Light and gibberellins (GAs) antagonistically regulate hypocotyl elongation in plants. It has been demonstrated that DELLAs, which are negative regulators of GA signalling, inhibit phytochrome-interacting factors 3 and 4 (PIF3 and PIF4) by sequestering their DNA-recognition domains. However, it is unclear whether there are other mechanisms of regulatory crosstalk between DELLAs and PIFs. Here, we demonstrate that DELLAs negatively regulate the abundance of four PIF proteins through the ubiquitin–proteasome system. Reduction of PIF3 protein abundance by DELLAs correlates closely with reduced hypocotyl elongation. Both sequestration and degradation of PIF3 by DELLAs contribute to a reduction in PIF3 binding to its target genes. Thus, we show that promotion of PIF degradation by DELLAs is required to coordinate light and GA signals, and the dual regulation of transcription factors by DELLAs by both sequestration and degradation may be a general mechanism.
Light elicits different growth responses in different organs of plants. These organ-specific responses are prominently displayed during de-etiolation. While major light-responsive components and early signaling pathways in this process have been identified, this information has yet to explain how organ-specific light responses are achieved. Here, we report that members of the TEOSINTE BRANCHED1, CYCLOIDEA, and PCF (TCP) transcription factor family participate in photomorphogenesis and facilitate light-induced cotyledon opening in Arabidopsis (Arabidopsis thaliana). Chromatin immunoprecipitation sequencing and RNA sequencing analyses indicated that TCP4 targets a number of SMALL AUXIN UPREGULATED RNA (SAUR) genes that have previously been shown to exhibit organ-specific, light-responsive expression. We demonstrate that TCP4-like transcription factors, which are predominantly expressed in the cotyledons of both light-and dark-grown seedlings, activate SAUR16 and SAUR50 expression in response to light. Light regulates the binding of TCP4 to the promoters of SAUR14, SAUR16, and SAUR50 through PHYTOCHROME-INTERACTING FACTORs (PIFs). PIF3, which accumulates in etiolated seedlings and its levels rapidly decline upon light exposure, also binds to the SAUR16 and SAUR50 promoters, while suppressing the binding of TCP4 to these promoters in the dark. Our study reveals that the interplay between light-responsive factors PIFs and the developmental regulator TCP4 determines the cotyledon-specific light regulation of SAUR16 and SAUR50, which contributes to cotyledon closure and opening before and after de-etiolation.
One-sentence summary: SAUR17 is highly expressed in apical hooks and cotyledons in the dark, where it promotes etiolation by protecting the phosphatase activity of PP2C-D1 against cell-expansion-inducing SAURs such as SAUR50.
Phytochrome A (phyA) is the primary plant photoreceptor responsible for perceiving and mediating various responses to farred (FR) light and is essential for survival in canopy shade. In this study, we identified two Arabidopsis thaliana mutants that grew longer hypocotyls in FR light. Genetic analyses showed that they were allelic and their FR phenotypes were caused by mutations in the gene named TANDEM ZINC-FINGER/PLUS3 (TZP), previously shown to encode a nuclear protein involved in blue light signaling and phyB-dependent regulation of photoperiodic flowering. We show that the expression of TZP is dramatically induced by light and that TZP proteins are differentially modified in different light conditions. Furthermore, we show that TZP interacts with both phyA and FAR-RED ELONGATED HYPOCOTYL1 (FHY1) and regulates the abundance of phyA, FHY1, and ELONGATED HYPOCOTYL5 proteins in FR light. Moreover, our data indicate that TZP is required for the formation of a phosphorylated form of phyA in the nucleus in FR light. Together, our results identify TZP as a positive regulator of phyA signaling required for phosphorylation of the phyA photoreceptor, thus suggesting an important role of phosphorylated phyA in inducing the FR light response.
