-related genes are enriched in FHY3/FAR1-regulated genes (Liu et al. 2019). By using the 28-d-old adult plants, loss-of-function mutant of FHY3 and FAR1 displayed the acceleration of senescence, such as necrotic lesions in leaves. Microarray analysis showed that FHY3 and FAR1 might negatively regulate the genes that respond to biotic and abiotic stresses, for example, WRKY and PR genes (Wang et al. 2016). Due to the defect of seed dormancy and germination in the fhy3 mutant, Liu et al. (2021) conducted RNA-seq analysis using the seed sample. They found that FHY3 suppresses RVE2 and RVE7 but promotes SPT during seed germination (Liu et al. 2021). FHY3 is also required for floral meristem determinacy and shoot apical meristem maintenance in the reproductive growth stage. RNA-seq analysis of FHY3-regulated genes in floral organs showed that many flower-specific genes were upregulated in the fhy3 mutant, suggesting a repressive role for FHY3 in flower development (Li et al. 2016).
In two studies, FHY3’s binding sites on the genome level were identified by chromatin immunoprecipitation (ChIP)-based sequencing. One study used seedlings growing under dark and far-red light conditions, while another examined its binding site in flowers (Ouyang et al. 2011, Li et al. 2016). Both studies uncovered thousands of genome loci, approximately half of which were assigned to genic promoter regions, confirming the role of FHY3 as a Transcription factor. In addition, Gene Ontology analysis of FHY3-bound genes showed that they are enriched in metabolism, development, and environmental and hormone responses. These observations support the role of FHY3 in multiple cellular activities and biological processes.
Regulation of FHY3 Transcriptional Activity
Several FHY3-binding partners have been identified through direct protein–protein analyses coupled with functional assays (Fig. 1, Table 1). These studies shed light on how the transcriptional activity of FHY3 and FAR1 is regulated within transcriptional modules that allow the integration of light and other cellular pathways.
Posttranscriptional and posttranslational regulation of FHY3 and FAR1. FHY3 and FAR1 binding proteins exert the regulation transcriptional activities of FHY3 and FAR1 by acting as coregulators (gray circles), inhibiting their ability to bind to DNA (green circles) or repressing their capacity to activate transcription (blue circles). In addition, light conditions and age signal also affect their protein accumulation.
The genes and proteins that interact with FHY3 and FAR1
| Categories | Gene and protein | Biological process | References |
|---|---|---|---|
| FHY3/FAR1-interacting promoters of target genes | RVE2, RVE7, and SPT | Seed dormancy and germination | Liu et al. (2021) |
| CCA1 and ELF4 | Circadian clock; flowering | Liu et al. (2020) and Li et al. (2011) | |
| FHY1 | FR signaling | Lin et al. (2007) | |
| PHR1 | Pi starvation responses | Liu et al. (2017) | |
| WRKY28 | Leaf senescence | Tian et al. (2020) | |
| ABI5 | ABA-regulated processes | Tang et al. (2013) | |
| SMXL6 and SMXL7 | SL signaling | Xie et al. (2020a) | |
| COP1 | UV-B signaling | Huang et al. (2012) | |
| FHY3/FAR1-interacting proteins | HY5 | Light signaling | Li et al. (2010) |
| TOC1 and CCA1 | Circadian clock | Liu et al. (2020) and Li et al. (2011) | |
| PIF5 and DET1 | Circadian clock; ABA signaling | Liu et al. (2020) and Xu et al. (2020) | |
| EIN3 and EIL1 | Ethylene regulated phosphate starvation responses | Liu et al. (2017) | |
| MYC2/3/4 and JAZs | JA signaling and shade avoidance | Liu et al. (2019) | |
| SPL9/15 | Branching | Xie et al. (2020a) | |
| SPL3/4/5 | Flowering | Xie et al. (2020b) |
| Categories | Gene and protein | Biological process | References |
|---|---|---|---|
| FHY3/FAR1-interacting promoters of target genes | RVE2, RVE7, and SPT | Seed dormancy and germination | Liu et al. (2021) |
| CCA1 and ELF4 | Circadian clock; flowering | Liu et al. (2020) and Li et al. (2011) | |
| FHY1 | FR signaling | Lin et al. (2007) | |
| PHR1 | Pi starvation responses | Liu et al. (2017) | |
| WRKY28 | Leaf senescence | Tian et al. (2020) | |
| ABI5 | ABA-regulated processes | Tang et al. (2013) | |
| SMXL6 and SMXL7 | SL signaling | Xie et al. (2020a) | |
| COP1 | UV-B signaling | Huang et al. (2012) | |
