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Overexpression of the regulator of G-protein signalling protein enhances ABA-mediated inhibition of root elongation and drought tolerance in Arabidopsis
Author(s) -
Ying Chen
Publication year - 2006
Publication title -
journal of experimental botany
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.616
H-Index - 242
eISSN - 1460-2431
pISSN - 0022-0957
DOI - 10.1093/jxb/erj167
Subject(s) - abscisic acid , arabidopsis , biology , genetically modified crops , transgene , microbiology and biotechnology , regulator , signal transduction , drought tolerance , gene , botany , biochemistry , mutant
Regulator of G-protein signalling (RGS) proteins identified recently in Arabidopsis have been involved in the regulation of several physiological processes, but largely nothing is known about their roles at both the physiological and the molecular level. In the experiments reported here, the overexpression approach was used to present evidence that RGS1 protein plays critical roles in plant development and in modulating abscisic acid (ABA) and drought stress signal transduction. RGS1 affected the shapes of leaves, the development of floral buds, the elongation of stems, siliques, and hypocotyls, and the time of flowering. Post-germination growth was inhibited by 1 microM ABA, and root growth was hypersensitive to ABA for 35S-RGS1 transgenic plants. RGS1 overexpression conferred more drought tolerance to transgenic plants, as compared with the wild type (Columbia). Reverse transcription-PCR (RT-PCR) results indicated that RGS1 overexpresssion significantly stimulated the expression of NCED and ABA2, that encode two key enzymes catalysing ABA biosynthesis. Furthermore, the expression of several stress-regulated genes was either up- or down-regulated in RGS1-overexpressing transgenic plants. Combining the results above with previous results, it is suggested that RGS1 exerted its effects on plant responsiveness to ABA and drought tolerance largely through changing the expression either of genes responsible for ABA biosynthesis, which leads to changes in endogenous ABA levels, or of stress-responsive genes.

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