Linked Life Data

16045470

Source:http://linkedlifedata.com/resource/pubmed/id/16045470

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-7-27
pubmed:abstractText
In dicotyledonous plants broad-spectrum resistance to pathogens is established after the induction of the systemic acquired resistance (SAR) response. In Arabidopsis the NPR1 protein can regulate SAR by interacting with members of the TGA class of basic, leucine-zipper transcription factors to alter pathogenesis-related (PR) gene expression. Overexpression of (At)NPR1 in Arabidopsis enhances resistance to multiple pathogens. Similarly, overexpression of (At)NPR1 in rice enhances resistance to the bacterial pathogen, Xanthomonas oryzae pv. oryzae (Xoo). These results suggest that components of the (At)NPR1-mediated SAR defense response may be conserved between monocots and dicots. To determine whether or not rice TGA factors are involved in disease resistance responses, the effect of altering the function of rice TGA2.1 was analyzed in transgenic plants. Transgenic rice overexpressing an rTGA2.1 mutant, that can no longer bind DNA, and transgenic rice that have the endogenous rTGA2.1 silenced by dsRNA-mediated silencing were generated. Both types of transgenic rice displayed increased tolerance to Xoo, were dwarfed, and had altered accumulation of PR genes. The results presented in this study suggest that wild-type rTGA2.1 has primarily a negative role in rice basal defense responses to bacterial pathogens.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0960-7412
pubmed:author
pubmed:issnType
Print
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
335-47
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Alteration of TGA factor activity in rice results in enhanced tolerance to Xanthomonas oryzae pv. oryzae.
pubmed:affiliation
Department of Plant Pathology, University of California, Davis, CA 95616, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.