Linked Life Data

18607631

Source:http://linkedlifedata.com/resource/pubmed/id/18607631

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-8-15
pubmed:abstractText
Injured plants induce a wide range of genes whose products are thought to help to repair the plant or to defend against opportunistic pathogens that might infect the wounded plant. In Arabidopsis thaliana L., oligogalacturonides (OGAs) and jasmonic acid (JA) are the main regulators of the signaling pathways that control the local and systemic wound response, respectively. RNS1, a secreted ribonuclease, is induced by wounding in Arabidopsis independent of these two signals, thus indicating that another wound-response signal exists. Here we show that abscisic acid (ABA), which induces wound-responsive genes in other systems, also induces RNS1. In the absence of ABA signaling, wounding induces only approximately 45% of the endogenous levels of RNS1 mRNA. However, significant levels of RNS1 still accumulate in the absence of ABA signaling. Our results suggest that wound-responsive increases in ABA production may amplify induction of RNS1 by a novel ABA-independent pathway. To elucidate this novel pathway, we show here that the wound induction of RNS1 is due in part to transcriptional regulation by wounding and ABA. We also show evidence of post-transcriptional regulation which may contribute to the high levels of RNS1 transcript accumulation in response to wounding.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1617-4615
pubmed:author
pubmed:issnType
Print
pubmed:volume
280
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
249-61
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Impact of transcriptional, ABA-dependent, and ABA-independent pathways on wounding regulation of RNS1 expression.
pubmed:affiliation
Interdepartmental Genetics Program, Iowa State University, Ames, IA 50011, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't