The PIF1/PIF3-MED25-HDA19 transcriptional repression complex regulates phytochrome signaling in Arabidopsis.

Light signals are perceived by photoreceptors, triggering the contrasting developmental transition in dark-germinated seedlings. Phytochrome-interacting factors (PIFs) are key regulators of this transition. Despite their prominent functions in transcriptional activation, little is known about PIFs' roles in transcriptional repression. Here, we provide evidence that histone acetylation is involved in regulating phytochrome-PIFs signaling in Arabidopsis. The histone deacetylase HDA19 interacts and forms a complex with PIF1 and PIF3 and the Mediator subunit MED25. The med25/hda19 double mutant mimics and enhances the phenotype of pif1/pif3 in both light and darkness. HDA19 and MED25 are recruited by PIF1/PIF3 to the target loci to reduce histone acetylation and chromatin accessibility, providing a mechanism for PIF1/PIF3-mediated transcriptional repression. Furthermore, MED25 forms liquid-like condensates, which can compartmentalize PIF1/PIF3 and HDA19 in vitro and in vivo, and the number of MED25 puncta increases in darkness. Collectively, our study establishes a mechanism wherein PIF1/PIF3 interact with HDA19 and MED25 to mediate transcriptional repression in the phytochrome signaling pathway and suggests that condensate formation with Mediator may explain the distinct and specific transcriptional activity of PIF proteins.

Cloning, expression, and bioinformatics analysis of heavy metal resistance-related genes fd-I and fd-II from Acidithiobacillus ferrooxidans.

Five heavy metals were introduced into the bacterial heavy metal resistance tests. The results showed that apparent inhibition effects of Cd2+ and Cu2+ on the growth of Acidithiobacillus ferrooxidans BYSW1 occurred at high concentrations (>0.04 mol l-1). Significant differences (P < 0.001) were both noticed in the expression of two ferredoxin-encoding genes (fd-I and fd-II) related to heavy metal resistance in the presence of Cd2+ and Cu2+ . When exposed to 0.06 mol l-1 Cd2+, the relative expression levels of fd-I and fd-II were about 11 and 13 times as much as those of the control, respectively. Similarly, exposure to 0.04 mol l-1 Cu2+ caused approximate 8 and 4 times higher than those of the control, respectively. These two genes were cloned and expressed in Escherichia coli, and the structures, functions of two corresponding target proteins, i.e. Ferredoxin-I (Fd-I) and Ferredoxin-II (Fd-II), were predicted. The recombinant cells inserted by fd-I or fd-II were more resistant to Cd2+ and Cu2+ compared with wild-type cells. This study was the first investigation regarding the contribution of fd-I and fd-II to enhancing heavy metal resistance of this bioleaching bacterium, and laid a foundation for further elucidation of heavy metal resistance mechanisms caused by Fd.

Arabidopsis EXECUTER1 interacts with WRKY transcription factors to mediate plastid-to-nucleus singlet oxygen signaling.

Chloroplasts produce singlet oxygen (1O2), which causes changes in nuclear gene expression through plastid-to-nucleus retrograde signaling to increase plant fitness. However, the identity of this 1O2-triggered pathway remains unclear. Here, we identify mutations in GENOMES UNCOUPLED4 (GUN4) and GUN5 as suppressors of phytochrome-interacting factor1 (pif1) pif3 in regulating the photo-oxidative response in Arabidopsis thaliana. GUN4 and GUN5 specifically interact with EXECUTER1 (EX1) and EX2 in plastids, and this interaction is alleviated by treatment with Rose Bengal (RB) or white light. Impaired expression of GUN4, GUN5, EX1, or EX2 leads to insensitivity to excess light and overexpression of EX1 triggers photo-oxidative responses. Strikingly, upon light irradiation or RB treatment, EX1 transiently accumulates in the nucleus and the nuclear fraction of EX1 shows a similar molecular weight as the plastid-located protein. Point mutagenesis analysis indicated that nuclear localization of EX1 is required for its function. EX1 acts as a transcriptional co-activator and interacts with the transcription factors WRKY18 and WRKY40 to promote the expression of 1O2-responsive genes. This study suggests that EX1 may act in plastid-to-nucleus signaling and establishes a 1O2-triggered retrograde signaling pathway that allows plants adapt to changing light environments during chloroplast development.