| FHY3/FAR1-interacting proteins | HY5 | Light signaling | Li et al. (2010) |
| TOC1 and CCA1 | Circadian clock | Liu et al. (2020) and Li et al. (2011) | |
| PIF5 and DET1 | Circadian clock; ABA signaling | Liu et al. (2020) and Xu et al. (2020) | |
| EIN3 and EIL1 | Ethylene regulated phosphate starvation responses | Liu et al. (2017) | |
| MYC2/3/4 and JAZs | JA signaling and shade avoidance | Liu et al. (2019) | |
| SPL9/15 | Branching | Xie et al. (2020a) | |
| SPL3/4/5 | Flowering | Xie et al. (2020b) |
The genes and proteins that interact with FHY3 and FAR1
| Categories | Gene and protein | Biological process | References |
|---|---|---|---|
| FHY3/FAR1-interacting promoters of target genes | RVE2, RVE7, and SPT | Seed dormancy and germination | Liu et al. (2021) |
| CCA1 and ELF4 | Circadian clock; flowering | Liu et al. (2020) and Li et al. (2011) | |
| FHY1 | FR signaling | Lin et al. (2007) | |
| PHR1 | Pi starvation responses | Liu et al. (2017) | |
| WRKY28 | Leaf senescence | Tian et al. (2020) | |
| ABI5 | ABA-regulated processes | Tang et al. (2013) | |
| SMXL6 and SMXL7 | SL signaling | Xie et al. (2020a) | |
| COP1 | UV-B signaling | Huang et al. (2012) | |
| FHY3/FAR1-interacting proteins | HY5 | Light signaling | Li et al. (2010) |
| TOC1 and CCA1 | Circadian clock | Liu et al. (2020) and Li et al. (2011) | |
| PIF5 and DET1 | Circadian clock; ABA signaling | Liu et al. (2020) and Xu et al. (2020) | |
| EIN3 and EIL1 | Ethylene regulated phosphate starvation responses | Liu et al. (2017) | |
| MYC2/3/4 and JAZs | JA signaling and shade avoidance | Liu et al. (2019) | |
| SPL9/15 | Branching | Xie et al. (2020a) | |
| SPL3/4/5 | Flowering | Xie et al. (2020b) |
| Categories | Gene and protein | Biological process | References |
|---|---|---|---|
| FHY3/FAR1-interacting promoters of target genes | RVE2, RVE7, and SPT | Seed dormancy and germination | Liu et al. (2021) |
| CCA1 and ELF4 | Circadian clock; flowering | Liu et al. (2020) and Li et al. (2011) | |
| FHY1 | FR signaling | Lin et al. (2007) | |
| PHR1 | Pi starvation responses | Liu et al. (2017) | |
| WRKY28 | Leaf senescence | Tian et al. (2020) | |
| ABI5 | ABA-regulated processes | Tang et al. (2013) | |
| SMXL6 and SMXL7 | SL signaling | Xie et al. (2020a) | |
| COP1 | UV-B signaling | Huang et al. (2012) | |
| FHY3/FAR1-interacting proteins | HY5 | Light signaling | Li et al. (2010) |
| TOC1 and CCA1 | Circadian clock | Liu et al. (2020) and Li et al. (2011) | |
| PIF5 and DET1 | Circadian clock; ABA signaling | Liu et al. (2020) and Xu et al. (2020) | |
| EIN3 and EIL1 | Ethylene regulated phosphate starvation responses | Liu et al. (2017) | |
| MYC2/3/4 and JAZs | JA signaling and shade avoidance | Liu et al. (2019) | |
| SPL9/15 | Branching | Xie et al. (2020a) | |
| SPL3/4/5 | Flowering | Xie et al. (2020b) |
Inhibition of FHY3 binding to DNA
Among all the FHY3-binding partners, the Basic Leucine Zipper (bZIP) transcription factor HY5 function as a positive regulator of light signaling (Oyama et al. 1997, Li et al. 2010). In various growth and developmental events, HY5 and FHY3 are tightly linked and simultaneously occupy the promoters of some common target genes to coregulate gene expression. Comparison of the FHY3 direct target genes with two ChIP-chip data of HY5 showed that 572 and 331 genes were coregulated by FHY3 and HY5 (Lee et al. 2007, Ouyang et al. 2011, Zhang et al. 2011). In most cases, FHY3 and HY5 have the same role of activating downstream targets, such as CCA1, ELF4 and COP1 (Li et al. 2011, Huang et al. 2012, Liu et al. 2020). As the interaction of FHY3 and HY5 is mediated through their DNA-binding domains, in some cases where the FBS element and the ACE element (ACGT-containing element, The element contains four consecutive AGCT bases) are very close, FHY3 and HY5 compete with each other for binding to downstream promoters of target genes. For example, FHY3 is a positive regulator of FR signaling and Pi starvation responses through activating FHY1 and PHR1, respectively, whereas HY5 interferes with FHY3 for binding to their promoters (Li et al. 2010, Liu et al. 2017). The FHY3–HY5 interactions are proposed to form non-DNA-binding heterodimers and may create a negative feedback loop that limits the over-response of some light-mediated developmental regulation.
