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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2011-6-15
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pubmed:abstractText |
Previous studies reveal that both Ca(2+) and nitric oxide (NO) play pivotal roles in the plant senescence signaling cascade. However, not much is known about the molecular identity of the Ca(2+) entry during senescence programming and its relationship to the downstream NO signal. Our recent study shows that Arabidopsis cyclic nucleotide gated channel2 (CNGC2) contributes to Ca(2+) uptake and senescence signaling. The CNGC2 loss-of-function mutant dnd1 displays reduced Ca(2+) accumulation in leaves and a series of early senescence phenotypes compared to wild type (WT). Notably, endogenous NO content in dnd1 leaves is lower than leaves of WT. Application of an NO donor can effectively rescue a number of early senescence phenotypes found in the dnd1 plants. Current evidence supports the notion that NO functions as a negative regulator in senescence signaling and our model supports this point. In this article, we expand our discussion of CNGC2 mediated Ca(2+) uptake and other related signaling components involved in the plant senescence signaling cascade.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1559-2324
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
413-5
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pubmed:meshHeading |
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pubmed:year |
2011
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pubmed:articleTitle |
Cyclic nucleotide gated channel and Ca²?-mediated signal transduction during plant senescence signaling.
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pubmed:affiliation |
Department of Energy Plant Research Laboratory, Michigan State University, East Lansing, MI, USA. mawei@msu.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.
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