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Identification and characterization of two enhancers of the suppressor of npr1, constitutive 1 (snc1)

University of British Columbia

Out of necessity, plants have evolved robust, multi-layered defence responses to combat pathogen attack. Resistance (R) protein-mediated defence is one such layer that provides resistance to pathogens that have successfully overcome plant cell surface defences. R proteins, such as SNC1 (SUPPRESSOR OF NPR1, CONSTITUTIVE 1), recognize pathogenic molecules within the plant cell and initiate down-stream defence responses. A gain-of-function mutation in SNC1, snc1, results in constitutive defence responses, dwarf stature and dark green, deformed leaves. Using the snc1 mutant, many MODIFIER OF SNC1 (MOS) genes were found through a snc1 suppressor screen, which identified mutants based on increased size and decreased resistance responses. The wild-type-like phenotype of mos snc1 mutants, allowed another screen to identify enhancers of snc1 termed MUTANT, SNC1 ENHANCING (MUSE) genes. Here I describe the discovery of snc1-4d, an allele of snc1, and muse8, a partial loss-of-function mutant of AtCDC48A. snc1-4d is a unique allele of snc1 in that it possesses a mutation in the Nucleotide-Binding (NB) region of this R-like protein. The enhanced snc1 phenotype observed in this mutant is thought to be due to an increase in SNC1 activity as western blot analysis revealed no increase in snc1 protein level. This novel allele of SNC1 provides a unique opportunity to investigate the nature of the NB region of R proteins and how it may contribute to R protein activation. The partial loss-of-function allele of AtCDC48A, muse8, is also distinctive, as unlike previously characterized alleles, it remains viable when homozygous. This novel allele will be instrumental in the study of AtCDC48A’s many functions and provides the first evidence of AtCDC48’s involvement in plant innate immunity.

Text

2016-05-31

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/43797

Botany

University of British Columbia

UBCV

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