Regulation of FHY3 transcriptional activity
Recently, some proteins that interact with FHY3 and FAR1 and repress their transcriptional activity in various scenarios have been illustrated. FHY3 and FAR1 play an essential role in light input into the circadian clock by directly activating the central clock genes CCA1 and ELF4 (Li et al. 2011, Liu et al. 2020). TOC1 and CCA1 can directly interact with FHY3 and FAR1 and repress their activating activity, thereby leading to the oscillation of CCA1 and ELF4 in every diurnal cycle. Additionally, the phytochrome-interacting factor PIF5 interacts with FHY3 and represses its transcriptional activity. In the regulation of CCA1 expression, PIF5 also has the capacity to repress FHY3 (Liu et al. 2020). Unlike CCA1 and TOC1, which are general transcriptional repressors, the mechanism of PIF5 repression activity on FHY3 is obscure. Another positive regulator of skotomorphogenesis DET1 also interacts with FHY3 and represses its activity by recruiting the histone deacetylase HDA6. Molecular evidence indicates that the alteration of H3K27ac and H3K4me3 modification on the promoter of FHY3 targets is mediated by DET1 and HDA6, thus leading to the transcription changes (Xu et al. 2020).
Regulation of FHY3 protein level by light conditions
Under light conditions, the transcription level of FHY3 is almost unchanged, whereas its protein level is accumulated significantly, and this process is very sensitive. Liu et al. (2020) found that 1-min white light exposure to dark-grown Arabidopsis seedlings resulted in significantly enhanced FHY3 protein accumulation. Molecular evidence demonstrated that FHY3 interacts with the active Pfr form of phyB. This light-triggered phyB–FHY3 interaction promotes FHY3 protein accumulation under light (Liu et al. 2021). Consistent with this finding, EOD-FR-treated plants (the plants with far-red light (15 μmol m−2 s−1) for 30 min at the end of each light period before returning to darkness) in which active phyB is inactivated by FR light treatment at the end of each light period led to declined FHY3 protein accumulation in the following dark night (Xie et al. 2020a). However, the underlying mechanism of this post-translational regulation requires further investigation. Although FHY3 and HY5 display similar protein accumulation patterns under light and dark conditions, FHY3 does not interact with the photomorphogenic repressor protein COP1, the E3 ubiquitin ligase that directly targets HY5 for degradation (Osterlund et al. 2000).
Interface with Hormone Pathways
Recent studies implicated in the interacting protein and target gene of FHY3 and FAR1 have shed light on its important role in growth and development. FHY3 and FAR1 are emerging as integrators of light and various hormones, including ethylene, jasmonate (JA), salicylic acid (SA), ABA, auxin and strigolactone (SL) (Fig. 2).
FHY3 and FAR1 integrate multiple internal and external information to regulate plant growth and developmental responses and for the adaption to environmental changes. Arrow, activation; bar, suppression; dummy line, insufficient evidence; red fonts, directly regulated target genes; black fonts, indirectly regulated target genes.
Ethylene is a gaseous phytohormone that interacts with light signaling to control a wide range of physiological responses (Johnson and Ecker 1998). The ethylene precursor ACC can promote FHY3 protein accumulation. Additionally, EIN3 and EIL1, the master regulators of the ethylene signaling pathway, interact with FHY3 and FAR1 physically to coregulate a large number of downstream genes (Liu et al. 2017). For example, FHY3 and EIN3 directly bind to the PHR1 promoter and act synergistically to activate its expression and phosphate starvation responses (Liu et al. 2017). Interestingly, in the process of plant senescence, FHY3 represses the transcriptional activation activity of EIN3 by interfering with its DNA-binding activity on the promoters of SAGs, for example, ORE1 (Xie et al. 2021). These studies provide new clues to understand whether FHY3 will be implicated in other ethylene-mediated developmental processes, such as seedling emergence and fruit ripening, and whether FHY3 and EIN3 acted corporately or antagonistically in these processes. Previous transcriptome and molecular analysis showed that PIFs and EIN3/EIL1 work together to mediate a wide range of light- and hormone-controlled developmental changes (Shi et al. 2018, Zhang et al. 2018). Although they act in parallel, direct interaction is not observed. A recent study confirmed the role of FHY3 as a bridge to connect PIF5 and EIN3 through physical interaction; thus, FHY3, EIN3 and PIFs might function together as a complex to regulate common pathways (Xie et al. 2021).