The RNA helicase UAP56 and the E3 ubiquitin ligase COP1 coordinately regulate alternative splicing to repress photomorphogenesis in Arabidopsis.

Light is a key environmental signal that regulates plant growth and development. While posttranscriptional regulatory mechanisms of gene expression include alternative splicing (AS) of pre-messenger RNA (mRNA) in both plants and animals, how light signaling affects AS in plants is largely unknown. Here, we identify DExD/H RNA helicase U2AF65-associated protein (UAP56) as a negative regulator of photomorphogenesis in Arabidopsis thaliana. UAP56 is encoded by the homologs UAP56a and UAP56b. Knockdown of UAP56 led to enhanced photomorphogenic responses and diverse developmental defects during vegetative and reproductive growth. UAP56 physically interacts with the central light signaling repressor constitutive photomorphogenic 1 (COP1) and U2AF65. Global transcriptome analysis revealed that UAP56 and COP1 co-regulate the transcription of a subset of genes. Furthermore, deep RNA-sequencing analysis showed that UAP56 and COP1 control pre-mRNA AS in both overlapping and distinct manners. Ribonucleic acid immunoprecipitation assays showed that UAP56 and COP1 bind to common small nuclear RNAs and mRNAs of downstream targets. Our study reveals that both UAP56 and COP1 function as splicing factors that coordinately regulate AS during light-regulated plant growth and development.

Mutual upregulation of HY5 and TZP in mediating phytochrome A signaling.

Phytochrome A (phyA) is the far-red (FR) light photoreceptor in plants that is essential for seedling de-etiolation under FR-rich environments, such as canopy shade. TANDEM ZINC-FINGER/PLUS3 (TZP) was recently identified as a key component of phyA signal transduction in Arabidopsis thaliana; however, how TZP is integrated into the phyA signaling networks remains largely obscure. Here, we demonstrate that ELONGATED HYPOCOTYL5 (HY5), a well-characterized transcription factor promoting photomorphogenesis, mediates FR light induction of TZP expression by directly binding to a G-box motif in the TZP promoter. Furthermore, TZP physically interacts with CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1), an E3 ubiquitin ligase targeting HY5 for 26S proteasome-mediated degradation, and this interaction inhibits COP1 interaction with HY5. Consistent with those results, TZP post-translationally promotes HY5 protein stability in FR light, and in turn, TZP protein itself is destabilized by COP1 in both dark and FR light conditions. Moreover, tzp hy5 double mutants display an additive phenotype relative to their respective single mutants under high FR light intensities, indicating that TZP and HY5 also function in largely independent pathways. Together, our data demonstrate that HY5 and TZP mutually upregulate each other in transmitting the FR light signal, thus providing insights into the complicated but delicate control of phyA signaling networks.

The SNL-HDA19 histone deacetylase complex antagonizes HY5 activity to repress photomorphogenesis in Arabidopsis.

Reprogramming of the transcriptome during photomorphogenesis requires dynamic changes in chromatin and distribution of histone modifications. However, the chromatin-based regulation of this process remains to be elucidated. Here, we identify the conserved SWI-INDEPENDENT3 LIKE (SNL)-HISTONE DEACETYLASE19 (HDA19) deacetylase complex, including HDA19 and SNL1-SNL6, as a negative regulator of the light signaling pathway. Light-repression of HDA19 and SNLs expression is mediated by photoreceptors. HDA19 and SNLs are required for histone deacetylation and chromatin inactivation of PHYA gene. We further examined the interaction between SNL-HDA19 complex and ELONGATED HYPOCOTYL5 (HY5), and their antagonistic regulation on the expressions of target genes. The HDA19 deacetylase complex is recruited by HY5 to the chromatin regions of two positive light signaling genes, HY5 and B-BOX CONTAINING PROTEIN 22 (BBX22), thereby reduces the accessibility and histone acetylation and represses their expression. HDA19, SNL1, and HY5 associate with the same regulatory regions of HY5 and BBX22, and HY5 binding to these loci is enhanced upon SNL-HDA19 dysfunction. Our study reveals a crucial role for the HDA19 deacetylase complex in light signaling and demonstrates that the functional interplay between chromatin regulators and transcription factors regulates photomorphogenetic responses to the changing light environments.

AGAMOUS-LIKE67 Cooperates with the Histone Mark Reader EBS to Modulate Seed Germination under High Temperature.

Seed germination is a vital developmental process that is tightly controlled by environmental signals, ensuring germination under favorable conditions. High temperature (HT) suppresses seed germination. This process, known as thermoinhibition, is achieved by activating abscisic acid and inhibiting gibberellic acid biosynthesis. The zinc-finger protein SOMNUS (SOM) participates in thermoinhibition of seed germination by altering gibberellic acid/abscisic acid metabolism, but the underlying regulatory mechanism is poorly understood. In this study, we report that SOM binds to its own promoter and activates its own expression in Arabidopsis (Arabidopsis thaliana) and identify the MADS-box transcription factor AGAMOUS-LIKE67 (AGL67) as a critical player in SOM function, based on its ability to recognize CArG-boxes within the SOM promoter and mediate the trans-activation of SOM under HTs. In addition, AGL67 recruits the histone mark reader EARLY BOLTING IN SHORT DAY (EBS), which recognizes H3K4me3 at SOM chromatin. In response to HTs, AGL67 and EBS are highly enriched around the SOM promoter. The AGL67-EBS complex is also necessary for histone H4K5 acetylation, which activates SOM expression, ultimately inhibiting seed germination. Taken together, our results reveal an essential mechanism in which AGL67 cooperates with the histone mark reader EBS, which bridges the process of H3K4me3 recognition with H4K5 acetylation, thereby epigenetically activating SOM expression to suppress seed germination under HT stress.

PHYTOCHROME-INTERACTING FACTOR-LIKE14 and SLENDER RICE1 Interaction Controls Seedling Growth under Salt Stress.

Early seedling development and emergence from the soil, which are critical for plant growth and important for crop production, are controlled by internal factors, such as phytohormones, and external factors, such as light and salt. However, little is known about how light and salt signals are integrated with endogenous cues in controlling plant physiological processes. Here, we show that overexpression of rice (Oryza sativa) PHYTOCHROME-INTERACTING FACTOR-LIKE14 (OsPIL14) or loss of function of the DELLA protein SLENDER RICE1 (SLR1) promotes mesocotyl and root growth, specifically in the dark and under salt stress. Furthermore, salt induces OsPIL14 turnover but enhances SLR1 accumulation. OsPIL14 directly binds to the promoter of cell elongation-related genes and regulates their expression. SLR1 physically interacts with OsPIL14 and negatively regulates its function. Our study reveals a mechanism by which the OsPIL14-SLR1 transcriptional module integrates light and gibberellin signals to fine-tune seedling growth under salt stress, enhancing understanding about how crops adapt to saline environments.

Transcriptional regulatory network of the light signaling pathways.

The developmental program by which plants respond is tightly controlled by a complex cascade in which photoreceptors perceive and transduce the light signals that drive signaling processes and direct the transcriptional reprogramming, yielding specific cellular responses. The molecular mechanisms involved in the transcriptional regulation include light-regulated nuclear localization (the phytochromes and UVR8) and nuclear accumulation (the cryptochrome, cry2) of photoreceptors. This regulatory cascade also includes master regulatory transcription factors (TFs) that bridge photoreceptor activation with chromatin remodeling and regulate the expression of numerous light-responsive genes. Light signaling-related TFs often function as signal convergence points in concert with TFs in other signaling pathways to integrate complex endogenous and environmental cues that help the plant adapt to the surrounding environment. Increasing evidence suggests that chromatin modifications play a critical role in regulating light-responsive gene expression and provide an additional layer of light signaling regulation. Here, we provide an overview of our current knowledge of the transcriptional regulatory network involved in the light response, particularly the roles of TFs and chromatin in regulating light-responsive gene expression.

PIF1 and RVE1 form a transcriptional feedback loop to control light-mediated seed germination in Arabidopsis.

