Phytochrome B regulates jasmonic acid-mediated defense response against Botrytis cinerea in Arabidopsis

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-lle,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 pifl/3/4/5(pi/q)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.

AtWRKY75 positively regulates age-triggered leaf senescence through gibberellin pathway

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 agetriggered 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。

GhWRKY33 negatively regulates jasmonate-mediated plant defense to Verticillium dahliae

Verticillium wilt,caused by Verticillium dahliae,seriously restricts the yield and quality improvement of cotton.Previous studies have revealed the involvement of WRKY members in plant defense against V.dahliae,but the underlying mechanisms involved need to be further elucidated.Here,we demonstrated that Gossypium hirsutum WRKY DNA-binding protein 33(GhWRKY33) functions as a negative regulator in plant defense against V.dahliae.GhWRKY33 expression is induced rapidly by V.dahliae and methyl jasmonate,and overexpression of GhWRKY33 reduces plant tolerance to V.dahliae in Arabidopsis.Quantitative RT-PCR analysis revealed that expression of several JA-associated genes was significantly repressed in GhWRKY33 overexpressing transgenic plants.Yeast one-hybrid analysis revealed that GhWRKY33 may repress the transcription of both AtERF1 and GhERF2 through its binding to their promoters.Protein-protein interaction analysis suggested that GhWRKY33 interacts with G.hirsutum JASMONATE ZIM-domain protein 3(GhJAZ3).Similarly,overexpression of GhJAZ3 also decreases plant tolerance to V.dahliae.Furthermore,GhJAZ3 acts synergistically with GhWRKY33 to suppress both AtERF1 and GhERF2 expression.Our results imply that GhWRKY33 may negatively regulate plant tolerance to V.dahliae via the JA-mediated signaling pathway.