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Characterization and cloning of suppressor of chs3-2D in Arabidopsis

University of British Columbia

Plant innate immunity depends on the function of a large number of intracellular immune receptor proteins, the majority of which are structurally similar to mammalian NUCLEOTIDE-BINDING OLIGOMERIZATION DOMAIN (NOD)-LIKE RECEPTOR (NLR) proteins. CHILLING SENSITIVE 3 (CHS3) encodes an atypical Toll/Interleukin 1 Receptor (TIR)-type NLR protein with an additional Lin-11, Isl-1 and Mec-3 (LIM) domain at its C terminus. The gain-of-function mutant allele chs3-2D exhibits severe dwarfism and constitutively activated defense responses, including enhanced resistance to virulent pathogens, high PATHOGENESIS-RELATED (PR) gene expression, and salicylic acid accumulation. To search for novel regulators involved in the CHS3-mediated immune signaling pathway, we conducted suppressor screens in the chs3-2D and chs3-2D pad4-1 genetic backgrounds. Alleles of sag101 and eds1-90 were isolated as complete suppressors of chs3-2D, and alleles of sgt1b were isolated as partial suppressors of chs3-2D pad4-1. This suggests that SAG101, EDS1-90, and SGT1b are all positive regulators of CHS3-mediated defense signaling. Additionally, the TIR-type NLR-encoding CSA1 locus located in the Arabidopsis genome adjacent to CHS3 was found to be required for CHS3-mediated signaling. CSA1 is located 3.9kb upstream of CHS3 and is transcribed in the opposite direction. Altogether, these data illustrate the distinct genetic requirements for CHS3-mediated defense signaling.

Text

2015-08-31

Attribution-NonCommercial-NoDerivs 2.5 Canada

http://hdl.handle.net/2429/52083

Botany

University of British Columbia

UBCV

http://creativecommons.org/licenses/by-nc-nd/2.5/ca/