Abstract
Nitric oxide (NO) orchestrates a plethora of incongruent plant immune responses, including the reprograming of global gene expression. However, the cognate molecular mechanisms remain largely unknown. Here we show a zinc finger transcription factor (ZF-TF), SRG1, is a central target of NO bioactivity during plant immunity, where it functions as a positive regulator. NO accumulation promotes SRG1 expression and subsequently SRG1 occupies a repeated canonical sequence within target promoters. An EAR domain enables SRG1 to recruit the corepressor TOPLESS, suppressing target gene expression. Sustained NO synthesis drives SRG1 S-nitrosylation predominantly at Cys87, relieving both SRG1 DNA binding and transcriptional repression activity. Accordingly, mutation of Cys87 compromises NO-mediated control of SRG1-dependent transcriptional suppression. Thus, the SRG1-SNO formation may contribute to a negative feedback loop that attenuates the plant immune response. SRG1 Cys87 is evolutionary conserved and thus may be a target for redox regulation of ZF-TF function across phylogenetic kingdoms.
Highlights
Nitric oxide (NO) orchestrates a plethora of incongruent plant immune responses, including the reprograming of global gene expression
While NO is well established as a global regulator of plant defence gene expression[9,10,21,23,24,25,26], how this small, mobile signal might function in the nucleus to control the transcription of a plethora of incongruent defence-related genes remains to be established
Our findings suggest a molecular framework for SNO-regulated gene1 (SRG1) activity during plant immune function (Fig. 6g)
Summary
Nitric oxide (NO) orchestrates a plethora of incongruent plant immune responses, including the reprograming of global gene expression. There is a rapid synthesis of reactive oxygen intermediates (ROIs)[3,4] These small, redox-active molecules orchestrate a plethora of immune responses in plants including cell wall structural protein cross-linking[5], salicylic acid (SA) synthesis[6,7,8] and signalling and pathogen-triggered, programmed cell death development[9,10,11]. The total cellular level of S-nitrosylation is controlled indirectly by the action of the enzyme S-nitrosoglutathione reductase (GSNOR), which turns over the natural NO donor, S-nitrosoglutathione (GSNO)[6,17,18] This enzyme is required for plant development in addition to biotic and abiotic responses[17,19,20]. NO has been proposed to control the translocation of the transcriptional co-activator NPR1 into the nucleus[7,28] and the specific DNA-binding activity of its protein interactor, the basic leucine-zipper transcription factor, TGA1, which regulates the expression of Pathogenesis Related (PR) genes[28]
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