Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-12-22
pubmed:abstractText
The continuing rise in atmospheric CO2 causes stomatal pores in leaves to close and thus globally affects CO2 influx into plants, water use efficiency and leaf heat stress. However, the CO2-binding proteins that control this response remain unknown. Moreover, which cell type responds to CO2, mesophyll or guard cells, and whether photosynthesis mediates this response are matters of debate. We demonstrate that Arabidopsis thaliana double-mutant plants in the beta-carbonic anhydrases betaCA1 and betaCA4 show impaired CO2-regulation of stomatal movements and increased stomatal density, but retain functional abscisic-acid and blue-light responses. betaCA-mediated CO2-triggered stomatal movements are not, in first-order, linked to whole leaf photosynthesis and can function in guard cells. Furthermore, guard cell betaca-overexpressing plants exhibit instantaneous enhanced water use efficiency. Guard cell expression of mammalian alphaCAII complements the reduced sensitivity of ca1 ca4 plants, showing that carbonic anhydrase-mediated catalysis is an important mechanism for betaCA-mediated CO2-induced stomatal closure and patch clamp analyses indicate that CO2/HCO3- transfers the signal to anion channel regulation. These findings, together with ht1-2 (ref. 9) epistasis analysis demonstrate that carbonic anhydrases function early in the CO2 signalling pathway, which controls gas-exchange between plants and the atmosphere.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-11292871, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-11346781, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-11740564, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-12119381, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-12938931, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-14535880, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-14973164, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-15107451, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-15469500, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-15494745, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-15604670, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-16002616, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-16040633, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-16103214, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-16166256, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-16407445, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-16518390, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-16651523, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-16687407, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-16898020, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-17201685, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-17407539, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-17827274, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-18160292, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-18305482, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-18305484, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-18349152, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-18354450, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-18452588, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-18541006, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-18664613, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-18776898, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-19114538, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-19131626, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-657464, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-8980535, http://linkedlifedata.com/resource/pubmed/commentcorrection/20010812-9276963
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1476-4679
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
87-93; sup pp 1-18
pubmed:dateRevised
2011-7-22
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Carbonic anhydrases are upstream regulators of CO2-controlled stomatal movements in guard cells.
pubmed:affiliation
Division of Biological Sciences, Cell and Developmental Biology Section, University of California San Diego, La Jolla, CA 92093-0116, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural