CAMTA-Mediated Regulation of Salicylic Acid Immunity Pathway Genes in Arabidopsis Exposed to Low Temperature and Pathogen Infection
First author:Yong Sig Kim; Affiliations: Michigan State University(密歇根州立大学): East Lansing, USA
Corresponding author:Michael Thomashow
Arabidopsis thaliana Calmodulin-binding Transcription Activation (CAMTA; 钙调素结合转录激活) factors repress the expression of genes involved in salicylic acid (SA) biosynthesis and SA-mediated immunity in healthy plants grown at warm temperature (22°C). This repression is overcome in plants exposed to low temperature (4°C) for more than a week and in plants infected by biotrophic and hemibiotrophic pathogens (活体和半活体营养的病原菌). Here we present evidence that CAMTA3-mediated repression of SA pathway genes in non-stressed plants involves the action of an N-terminal repression module (NRM) that acts independently of calmodulin (CaM) binding to the IQ and CaM-binding (CaMB) domain, a finding that is contrary to current thinking that CAMTA3 repression activity requires binding of CaM to the CaMB domain. Induction (诱发) of SA-pathway genes in response to low temperature did not occur in plants expressing only the CAMTA3-NRM region of the protein. Mutational analysis provided evidence that the repression activity of the NRM was suppressed by action of the IQ and CaMB domains responding to signals generated in response to low temperature. Plants expressing the CAMTA3-NRM region were also impaired (有缺陷的) in defense against the bacterial hemibiotrophic pathogen Pseudomonas syringae (丁香假单胞菌) pv. tomato DC3000. Our results indicate that the regulation of CAMTA3 repression activity by low temperature and pathogen infection involves related mechanisms, but with distinct differences.