The phytochrome B (phyB) photoreceptor plays a major role that inputs light signals to regulate seed dormancy and germination. PHYTOCHROME-INTERACTING FACTOR1 (PIF1) is a key transcription factor repressing phyB-mediated seed germination, while REVEILLE1 (RVE1) factor functions as a curial regulator in controlling both seed dormancy and germination. However, the relationship between the PIF1- and RVE1-modulated signaling pathways remains mostly unknown. Here, we find that PIF1 physically interacts with RVE1. Genetic analysis indicates that RVE1 inhibition on seed germination requires PIF1; reciprocally, the repressive effect of PIF1 is partially dependent on RVE1. Strikingly, PIF1 and RVE1 directly bind to the promoter and activate the expression of each other. Furthermore, PIF1 and RVE1 coordinately regulate the transcription of many downstream genes involved in abscisic acid and gibberellin pathways. Moreover, PIF1 enhances the DNA-binding ability and transcriptional repression activity of RVE1 in regulating GIBBERELLIN 3-OXIDASE2, and RVE1 promotes PIF1's DNA-binding ability in modulating ABSCISIC ACID-INSENSITIVE3 expression. Thus, this study demonstrates that PIF1 and RVE1 form a transcriptional feedback loop that coordinately inhibits seed germination, providing a mechanistic understanding of how phyB-mediated light signal is transduced to the seeds.

Functional analysis of ZmCOP1 and ZmHY5 reveals conserved light signaling mechanism in maize and Arabidopsis.

Plants have evolved light signaling mechanisms to optimally adapt developmental patterns to the ambient light environments. CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) and LONG HYPOCOTYL5 (HY5) are two critical components in the light signaling pathway in Arabidopsis thaliana. COP1 acts as an E3 ubiquitin ligase that targets positive regulators, such as HY5, leading to their degradation in darkness. However, functional analysis of the COP1-HY5 module in maize (Zea mays) has not been reported. Here, we investigated the expression patterns and roles of the COP1 and HY5 orthologs, ZmCOP1 and ZmHY5, in regulating photomorphogenesis. These two genes have high amino acid identities with their Arabidopsis homolog and were both regulated by light. Subcellular localization assay showed that ZmCOP1 was distributed in the cytosol and ZmHY5 localized in the nucleus. Exogenous expression of ZmCOP1 rescued the physiological defects of the cop1-4 mutant, and expression of ZmHY5 complemented the long hypocotyl phenotype of the hy5-215 mutant in Arabidopsis. Yeast two-hybrid and fluorescence resonance energy transfer assays showed that ZmCOP1 interacted with ZmHY5. Our study gains insight into the conserved function and regulatory mechanism of the COP1-HY5 signaling pathway in maize and Arabidopsis.

PHYTOCHROME-INTERACTING FACTORS Interact with the ABA Receptors PYL8 and PYL9 to Orchestrate ABA Signaling in Darkness.

PHYTOCHROME-INTERACTING FACTORS (PIFs) are a group of basic helix-loop-helix transcription factors that can physically interact with photoreceptors, including phytochromes and cryptochromes. It was previously demonstrated that PIFs accumulated in darkness and repressed seedling photomorphogenesis, and that PIFs linked different photosensory and hormonal pathways to control plant growth and development. In this study, we show that PIFs positively regulate the ABA signaling pathway during the seedling stage specifically in darkness. We found that PIFs positively regulate ABI5 transcript and protein levels in darkness in response to exogenous ABA treatment by binding directly to the G-box motifs in the ABI5 promoter. Consistently, PIFs and the G-box motifs in the ABI5 promoter determine ABI5 expression in darkness, and overexpression of ABI5 could rescue the ABA-insensitive phenotypes of pifq mutants in the dark. Moreover, we discovered that PIFs can physically interact with the ABA receptors PYL8 and PYL9, and that this interaction is not regulated by ABA. Further analyses showed that PYL8 and PYL9 promote PIF4 protein accumulation in the dark and enhance PIF4 binding to the ABI5 promoter, but negatively regulate PIF4-mediated ABI5 activation. Taken together, our data demonstrate that PIFs interact with ABA receptors to orchestrate ABA signaling in darkness by controlling ABI5 expression, providing new insights into the pivotal roles of PIFs as signal integrators in regulating plant growth and development.

The Evening Complex and the Chromatin-Remodeling Factor PICKLE Coordinately Control Seed Dormancy by Directly Repressing DOG1 in Arabidopsis.

