Open AccessA rabidopsis GOLDEN2‐LIKE ( GLK ) transcription factors activate jasmonic acid ( JA )‐dependent disease susceptibility to the biotrophic pathogen H yaloperonospora arabidopsidis , as well as JA ‐independent plant immunity against the necrotrophic pathogen B otrytis cinerea
Author(s) -
Murmu Jhadeswar,
Wilton Michael,
Allard Ghislaine,
Pandeya Radhey,
Desveaux Darrell,
Singh Jas,
Subramaniam Rajagopal
Publication year - 2014
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12077
Subject(s) - jasmonic acid , biology , mutant , pathogen , npr1 , plant disease resistance , salicylic acid , transcription factor , oomycete , microbiology and biotechnology , gene , genetics , medicine , heart failure , natriuretic peptide
Summary A rabidopsis thaliana GOLDEN2 ‐ LIKE ( GLK1 and 2) transcription factors regulate chloroplast development in a redundant manner. Overexpression of AtGLK1 (35S: AtGLK1 ) in A rabidopsis also confers resistance to the cereal pathogen F usarium graminearum. To further elucidate the role of GLK transcription factors in plant defence, the A rabidopsis glk1 glk2 double‐mutant and 35S : AtGLK1 plants were challenged with the virulent oomycete pathogen H yaloperonospora arabidopsidis ( H pa ) N oco2. Compared with C ol‐0 , glk1 glk2 plants were highly resistant to H pa N oco2, whereas 35S: AtGLK1 plants showed enhanced susceptibility to this pathogen. Genetic studies suggested that AtGLK ‐mediated plant defence to H pa N oco2 was partially dependent on salicylic acid ( SA ) accumulation, but independent of the SA signalling protein NONEXPRESSOR OF PATHOGENESIS ‐ RELATED 1 ( NPR1 ). Pretreatment with jasmonic acid ( JA ) dramatically reversed H pa N oco2 resistance in the glk1 glk2 double mutant, but only marginally affected the 35S: AtGLK1 plants. In addition, overexpression of AtGLK1 in the JA signalling mutant coi1‐16 did not increase susceptibility to H pa N oco2. Together, our GLK gain‐of‐function and loss‐of‐function experiments suggest that GLK acts upstream of JA signalling in disease susceptibility to H pa N oco2. In contrast, glk1 glk2 plants were more susceptible to the necrotrophic fungal pathogen B otrytis cinerea , whereas 35S: AtGLK1 plants exhibited heightened resistance which could be maintained in the absence of JA signalling. Together, the data reveal that AtGLK1 is involved in JA ‐dependent susceptibility to the biotrophic pathogen H pa N oco2 and in JA ‐independent resistance to the necrotrophic pathogen B . cinerea .