The plant hormone jasmonic acid plays essential roles in regulating many physiological processes and mediating plant responses to biotic and abiotic stresses. JA application also remarkably promotes FHY3 protein accumulation. In the process of JA-mediated defense responses, the fhy3 far1 double mutant displayed more susceptibility to the necrotrophic fungus Botrytis cinerea, accompanied by significantly reduced JA-responsive gene expression (Liu et al. 2019). Biochemical evidence suggested that FHY3 and MYC2/3/4 interact with each other and coregulate JA-responsive gene expression. JAZ, the key repressor of JA signaling, also interacts with FHY3 and represses its activity. Based on the molecular and biochemical data presented in this work, it is proposed that FHY3 function as the positive regulator of JA pathway-mediated growth and defense responses. Consistent with this suggestion, loss-of-function mutant of FHY3 and FAR1 led to the insensitivity to JA-mediated inhibition of hypocotyl growth (Liu et al. 2019). As a defense-related hormone, JA signaling is upregulated to promote plant defense at the expense of growth responses. When taking hypocotyl growth as a paradigm, on one hand, JAZ alleviates the repression effect of PIFs by DELLA (Yang et al. 2012); on the other hand, JAZ represses FHY3 activity, ultimately influencing the downstream growth gene, such as PAR1/2. Like FHY3, PIFs also interact with MYC2 (Zhang et al. 2018); thus, PIFs, FHY3 and MYC2 might work together to fine-tune adaptive growth and defense in response to JA and light signals.
SA is a plant hormone that plays a central role in the induction of systemic acquired resistance. FHY3 and FAR1 seemed to regulate the SA signaling pathway negatively. Wang et al. (2016) showed that the fhy3 far1 double mutant displayed a high SA level and increased resistance to Pseudomonas syringae pathogen infection. Consistently, some SA biosynthesis and signaling genes, including EDS1, PAD4, SID2, EDS1 and NPR1, were upregulated in the fhy3 far1 mutant. Interestingly, some fhy3 far1 double mutants growing under short-day conditions exhibit autoimmune phenotypes, including dwarf morphology, spontaneous cell death and constitutive R gene expression, mimicking the growth situation of autoimmune mutants (Zhang et al. 2012, Wang et al. 2016). Overexpression of HEMB1, which encodes a 5-aminolevulinic acid dehydratase in the chlorophyll biosynthetic pathway, can rescue the phenotype of fhy3 far1 by affecting SA metabolism (Wang et al. 2016). Another molecular evidence further supports the role of FHY3 and FAR1 in regulating SA biosynthesis. FHY3 and FAR1 can directly bind to the promoter of WRKY28 and repress its transcription. As WRKY28 promotes SA biosynthesis by activating SID2/ICS1 (van Verk et al. 2011, Tian et al. 2020); thus, FHY3 and FAR1 might indirectly repress SA levels via modulating WRKY28 level. The detailed mechanism of the negative regulation of plant immunity by FHY3 and FAR1 remains largely unclear.
The phytohormone ABA plays essential roles in seed dormancy and germination, stomatal closure, seedling growth and plant adaptation to various environmental challenges. Transduction of ABA signaling to downstream gene expression is mainly mediated by the bZIP transcription factors ABFs, of which ABI5 was shown to play fundamental roles (Finkelstein 1994, Finkelstein and Lynch 2000). FHY3 and FAR1 can directly activate ABI5 transcription by binding to the FBS element in the ABI5 promoter (Tang et al. 2013). Consistently, fhy3 and fhy3 far1 mutants displayed reduced sensitivity in ABA-mediated inhibition of seed germination. Additionally, other ABA-mediated phenotypes, like root elongation, stomatal movement and drought tolerance, are impaired in fhy3 and fhy3 far1 mutants, indicating that FHY3 and FAR1 regulate multiple aspects of ABA responses. Besides FHY3, other light-signaling transcription factors, like HY5 and PIFs, also directly activate ABI5 expression (Chen et al. 2008, Qi et al. 2020). Thus, it is supposed that FHY3 and HY5 are major transcription factors responsible for the induction of ABI5 in light, while in dark, ABI5 is mainly activated by PIFs (Qi et al. 2020). The regulation of ABI5 at multiple layers ensures the young seedlings to better adapt to dynamic light conditions.
