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A dual regulatory role of Arabidopsis calreticulin‐2 in plant innate immunity
Author(s) -
Qiu Yongjian,
Xi Jing,
Du Liqun,
Roje Sanja,
Poovaiah B.W.
Publication year - 2012
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2011.04807.x
Subject(s) - calreticulin , arabidopsis , biology , pseudomonas syringae , salicylic acid , plant immunity , innate immune system , microbiology and biotechnology , effector , plant defense against herbivory , endoplasmic reticulum , receptor , mutant , genetics , gene
Summary Calreticulin (CRT) is an endoplasmic reticulum‐resident calcium‐binding molecular chaperone that is highly conserved in multi‐cellular eukaryotes. Higher plants contain two distinct groups of CRTs: CRT1/CRT2 and CRT3 isoforms. Previous studies have shown that bacterial elongation factor Tu receptor (EFR), a pattern‐recognition receptor that is responsible for pathogen‐associated molecular pattern‐triggered immunity, is a substrate for Arabidopsis CRT3, suggesting a role for CRT3 in regulating plant defense against pathogens. Here we report that Arabidopsis CRT2 is another regulator of plant innate immunity. Despite significantly increased salicylic acid levels and constitutive expression of the systemic acquired resistance‐associated marker genes PR1 , PR2 and PR5 , transgenic plants over‐expressing CRT2 displayed reduced resistance to virulent Pseudomonas syringae pv. tomato DC3000 ( Pst DC3000 ). A 45 Ca 2+ overlay assay and a domain‐swapping experiment further demonstrated that the negatively charged C‐terminal tail of CRT2 is responsible for its high calcium‐binding capacity and function in regulating the endogenous salicylic acid level. In addition, over‐expression of the His173 mutant of CRT2 greatly enhanced plant defense against Pst DC3000 , supporting the existence of a self‐inhibition mechanism that can counteract the effects of salicylic acid‐dependent immune responses. These results suggest that CRT2 functions through its N‐terminal domain(s) as a self‐modulator that can possibly prevent the salicylic acid‐mediated runaway defense responses triggered by its C‐terminal calcium‐buffering activity in response to pathogen invasion.