Please use this identifier to cite or link to this item:
|Title:||Inactivation of AtRac1 by abscisic acid is essential for stomatal closure||Authors:||Lemichez, E.
|Issue Date:||15-Jul-2001||Citation:||Lemichez, E., Wu, Y., Sanchez, J.-P., Mettouchi, A., Mathur, J., Chua, N.-H. (2001-07-15). Inactivation of AtRac1 by abscisic acid is essential for stomatal closure. Genes and Development 15 (14) : 1808-1816. ScholarBank@NUS Repository. https://doi.org/10.1101/gad.900401||Abstract:||Plant water homeostasis is maintained by the phytohormone abscisic acid (ABA), which triggers stomatal pore closure in response to drought stress. We identified the Arabidopsis small guanosine triphosphatase (GTPase) protein AtRac1 as a central component in the ABA-mediated stomatal closure process. ABA treatment induced inactivation of AtRac GTPases and disruption of the guard cell actin cytoskeleton. In contrast, in the ABA-insensitive mutant abi1-1, which is impaired in stomatal closure, neither AtRac inactivation nor actin cytoskeleton disruption was observed on ABA treatment. These observations indicate that AtRac1 inactivation is a limiting step in the ABA-signaling cascade leading to stomatal closure. Consistent with these findings, expression of a dominant-positive mutant of AtRac1 blocked the ABA-mediated effects on actin cytoskeleton and stomatal closure in wild-type plants, whereas expression of a dominant-negative AtRac1 mutant recapitulated the ABA effects in the absence of the hormone. Moreover, the dominant-negative form of AtRac1 could also restore stomatal closure in abi1-1. These results define AtRac1 as a central element for plant adaptation to drought.||Source Title:||Genes and Development||URI:||http://scholarbank.nus.edu.sg/handle/10635/132752||ISSN:||08909369||DOI:||10.1101/gad.900401|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Sep 30, 2020
WEB OF SCIENCETM
checked on Sep 22, 2020
checked on Sep 25, 2020
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.