Besides the above-mentioned hormones, the participation of FHY3 in other growth-related hormones, such as auxin and SL, has recently emerged. The development of shoot branches is a multistep process coordinately regulated by light and hormones. Plants deficient in phytochrome B exhibit reduced branching and elevated IAA levels (Krishna Reddy and Finlayson 2014). Mutation of FHY3 also inhibits shoot branching and can partially rescue the highly branched max2-1 mutant (Stirnberg et al. 2012). Genetic evidence suggested that FHY3 relieves auxin-mediated bud inhibition through attenuating AXR1-dependent auxin signaling. The inhibition function of FHY3 on branching has been supported by a recent study, which uncovers its role in integrating light and SL signaling. SMXL6 and SMXL7, two key repressors of the SL signaling pathway, are directly activated by FHY3 and FAR1. The activated SMXL6/7 (D53 in rice) and FHY3/FAR1 can interact with SPL9/15 (IPA1 in rice) and suppress their transcriptional activation on BRC1, thus promoting branching (Song et al. 2017; Xie et al. 2020a). It is noteworthy that SPL9 and SPL15 levels are upregulated in PIF overexpression plants as their canonical regulator miR156 is transcriptionally repressed by PIFs (Xie et al. 2017). Also, PIFs have the capacity to promote auxin biosynthesis by activating YUCCA expression (Hornitschek et al. 2012, Li et al. 2012). Therefore, the integration of light, auxin and SL in regulating plant branching requires both FHY3 and PIFs, and the functional interplay between them needs further investigation.
The Antagonistic Interplay between FHY3 and PIFs in Growth and Stress Responses
Phytochrome-interacting factors that interacted specifically with the phytochrome photoreceptors are central regulators of photomorphogenic development. Studies in the last decade have established PIFs as central components of a regulatory node that integrates multiple internal and external signals to optimize plant development and environmental adaption. Given the involvement of FHY3 in multiple development and stress regulations and the direct interactions between FHY3 and PIFs (Tang et al. 2012; Liu et al. 2020), it is supposed that FHY3 and PIFs might be intricately interconnected. In contrast to PIFs, whose activity and accumulation are inhibited by phyB at the post-translational level (Favero 2020), the association between phyB and FHY3 promotes FHY3 stability (Liu et al. 2021). In most case studies presented in this review, FHY3 and PIFs act antagonistically to regulate plant growth and development, including hypocotyl growth, flowering, senescence, branching and shade avoidance (Fig. 3). Like PIFs, the transcript or protein levels of FHY3 also respond to various hormones (Fig. 2). Recent evidence has established that FHY3 are themselves direct regulators of multiple hormone responses. Mechanistically, some evidence suggested that FHY3 and PIFs suppress the activity of each other. For example, PIF5 represses the transcriptional activity of FHY3, whereas in turn, FHY3 inhibits the DNA-binding activity of PIF5 (Liu et al. 2020, Xie et al. 2021). The reciprocal suppression between FHY3 and PIFs is very likely presented in many responses that require the integration of developmental and external information.
FHY3 and PIFs act downstream of phyB to antagonistically regulate diverse growth and development processes. Arrow, activation; bar, suppression.
Perspective
Owing to the recent progress made in understanding the role of FHY3 and FAR1, FHY3 and FAR1 are emerging as central components of a regulatory node that integrate multiple internal and external signals to optimize plant development. Although the general framework for the FHY3 regulatory network has been established, many essential questions are not answered. First, compared with the thorough understanding of PIFs’ functions, the role of FHY3 and FAR1 in many aspects of physiological and environmental responses still needs to be explored. Second, recent work indicated that FHY3 and FAR1 might have the capacity to mediate the tolerance to multiple abiotic stresses, such as cold, heat and salt stress in other plant species (Dai et al. 2022, Wang et al. 2022, Cai et al. 2023). The interacting partners and whether these abiotic stresses can regulate FHY3 levels are yet to be studied. Third, in addition to the above-mentioned studies, whether FHY3 and FAR1 play a role in other hormone signaling pathways, such as GA and BR, remains to be determined. Therefore, FHY3 and FAR1 may have more diverse functions than previously thoughts. More molecular mechanisms will emerge through functional analysis and binding component screening in the future, which will expand our understanding of the role of FHY3 and finally see its whole picture.
Data Availability
No new data were generated in this review article.
Funding
Chinese Universities Scientific Fund (15053348); 315 Talent Program of China Agricultural University and Construction of Beijing Science and Technology Innovation and Service Capacity in Top Subjects (CEFF-PXM2019_014207_000032).
Disclosures
The authors have no conflicts of interest to declare.
References
Author notes
contributed equally.
