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Changes in the proteome of pad2-1, a glutathione depleted Arabidopsis mutant, during Pseudomonas syringae infection.
- Source :
-
Journal of Proteomics . Aug2015, Vol. 126, p82-93. 12p. - Publication Year :
- 2015
-
Abstract
- The involvement of glutathione (GSH) in plant defense against pathogen invasion is an established fact. However, the molecular mechanism conferring this tolerance remains to be explored. Here, proteomic analysis of pad2-1 , an Arabidopsis thaliana GSH-depleted mutant, in response to Pseudomonas syringae infection has been performed to explore the intricate position of GSH in defense against biotrophic pathogens. The pad2-1 mutant displayed severe susceptibility to P. syringae infection compared to the wild-type (Col-0) thus re-establishing a fundamental role of GSH in defense. Apart from general up-accumulation of energy metabolism-related protein-species in both infected Col-0 and pad2-1 , several crucial defense-related protein-species were identified to be differentially accumulated. Leucine-rich repeat-receptor kinase (LRR-RK) and nucleotide-binding site–leucine-rich repeat resistance protein (NBS–LRR), known to play a pioneering role against pathogen attack, were only weakly up-accumulated in pad2-1 after infection. Transcriptional and post-transcriptional regulators like MYB-P1 and glycine-rich repeat RNA-binding protein (GRP) and several other stress-related protein-species like heat shock protein 17 (HSP17) and glutathione-S-transferase (GST) were also identified to be differentially regulated in pad2-1 and Col-0 in response to infection. Together, the present investigation reveals that the optimum GSH-level is essential for the efficient activation of plant defense signaling cascades thus conferring resistance to pathogen invasion. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 18743919
- Volume :
- 126
- Database :
- Academic Search Index
- Journal :
- Journal of Proteomics
- Publication Type :
- Academic Journal
- Accession number :
- 108655048
- Full Text :
- https://doi.org/10.1016/j.jprot.2015.04.036