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Huang, Weijie

University of British Columbia

Plant immune responses against pathogen infections can be activated by different receptors at the site of infection. Activation of local immune responses leads to establishment of systemic acquired resistance (SAR) at distal part of host plant. Salicylic acid (SA) and N-hydroxypipecolic acid (NHP) are two critical signaling molecules in plant immunity. Pathogen-induced increase of SA and NHP levels relies on their biosynthetic genes, which are transcriptionally regulated by two transcription factors, SAR Deficient 1 (SARD1) and CaM-Binding Protein 60 g (CBP60g). Arabidopsis snc2-1D (for suppressor of npr1-1, constitute 2D) is an autoimmune mutant carrying a gain-of-function mutation in the receptor-like protein SNC2. The constitutively activated defense responses in snc2-1D can be partially suppressed by cbp60g, and almost completely suppressed by sard1 cbp60g, suggesting that SARD1 and CBP60g are activated downstream of SNC2. My Ph. D. research aims to identify immune regulators downstream of SNC2 that lead to SARD1 activation. In a genetic screen searching for suppressors of cbp60g-1 snc2-1D, I identified a bda7 mutant. Mapping-by-sequencing revealed that BDA7 encodes the transcription factor CBP60b. Loss of CBP60b function causes partial suppression of the cbp60g-1 snc2-1D autoimmunity, including the elevated expression of SARD1 in cbp60g-1 snc2-1D. Transient expression of CBP60b and a reporter gene driven by the SARD1 promoter in Nicotiana benthamiana showed that SARD1 expression can be activated by co-expression of CBP60b. Chromatin immunoprecipitation assay revealed that CBP60b directly targets SARD1 promoter. In addition, Arabidopsis overexpression lines of CBP60b exhibit increased SARD1 expression level and enhanced disease resistance. These findings suggest that CBP60b functions downstream of SNC2 to activate SARD1 expression. Mutants of BDA6 were also identified from the cbp60g-1 snc2-1D suppressor screen. Mapping-by-sequencing showed that bda6 mutants carry mutations in the gene Adaptor Protein 4 µ subunit (AP4M). Loss-of-function mutations in AP4M suppress the autoimmunity of cbp60g-1 snc2-1D, suggesting that the AP4 complex is required for defense responses mediated by SNC2. In addition, various receptor mediated immune responses are compromised in deletion mutants of AP4M, indicating that the AP4 complex plays broad roles in plant immunity. Altogether, studies in this dissertation provide new insights on the regulation of SNC2-mediated immunity.

Text

2025-04-30

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/82963

Botany

University of British Columbia

UBCV

http://creativecommons.org/licenses/by-nc-nd/4.0/