Flowering time is tightly controlled by both endogenous and exogenous signals. Although several lines of evidence have suggested the involvement of WRKY transcription factors in floral initiation, the underlying mechanisms and signaling pathways involved remain elusive. Here, we newly identified Arabidopsis thaliana WRKY DNA binding protein75 (WRKY75) as a positive regulator of flowering initiation. Mutation of WRKY75 resulted in a delay in flowering, whereas overexpression of WRKY75 significantly accelerated flowering in Arabidopsis. Gene expression analysis showed that the transcript abundance of the flowering time integrator gene FLOWERING LOCUS T (FT) was lower in wrky75 mutants than in the WT, but greater in WRKY75-overexpressing plants. Chromatin immunoprecipitation assays revealed that WRKY75 directly binds to the promoter of FT. Both in vivo and in vitro biochemical analyses demonstrated that WRKY75 interacts with DELLA proteins. We found that both RGL1 and GAI can repress the activation ability of WRKY75, thereby attenuating expression of its regulon. Genetic analyses indicated that WRKY75 positively regulates flowering in a FT-dependent manner and overexpression of RGL1 or gain-of-function of GAI could partially rescues the early-flowering phenotype of WRKY75-overexpressing plants. Taken together, our results demonstrate that WRKY75 may function as a new component of the GA-mediated signaling pathway to positively regulate flowering in Arabidopsis.

Class II TCP TFs interact with FD and act directly at the AP1 promoter to control flowering.

The plant-specific VQ gene family participates in diverse physiological processes but little information is available on their role in leaf senescence. Here, we show that the VQ motif-containing proteins, Arabidopsis SIGMA FACTOR BINDING PROTEIN1 (SIB1) and SIB2 are negative regulators of abscisic acid (ABA)-mediated leaf senescence. Loss of SIB1 and SIB2 function resulted in increased sensitivity of ABA-induced leaf senescence. In contrast, overexpression of SIB1 significantly delayed this process. Moreover, biochemical studies revealed that SIBs interact with WRKY75 transcription factor. Loss of WRKY75 function decreased sensitivity to ABA-induced leaf senescence, while overexpression of WRKY75 significantly accelerated this process. Chromatin immunoprecipitation assays revealed that WRKY75 directly binds to the promoters of GOLDEN 2-LIKE1(GLK1) and GLK2, to repress their expression. SIBs repress the transcriptional function of WRKY75 and negatively regulate ABA-induced leaf senescence in a WRKY75-dependent manner. In contrast, WRKY75 positively modulates ABA-mediated leaf senescence in a GLK-dependent manner. In addition, SIBs inhibit WRKY75 function in ABA-mediated seed germination. These results demonstrate that SIBs can form a complex with WRKY75 to regulate ABA-mediated leaf senescence and seed germination.

WRKY transcription factors play essential roles during leaf senescence. However, the mechanisms by which they regulate this process remains largely unknown. Here, we identified the transcription factor WRKY75 as a positive regulator during leaf senescence. Mutations of WRKY75 caused a delay in age-triggered leaf senescence, whereas overexpression of WRKY75 markedly accelerated this process. Expression of senescence-associated genes (SAGs) was suppressed in WRKY75 mutants but increased in WRKY75-overexpressing plants. Further analysis demonstrated that WRKY75 directly associates with the promoters of SAG12 and SAG29, to activate their expression. Conversely, GAI and RGL1, two DELLA proteins, can suppress the WRKY75-mediated activation, thereby attenuating SAG expression during leaf senescence. Genetic analyses showed that GAI gain-of-function or RGL1 overexpression can partially rescue the accelerated senescence phenotype caused by WRKY75 overexpression. Furthermore, WRKY75 can positively regulate WRKY45 expression during leaf senescence. Our data thus imply that WRKY75 may positively modulate age-triggered leaf senescence through the gibberellin-mediated signaling pathway.

The phytochrome B mediated light signaling integrates with various phytohormone signalings to control plant immune response. However, it is still unclear whether phyB-mediated light signaling has an effect on the biosynthesis of jasmonate during plant defense response against Botrytis cinerea. In this study, we demonstrated that phyB-mediated light signaling has a role in this process. Initially, we confirmed that phyb plants were obviously less resistant to B. cinerea while phyB overexpressing plants showed significantly enhanced resistance. We also found that the expression of numerous JA biosynthesis genes was promoted upon treatment with red or white light when compared to that of darkness, and that this promotion is dependent on phyB. Consistent with the gene expression results, phyb plants accumulated reduced pool of JA-Ile, indicating that phyB-mediated light signaling indeed increased JA biosynthesis. Further genetic analysis showed that light-mediated JAZ9 degradation and phyB-enhanced resistance were dependent on the receptor COI1, and that pif1/3/4/5 (pifq) can largely rescue the severe symptom of phyb. Taken together, our study demonstrates that phyB may participate in plant defense against B. cinerea through the modulation of the biosynthesis of JA.