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-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.

The transcription factor WRKY75 positively regulates jasmonate-mediated plant defense to necrotrophic fungal pathogens.

Necrotrophic fungi cause devastating diseases in both horticultural and agronomic crops, but our understanding of plant defense responses against these pathogens is still limited. In this study, we demonstrated that WRKY75 positively regulates jasmonate (JA)-mediated plant defense against necrotrophic fungal pathogens Botrytis cinerea and Alternaria brassicicola, and also affects the sensitivity of plants to JA-inhibited seed germination and root growth. Quantitative analysis indicated that several JA-associated genes, such as OCTADECANOID-RESPONSIVE ARABIDOPSIS (ORA59) and PLANT DEFENSIN 1.2A (PDF1.2), were significantly reduced in expression in wrky75 mutants, and enhanced in WRKY75 overexpressing transgenic plants. Immunoprecipitation assays revealed that WRKY75 directly binds to the promoter of ORA59 and represses itstranscription. In vivo and in vitro experiments suggested that WRKY75 interacts with several JASMONATE ZIM-domain proteins, repressors of the JA signaling pathway. We determined that JASMONATE-ZIM-DOMAIN PROTEIN 8 (JAZ8) represses the transcriptional function of WRKY75, thereby attenuating the expression of its regulation. Overexpression of JAZ8 repressed plant defense responses to B. cinerea. Our study provides evidence that WRKY75 functions as a critical component of the JA-mediated signaling pathway to positively regulate Arabidopsis defense responses to necrotrophic pathogens.

The PIFs Redundantly Control Plant Defense Response against Botrytis cinerea in Arabidopsis.

Endogenous and exogenous signals are perceived and integrated by plants to precisely control defense responses. As a crucial environmental cue, light reportedly plays vital roles in plant defenses against necrotrophic pathogens. Phytochrome-interacting factor (PIF) is one of the important transcription factors which plays essential roles in photoreceptor-mediated light response. In this study, we revealed that PIFs negatively regulate plant defenses against Botrytis cinerea. Gene expression analyses showed that the expression level of a subset of defense-response genes was higher in pifq (pif1/3/4/5) mutants than in the wild-type control, but was lower in PIF-overexpressing plants. Chromatin immunoprecipitation assays proved that PIF4/5 binds directly to the ETHYLENE RESPONSE FACTOR1 (ERF1) promoter. Moreover, genetic analyses indicated that the overexpression of ERF1 dramatically rescues the susceptibility of PIF4-HA and PIF5-GFP transgenic plants, and that PIF controls the resistance to B. cinerea in a COI1- and EIN2-dependent manner. Our results provide compelling evidence that PIF, together with the jasmonate/ethylene pathway, is important for plant resistance to B. cinerea.

Arabidopsis Class II TCP Transcription Factors Integrate with the FT-FD Module to Control Flowering.

The appropriate timing of flowering is critical for plant reproductive success. Although the FLOWERING LOCUS T (FT)-FD module plays crucial roles in the photoperiodic flowering pathway, the underlying mechanisms and signaling pathways involved still remain elusive. Here, we demonstrate that class II TCP transcription factors (TFs) integrate into the FT-FD complex to control floral initiation in Arabidopsis (Arabidopsis thaliana). Class II CINCINNATA (CIN) TCP TFs function as transcriptional activators by directly binding to the promoters of downstream floral meristem identity genes, such as APETALA1 (AP1). In addition, these TCPs directly interact with FD, a basic Leu zipper TF that plays a critical role in photoperiodic flowering, which further activates AP1 expression. Genetic analyses indicated that class II CIN TCP TFs function synergistically with FT and FD, to positively regulate flowering in an AP1-dependent manner. Thus, our results provide compelling evidence that class II CIN TCP TFs act directly at the AP1 promoter to enhance its transcription, thus further elucidating the molecular mechanisms underlying the regulation of photoperiodic flowering in Arabidopsis.

Arabidopsis WRKY45 Interacts with the DELLA Protein RGL1 to Positively Regulate Age-Triggered Leaf Senescence.

Leaf senescence can be triggered and promoted by various environmental stressors, developmental cues, and endogenous hormone signals. Several lines of evidence have suggested the involvement of WRKY transcription factors in regulating leaf senescence, but the underlying mechanisms and signaling pathways involved remain elusive. In this study, we identified Arabidopsis thaliana WRKY DNA-binding protein 45 (WRKY45) as a positive regulator of age-triggered leaf senescence. Loss of WRKY45 function resulted in increased leaf longevity in age-triggered senescence, whereas overexpression of WRKY45 significantly accelerated age-triggered leaf senescence. Consistently, expression of SENESCENCE-ASSOCIATED GENEs (SAGs) was significantly reduced in wrky45 mutants but markedly enhanced in transgenic plants overexpressing WRKY45. Chromatin immunoprecipitation assays revealed that WRKY45 directly binds the promoters of several SAGs such as SAG12, SAG13, SAG113, and SEN4. Both in vivo and in vitro biochemical analyses demonstrated that WRKY45 interacts with the DELLA protein RGA-LIKE1 (RGL1), a repressor of the gibberellin (GA) signaling pathway. We found that RGL1 repressed the transcription activation function of WRKY45, thereby attenuating the expression of its regulon. Consistent with this finding, overexpression of RGL1 resulted in significantly increased leaf longevity in age-triggered senescence. Taken together, our results provide compelling evidence that WRKY45 functions as a critical component of the GA-mediated signaling pathway to positively regulate age-triggered leaf senescence.