MYB transcription factors are involved in many biological processes, including metabolism, development and responses to biotic and abiotic stresses. RADIALIS-LIKE SANT/MYB 1 (RSM1) belongs to a MYB-related subfamily, and previous transcriptome analysis suggests that RSM1 may play roles in plant development, stress responses and plant hormone signaling. However, the molecular mechanisms of RSM1 action in response to abiotic stresses remain obscure. We show that down-regulation or up-regulation of RSM1 expression alters the sensitivity of seed germination and cotyledon greening to abscisic acid (ABA), NaCl and mannitol in Arabidopsis. The expression of RSM1 is dynamically regulated by ABA and NaCl. Transcription factors ELONGATED HYPOCOTYL 5 (HY5) and HY5 HOMOLOG (HYH) regulate RSM1 expression via binding to the RSM1 promoter. Genetic analyses reveal that RSM1 mediates multiple functions of HY5 in responses of seed germination, post-germination development to ABA and abiotic stresses, and seedling tolerance to salinity. Pull-down and BiFC assays show that RSM1 interacts with HY5/HYH in vitro and in vivo. RSM1 and HY5/HYH may function as a regulatory module in responses to ABA and abiotic stresses. RSM1 binds to the promoter of ABA INSENSITIVE 5 (ABI5), thereby regulating its expression, while RSM1 interaction also stimulates HY5 binding to the ABI5 promoter. However, no evidence was found in the dual-luciferase transient expression assay to support that RSM enhances the activation of ABI5 expression by HY. In summary, HY5/HYH and RSM1 may converge on the ABI5 promoter and independently or somehow dependently regulate ABI5 expression and ABI5-downstream ABA and abiotic stress-responsive genes, thereby improving the adaption of plants to the environment.
The CRISPR/Cas9 genome-editing system has emerged as a popular powerful tool for biological research. However, the process of selecting efficiently edited Cas9-free plants is usually laborious and time consuming. Here, we demonstrated P2A to be the most efficient self-cleaving peptide for fusing Cas9 and GFP in Arabidopsis and then used Cas9-P2A-GFP to develop a novel CRISPR/Cas9 system. Additionally, a pair of isocaudomer restriction enzymes were selected to conveniently assemble multiple sgRNAs. In this system, the GFP fluorescence intensity in T1 transgenic plants indicates the expression level of the Cas9 protein, which correlates well with the editing efficiency. Furthermore, Cas9-free plants can be easily selected by examining GFP fluorescence in T2 transgenic plants. The efficient knockout of BRI1, BZR1 and BES1 demonstrated the robustness of our new system. Thus, we designed a novel CRISPR/Cas9 system that can generate Cas9-free multiplex mutants efficiently in Arabidopsis and possibly in other plant species.
Light and gravity are two key environmental factors that control plant growth and architecture. However, the molecular basis of the coordination of light and gravity signaling in plants remains obscure. Here, we report that two classes of transcription factors, PHYTOCHROME INTERACTING FACTORS (PIFs) and ELONGATED HYPOCOTYL5 (HY5), can directly bind and activate the expression of LAZY4, a positive regulator of gravitropism in both shoots and roots in Arabidopsis. In hypocotyls, light promotes degradation of PIFs to reduce LAZY4 expression, which inhibits the negative gravitropism of hypocotyls. LAZY4 overexpression can partially rescue the negative gravitropic phenotype of pifq in the dark without affecting amyloplast development. Our identification of the PIFs-LAZY4 regulatory module suggests the presence of another role for PIF proteins in gravitropism, in addition to a previous report demonstrating that PIFs positively regulate amyloplast development to promote negative gravitropism in hypocotyls. In roots, light promotes accumulation of HY5 proteins to activate expression of LAZY4, which promotes positive gravitropism in roots. Together, our data indicate that light exerts opposite regulation of LAZY4 expression in shoots and roots by mediating the protein levels of PIFs and HY5, respectively, to inhibit the negative gravitropism of shoots and promote positive gravitropism of roots in Arabidopsis.
Trichomes are specialized epidermal cells that act as barriers against biotic and abiotic stresses. Although the formation of trichomes on hairy organs is well studied, the molecular mechanisms of trichome inhibition on smooth organs are still largely unknown. Here, we demonstrate that the CINCINNATA (CIN)-like TEOSINTE BRANCHED1/CYCLOIDEA/PCF (TCP) transcription factors inhibit the formation of trichomes on cotyledons in Arabidopsis (Arabidopsis thaliana). The tcp2/3/4/5/10/13/17 septuple mutant produces cotyledons with ectopic trichomes on the adaxial sides. The expression patterns of TCP genes are developmentally regulated during cotyledon development. TCP proteins directly interact with GLABRA3 (GL3), a key component of the MYB transcription factor/basic helix–loop–helix domain protein/WD40-repeat proteins (MYB–bHLH–WD40, MBW) complex essential for trichome formation, to interfere with the transactivation activity of the MBW complex in cotyledons. TCPs also disrupt the MBW complex–R3 MYB negative feedback loop by directly promoting the expression of R3 MYB genes, which enhance the repression of the MBW complex. Our findings reveal a molecular framework in which TCPs suppress trichome formation on adaxial sides of cotyledons by repressing the activity of the MBW complex at the protein level and the transcripts of R3 MYB genes at the transcriptional level.
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