Primary seed dormancy is acquired during seed development and maturation, which is important for plant fitness and survival. DELAY OF GERMINATION1 (DOG1) plays a critical role in inducing seed dormancy. DOG1 expression increases rapidly during seed development, but the precise mechanism underlying this process remains elusive. In this study, we showed that mutants with a loss or reduced function of the chromatin-remodeling factor PICKLE (PKL) exhibit increased seed dormancy. PKL associates with DOG1 chromatin and inhibits its transcription. We found that PKL physically interacts with LUX ARRHYTHMO (LUX), a member of the evening complex (EC) of the circadian clock. Furthermore, LUX directly binds to a specific coding sequence of DOG1, and DOG1 acts genetically downstream of PKL and LUX. Mutations in either LUX or EARLY FLOWERING3 (ELF3) encoding another member of the EC led to increased DOG1 expression and enhanced seed dormancy. Surprisingly, these phenotypes were abolished when the parent plants were grown under continuous light. In addition, we observed that loss of function of either PKL or LUX decreased H3K27me3 levels at the DOG1 locus. Taken together, our study reveals a regulatory mechanism in which EC proteins coordinate with PKL to transmit circadian signals for directly regulating DOG1 expression and seed dormancy during seed development.

The Chromatin-Remodeling Factor PICKLE Antagonizes Polycomb Repression of FT to Promote Flowering.

Changing daylength (or photoperiod) is a seasonal cue used by many plants to adjust the timing of their floral transition to ensure reproductive success. An inductive long-day photoperiod triggers the expression of FLOWERING LOCUS T (FT), which promotes flowering. FT, encoding a major component of florigen, is induced in leaf veins specifically at dusk through the photoperiod pathway; however, the modulation of FT expression in response to photoperiod cues remains poorly understood. Here, we report that the balance between Polycomb group (PcG) and Trithorax group (TrxG) proteins sets appropriate FT expression in long days in Arabidopsis (Arabidopsis thaliana). In PcG mutant lines, FT was highly derepressed, but FT expression was decreased to an almost wild-type level and pattern upon the additional disruption of chromatin-remodeling factors PICKLE (PKL) and ARABIDOPSIS HOMOLOG OF TRITHORAX1 (ATX1), but not by disruption of photoperiod pathway components. PKL interacts with ATX1 to mediate trimethylation of histone H3 on lysine-4 at the FT locus, leading to antagonistic effects of PKL and ATX1 on PcG proteins in the regulation of FT expression. Therefore, the TrxG-like protein PKL prevents PcG-mediated silencing to ensure specific and appropriate expression of FT, thereby determining the proper flowering response.

The B3-Domain Transcription Factor VAL1 Regulates the Floral Transition by Repressing FLOWERING LOCUS T.

Many plants monitor changes in day length (or photoperiod) and adjust the timing of the floral transition accordingly to ensure reproductive success. In long-day plants, a long-day photoperiod triggers the production of florigen, which promotes the floral transition. FLOWERING LOCUS T (FT) in Arabidopsis (Arabidopsis thaliana) encodes a major component of florigen, and FT expression is activated in leaf veins specifically at dusk through the photoperiod pathway. Repression of FT mediated by Polycomb group (PcG) proteins prevents precocious flowering and adds another layer to FT regulation. Here, we identified high-level trimethylation of histone H3 at Lys 27 (H3K27me3) in the high trimethylation region (HTR) of the FT locus from the second intron to the 3' untranslated region. The HTR contains a cis-regulatory DNA element required for H3K27me3 enrichment that is recognized by the transcriptional repressor VIVIPAROUS1/ABSCISIC ACID INSENSITIVE3-LIKE1 (VAL1). VAL1 directly represses FT expression before dusk and at night, coinciding with the high abundance of both VAL1 mRNA and VAL1 homodimer. Furthermore, VAL1 recruits LIKE HETEROCHROMATIN PROTEIN1 and MULTICOPY SUPRESSOR OF IRA1 to FT chromatin, leading to an H3K27me3 peak at the HTR of FT These findings reveal a mechanism for PcG repression of FT mediated by an intronic cis-silencing element and suggest a possible role for VAL1 in modulating PcG repression of FT during the flowering response.

The chromatin-remodelling factor PICKLE interacts with CONSTANS to promote flowering in Arabidopsis.

