UBC Theses and Dissertations
Plant immunity regulation by transcription factors SARD1 and CBP60g : downstream, upstream and the amplification loop Sun, Tongjun
Activated plant defense responses consist of PAMP (pathogen associated molecular pattern)-triggered immunity (PTI) and effector-triggered immunity (ETI) at infected sites and a secondary immune response in distal parts of the host plant, termed systemic acquired resistance (SAR). Salicylic acid (SA) plays critical roles in plant immunity and its level increases upon pathogen infection. Pathogen-induced SA biosynthesis predominantly relies on ICS1 (ISOCHORISMATE SYNTHASE 1), whose induction mainly depends on transcription factors SARD1 (SAR DEFICIENT 1) and CBP60g (CALMODULIN BINDING PROTEIN 60 g). Meanwhile, the expression of SARD1 and CBP60g is also highly induced by pathogens. My Ph.D. research focuses on identification of immune regulators that function upstream and downstream of SARD1 and CBP60g. First, we performed chromatin immunoprecipitation-sequencing experiments to identify candidate targets of SARD1. We found that SARD1 and CBP60g directly control the expression of a large number of key regulators involved in PTI, ETI and SAR. Among them, two genes essential for SAR, ALD1 (AGD2-LIKE DEFENSE RESPONSE PROTEIN 1) and SARD4, are involved in the biosynthesis of pipecolic acid (Pip), a plant secondary metabolite required for SAR. Consistently, the sard1cbp60g double mutant accumulates less Pip than wild type, suggesting that SARD1 and CBP60g regulate Pip biosynthesis in addition to SA. Secondly, we showed that transcription factors TGA1 and TGA4 act upstream of SARD1 and CBP60g and thus regulate the biosynthesis of SA and Pip. Lastly, we revealed a novel mechanism of SA perception by its receptors NPR3 (NPR1-LIKE PROTEIN 3) and NPR4. NPR3/NPR4 interact with transcription factors TGA2, TGA5 and TGA6, and act as transcriptional repressors. SA inhibits the transcriptional repression activities of NPR3/NPR4 and promotes the transcriptional activation activity of NPR1 (NONEXPRESSER OF PR GENES 1); both contribute to SA-induced defense gene expression. We also found that SA induces SARD1 expression, revealing a feedback amplification loop between SA and SARD1, where SARD1 promotes SA biosynthesis via directly activating ICS1 expression and SA induces SARD1 expression by regulating the activities of NPR/TGA complexes. Altogether studies in this dissertation provide new insights on the functions of SARD1 and CBP60g in plant immunity and the mechanism of SA perception and signaling.
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