Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
21
pubmed:dateCreated
2001-10-18
pubmed:abstractText
Recent evidence suggests that slow anion channels in guard cells need to be activated to trigger stomatal closing and efficiently inactivated during stomatal opening. The patch-clamp technique was employed here to determine mechanisms that produce strong regulation of slow anion channels in guard cells. MgATP in guard cells, serving as a donor for phosphorylation, leads to strong activation of slow anion channels. Slow anion-channel activity was almost completely abolished by removal of cytosolic ATP or by the kinase inhibitors K-252a and H7. Nonhydrolyzable ATP, GTP, and guanosine 5'-[gamma-thio]triphosphate did not replace the ATP requirement for anion-channel activation. In addition, down-regulation of slow anion channels by ATP removal was inhibited by the phosphatase inhibitor okadaic acid. Stomatal closures in leaves induced by the plant hormone abscisic acid (ABA) and malate were abolished by kinase inhibitors and/or enhanced by okadaic acid. These data suggest that ABA signal transduction may proceed by activation of protein kinases and inhibition of an okadaic acid-sensitive phosphatase. This modulation of ABA-induced stomatal closing correlated to the large dynamic range for up- and down-regulation of slow anion channels by opposing phosphorylation and dephosphorylation events in guard cells. The presented opposing regulation by kinase and phosphatase modulators could provide important mechanisms for signal transduction by ABA and other stimuli during stomatal movements.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-1375754, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-1385219, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-1534380, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-16593851, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-16662049, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-16666553, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-16667813, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-1701140, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-2174559, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-2475930, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-3762694, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-7515176, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-7681395, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-7855884, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-7910981, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-8197457, http://linkedlifedata.com/resource/pubmed/commentcorrection/11607582-8280465
pubmed:language
eng
pubmed:journal
pubmed:status
PubMed-not-MEDLINE
pubmed:month
Oct
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
92
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9535-9
pubmed:dateRevised
2010-9-14
pubmed:year
1995
pubmed:articleTitle
Strong regulation of slow anion channels and abscisic acid signaling in guard cells by phosphorylation and dephosphorylation events.
pubmed:affiliation
Department of Biology, University of California, San Diego, La Jolla, CA 92093-0116, USA.
pubmed:publicationType
Journal Article