GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.

Have any questions? Please email us at ecoliwiki@gmail.com

TableEdit

Jump to: navigation, search

PMID:22381007

You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki

See Help for Help on this wiki. See the documentation for how to use the table editor

Citation

Choi, SM, Song, HR, Han, SK, Han, M, Kim, CY, Park, J, Lee, YH, Jeon, JS, Noh, YS and Noh, B (2012) HDA19 is required for the repression of salicylic acid biosynthesis and salicylic acid-mediated defense responses in Arabidopsis. Plant J. 71:135-46

Abstract

To cope with a lifetime of exposure to a variety of pathogens, plants have developed exquisite and refined defense mechanisms that vary depending on the type of attacking pathogen. Defense-associated transcriptional reprogramming is a central part of plant defense mechanisms. Chromatin modification has recently been shown to be another layer of regulation for plant defense mechanisms. Here, we show that the RPD3/HDA1-class histone deacetylase HDA19 is involved in the repression of salicylic acid (SA)-mediated defense responses in Arabidopsis. Loss of HDA19 activity increased SA content and increased the expression of a group of genes required for accumulation of SA as well as pathogenesis related (PR) genes, resulting in enhanced resistance to Pseudomonas syringae. We found that HDA19 directly associates with and deacetylates histones at the PR1 and PR2 promoters. Thus, our study shows that HDA19, by modifying chromatin to a repressive state, ensures low basal expression of defense genes, such as PR1, under unchallenged conditions, as well as their proper induction without overstimulation during defense responses to pathogen attacks. Thus, the role of HDA19 might be critical in preventing unnecessary activation and self-destructive overstimulation of defense responses, allowing successful growth and development.

Links

PubMed Online version:10.1111/j.1365-313X.2012.04977.x

Keywords

public



Cancel