In many flowering plants, successful reproductive development depends on the plant's ability to sense seasonal photoperiodic changes and adjust its vegetative growth accordingly. In Arabidopsis thaliana, the day-length-dependent accumulation of CONSTANS (CO) is crucial for the rhythmic activation of FLOWERING LOCUS T (FT) expression at dusk under long days. However, the regulation of photoperiod-dependent changes of the diurnal FT expression pattern at the chromatin level is largely unknown. In this study, we show that the ATPase-dependent chromatin-remodelling factor PICKLE (PKL) acts through the CO-FT regulatory module and contributes to FT activation in leaf vasculature. PKL physically interacts with CO, and this interaction facilitates their binding to the common regions of FT chromatin in response to photoperiod. Long-day signal triggers the FT chromatin switch between the active state at dusk and the inactive state at night, and PKL is responsible for the diurnal state switch. Thus, our study reveals that PKL activates FT transcription likely through facilitating access of CO to FT chromatin at dusk to synchronize flowering time in response to environmental cues.

Cloning, Expression, and Bioinformatics Analysis of Heavy Metal Resistance Gene afe_1862 from Acidithiobacillus ferrooxidans L1 in Escherichia coli.

Molecular studies of copper and cadmium resistances in acidophilic bacteria are significant in biomining. In this study, afe_1862, which encodes a heavy metal-binding protein in Acidithiobacillus ferrooxidans L1, was amplified using PCR, cloned into the pET32a plasmid, and sequenced. Following SDS-PAGE analysis, optimization of the expression conditions and heterologous overexpression of afe_1862 in Escherichia coli BL21 in the presence of Cu2+ and Cd2+ were studied as well. The results indicated that AFE_1862 has higher resistance to Cu2+ than Cd2+. Bioinformatics analysis illustrated that AFE_1862 has a conserved HMA domain containing heavy metal-binding sites, which may play a role in transporting or detoxifying heavy metals.

SEUSS and PIF4 Coordinately Regulate Light and Temperature Signaling Pathways to Control Plant Growth.

Plants continuously monitor environmental conditions (such as light and temperature) and adjust their growth and development accordingly. The transcription factor PHYTOCHROME-INTERACTING FACTOR4 (PIF4) regulates both light and temperature signaling pathways. Here, we identified ENHANCED PHOTOMORPHOGENIC2 (EPP2) as a new repressor of photomorphogenesis in red, far-red, and blue light. Map-based cloning revealed that EPP2 encodes the SEUSS (SEU) transcription regulator. The C terminus of SEU has transcriptional activation activity, and SEU physically interacts with PIF4. Moreover, SEU promotes the expression of many genes, including auxin biosynthetic and responsive genes, and regulates IAA levels in plants. SEU associates with the regulatory regions of INDOLE-3-ACETIC ACID INDUCIBLE6 (IAA6) and IAA19 in a PIF4-independent manner, whereas the binding of PIF4 to these genes requires SEU. Furthermore, mutations in SEU affect H3K4me3 methylation at IAA6 and IAA19, and SEU positively regulates warm temperature-mediated hypocotyl growth together with PIF4. Collectively, our results reveal that SEU acts as a central regulator integrating light and temperature signals to control plant growth by coordinating with PIF4.

PICKLE chromatin-remodeling factor controls thermosensory hypocotyl growth of Arabidopsis.

Temperature is a major signal that governs plant distribution and shapes plant growth. High ambient temperature promotes plant thermomorphogenesis without significant induction of heat-stress responses. Although much progress of warm temperature-mediated plant growth has been made during recent years, the thermomorphogenic signalling pathway is not well understood. We previously revealed that PICKLE (PKL), an ATP-dependent chromatin remodelling factor, negatively controls photomorphogenesis in Arabidopsis thaliana. Here, we show that mutations in PKL lead to reduced sensitivity in hypocotyl elongation to warm temperature (28 °C). We demonstrate that CIRCADIAN CLOCK-ASSOCIATED 1 (CCA1) directly binds to the specific promoter regions of PKL and its expression is reduced in the cca1 mutants. We find that the cca1 seedlings are also less sensitive to temperature-mediated growth than the wild-type plants. Furthermore, PKL affects the level of trimethylation of histone H3 Lys 27 associated with INDOLE-3-ACETIC ACID INDUCIBLE 19 (IAA19) and IAA29 and regulates their expression. We also identify 6 additional transcription factors as the upstream regulators of PKL. Our study thus reveals PKL and CCA1 as 2 novel factors in controlling plant growth in response to the elevated temperature environment and provides new insight into the integration of light and temperature signals through chromatin regulation.