The HEAT Repeat Protein ILITYHIA is Required for Plant Immunity
Author(s) -
Jacqueline Monaghan,
Xin Li
Publication year - 2010
Publication title -
plant and cell physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.975
H-Index - 152
eISSN - 1471-9053
pISSN - 0032-0781
DOI - 10.1093/pcp/pcq038
Subject(s) - arabidopsis , pseudomonas syringae , biology , genetics , effector , spliceosome , proteomics , plant immunity , systemic acquired resistance , innate immune system , mutant , microbiology and biotechnology , computational biology , gene , rna splicing , immune system , rna
Plant innate immunity is mediated in part by resistance (R) proteins that detect pathogens and mount a robust defense response to fight against infection. We previously characterized proteins in the MOS4-associated complex (MAC) that function in the regulation of plant immune responses downstream of the autoactivated R protein snc1. The MAC is a highly conserved spliceosome-associated complex homologous to the nineteen complex (NTC) in yeast and human. The availability of proteomics data sets in these organisms allowed us to systematically test the biological function of additional putative MAC proteins based on protein sequence homology and reverse genetics. In this study, we investigate the function of the GENERAL CONTROL NONDEREPRESSIBLE1 (GCN1) homolog in Arabidopsis. GCN1 was previously isolated as a novel component of the NTC in one proteomics study of the human spliceosome. We identified a single GCN1 homolog in Arabidopsis and partially characterized its function using available T-DNA insertion mutants. This locus, previously named ILITYHIA (ILA), is required for non-host and basal resistance against Pseudomonas syringae as well as resistance conditioned by specific nucleotide binding, leucine-rich repeat (NB-LRR) R proteins. Furthermore, ILA is required for systemic acquired resistance (SAR). Previous proteomic identification of MAC components in Arabidopsis did not identify ILA, and epistasis analysis between snc1 and ila revealed that ILA does not function in snc1-mediated resistance. Overall, our results show that ILA functions in immunity against bacterial infection.
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