|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
1
|
|
pubmed:dateCreated |
2005-1-5
|
|
pubmed:abstractText |
Accumulation of reactive oxygen species (ROS) is central to plant response to several pathogens. One of the sources of ROS is the chloroplast because of the photoactive nature of the chlorophylls. Chlorophyllase 1 (encoded by AtCLH1) of Arabidopsis thaliana is quickly induced after tissue damage (e.g., caused by the bacterial necrotroph Erwinia carotovora or the necrotrophic fungus Alternaria brassicicola). RNA interference silencing of AtCLH1 resulted in failure to degrade free chlorophyll after tissue damage and in resistance to E. carotovora. Both inoculation with E. carotovora and exposure to high light caused elevated accumulation of hydrogen peroxide in AtCLH1 silenced plants. This was accompanied by expression of marker genes for systemic acquired resistance and induction of antioxidant defenses. Interestingly, downregulation of AtCLH1 resulted in increased susceptibility to A. brassicicola, resistance to which requires jasmonate signaling. We propose that AtCLH1 is involved in plant damage control and can modulate the balance between different plant defense pathways.
|
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-10066616,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-10069079,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-10213690,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-10230064,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-10459001,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-10476063,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-10611389,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-10755306,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-10796016,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-11041881,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-11044719,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-11128006,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-11149948,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-11154919,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-11299350,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-11402212,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-11497468,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-11607539,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-11788307,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-11950974,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-12179966,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-12615947,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-12650449,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-12873535,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-1392589,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-14742872,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-15012523,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-7480322,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-8589621,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-8989885,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-9115193,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-9148737,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-9501136,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-9844023,
http://linkedlifedata.com/resource/pubmed/commentcorrection/15598807-9933622
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Jan
|
|
pubmed:issn |
1040-4651
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
17
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
282-94
|
|
pubmed:dateRevised |
2010-9-21
|
|
pubmed:meshHeading |
pubmed-meshheading:15598807-Antioxidants,
pubmed-meshheading:15598807-Arabidopsis,
pubmed-meshheading:15598807-Carboxylic Ester Hydrolases,
pubmed-meshheading:15598807-Chlorophyll,
pubmed-meshheading:15598807-Cyclopentanes,
pubmed-meshheading:15598807-Down-Regulation,
pubmed-meshheading:15598807-Gene Expression Regulation,
pubmed-meshheading:15598807-Hydrogen Peroxide,
pubmed-meshheading:15598807-Immunity, Innate,
pubmed-meshheading:15598807-Oxidative Stress,
pubmed-meshheading:15598807-Oxylipins,
pubmed-meshheading:15598807-Pectobacterium carotovorum,
pubmed-meshheading:15598807-Photic Stimulation,
pubmed-meshheading:15598807-Plant Diseases,
pubmed-meshheading:15598807-Signal Transduction,
pubmed-meshheading:15598807-Up-Regulation
|
|
pubmed:year |
2005
|
|
pubmed:articleTitle |
Chlorophyllase 1, a damage control enzyme, affects the balance between defense pathways in plants.
|
|
pubmed:affiliation |
Department of Biological and Environmental Sciences, Genetics, University of Helsinki, 00014 Helsinki, Finland.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
