Arabidopsis GOLDEN2-LIKE (GLK) transcription factors activate jasmonic (JA)-dependent disease susceptibility to the biotrophic pathogen Hyaloperonospera arabidopsidis, as well as JA-independent plant immunity against the necrotrophic pathogen Botrytis cinerea.
Murmu, J., Wilton, M., Allard, G.C., Pandeya, R.S., Desveaux, D., Singh, J., and Subramaniam, R. (2014). "Arabidopsis GOLDEN2-LIKE (GLK) transcription factors activate jasmonic (JA)-dependent disease susceptibility to the biotrophic pathogen Hyaloperonospera arabidopsidis, as well as JA-independent plant immunity against the necrotrophic pathogen Botrytis cinerea.", Molecular Plant Pathology, 15(2), pp. 174-184. doi : 10.1111/mpp.12077 Access to full text
Arabidopsis thaliana GOLDEN2-LIKE (GLK1 and 2) transcription factors regulate chloroplast development in a redundant manner. Overexpression of AtGLK1 (35S:AtGLK1) in Arabidopsis also confers resistance to the cereal pathogen Fusarium graminearum. To further elucidate the role of GLK transcription factors in plant defence, the Arabidopsis glk1 glk2 double-mutant and 35S:AtGLK1 plants were challenged with the virulent oomycete pathogen Hyaloperonospora arabidopsidis (Hpa) Noco2. Compared with Col-0, glk1 glk2 plants were highly resistant to Hpa Noco2, whereas 35S:AtGLK1 plants showed enhanced susceptibility to this pathogen. Genetic studies suggested that AtGLK-mediated plant defence to Hpa Noco2 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 Hpa Noco2 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 Hpa Noco2. Together, our GLK gain-of-function and loss-of-function experiments suggest that GLK acts upstream of JA signalling in disease susceptibility to Hpa Noco2. In contrast, glk1 glk2 plants were more susceptible to the necrotrophic fungal pathogen Botrytis 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 Hpa Noco2 and in JA-independent resistance to the necrotrophic pathogen B. cinerea.
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