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Regulating the plant innate immune system : the roles of three Arabidopsis MUSE proteins

University of British Columbia

The plant innate immune system is highly effective in impeding infection by a broad spectrum of microbial pathogens. Strict regulation of immune signaling in plants is required to both facilitate rapid defense response induction upon pathogen detection and prevent the precocious activation of immunity, the latter of which has associated fitness costs. Despite their significance, the regulatory mechanisms governing plant immunity have only been partially characterized. Previously, members of the Li research group employed a forward genetic screen to identify positive regulators of innate immunity. This suppressor screen was performed using the unique Arabidopsis autoimmune mutant snc1 (suppressor of npr1, constitutive 1), which contains a gain-of-function mutation in an NLR (NOD-LIKE RECEPTOR) protein. The identified MOS (MODIFIER OF SNC1) genes highlighted the importance of diverse biological processes in the regulation of disease resistance. More recently, a snc1 enhancer screen was conducted to identify negative regulators of plant immune signaling. This thesis describes the cloning and characterization of three mutants isolated from this MUSE (MUTANT, SNC1-ENHANCING) screen. The muse9 mutant carries a molecular lesion in the gene encoding the chromatin remodeler SPLAYED (SYD). Molecular analyses showed that SYD negatively regulates SNC1 expression and thus functions antagonistically to MOS1 and MOS9, both of which were previously shown to positively regulate SNC1 transcription. This study emphasizes the importance of finely-tuned transcriptional control in NLR-mediated immunity. The muse4 mutant contains a partial loss-of-function mutation in NRPC7, which encodes an RNA polymerase III (Pol III) subunit. This is the first reported viable Pol III mutant. Using RT-PCR, it was established that the mutation in NRPC7 affects the expression of a diverse suite of genes and results in distortions in alternative splicing. The mutation responsible for the muse7 phenotypes is in a gene that encodes a protein of unknown function. MUSE7 negatively regulates SNC1 at the protein level, although no interactions were detected between MUSE7 and other known regulators of NLR protein turnover. This suggests that MUSE7 either regulates protein synthesis or is involved in an alternate degradation pathway. Taken together, these characterizations underscore the complexity inherent in the molecular mechanisms that control plant immune signaling.

Text

2017-02-28

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/58749

Botany

University of British Columbia

UBCV

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