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The Mediator subunit SFR6/MED16 controls defence gene expression mediated by salicylic acid and jasmonate responsive pathways
Author(s) -
Wathugala Deepthi L.,
Hemsley Piers A.,
Moffat Caroline S.,
Cremelie Pieter,
Knight Marc R.,
Knight Heather
Publication year - 2012
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/j.1469-8137.2012.04138.x
Subject(s) - pseudomonas syringae , biology , mutant , jasmonic acid , gene expression , arabidopsis , microbiology and biotechnology , gene knockdown , gene , regulation of gene expression , ectopic expression , salicylic acid , regulon , genetics
Summary• Arabidopsis SENSITIVE TO FREEZING6 (SFR6) controls cold‐ and drought‐inducible gene expression and freezing‐ and osmotic‐stress tolerance. Its identification as a component of the MEDIATOR transcriptional co‐activator complex led us to address its involvement in other transcriptional responses. • Gene expression responses to Pseudomonas syringae , ultraviolet‐C (UV‐C) irradiation, salicylic acid (SA) and jasmonic acid (JA) were investigated in three sfr6 mutant alleles by quantitative real‐time PCR and susceptibility to UV‐C irradiation and Pseudomonas infection were assessed. • sfr6 mutants were more susceptible to both Pseudomonas syringae infection and UV‐C irradiation. They exhibited correspondingly weaker PR (pathogenesis‐related) gene expression than wild‐type Arabidopsis following these treatments or after direct application of SA, involved in response to both UV‐C and Pseudomonas infection. Other genes, however, were induced normally in the mutants by these treatments. sfr6 mutants were severely defective in expression of plant defensin genes in response to JA; ectopic expression of defensin genes was provoked in wild‐type but not sfr6 by overexpression of ERF5. • SFR6/MED16 controls both SA‐ and JA‐mediated defence gene expression and is necessary for tolerance of Pseudomonas syringae infection and UV‐C irradiation. It is not, however, a universal regulator of stress gene transcription and is likely to mediate transcriptional activation of specific regulons only.