Present address: Torrey Mesa Research Institute, Syngenta, 3115 Merryfield Row, San Diego, CA 92121, USA.
The abi1-1 mutation blocks ABA signaling downstream of cADPR action
Article first published online: 23 APR 2003
The Plant Journal
Volume 34, Issue 3, pages 307–315, May 2003
How to Cite
Wu, Y., Sanchez, J. P., Lopez-Molina, L., Himmelbach, A., Grill, E. and Chua, N.-H. (2003), The abi1-1 mutation blocks ABA signaling downstream of cADPR action. The Plant Journal, 34: 307–315. doi: 10.1046/j.1365-313X.2003.01721.x
- Issue published online: 23 APR 2003
- Article first published online: 23 APR 2003
- Received 22 December 2002; revised 16 January 2003; accepted 28 January 2003.
- abscisic acid;
- cyclic ADP-ribose;
- signal transduction pathway
Arabidopsis thaliana abscisic acid insensitive 1-1 (abi1-1) is a dominant mutant that is insensitive to the inhibition of germination and growth by the plant hormone, abscisic acid (ABA). The mutation severely decreases the catalytic activity of the ABI1 type 2C protein phosphatase (PP2C). However, the site of action of the abi1-1/ABI1 in the ABA signal transduction pathway has not yet been determined. Using single cell assays, we showed that microinjecting mutant abi1-1 protein inhibited the activation of RD29A-GUS and KIN2-GUS in response to ABA, cyclic ADP-ribose (cADPR), and Ca2+. The inhibitory effect of the mutant protein, however, was reversed by co-microinjection of an excess amount of the ABI1 protein. In transgenic Arabidopsis plants, overexpression of abi1-1 rendered the plants insensitive to ABA during germination, whereas overexpression of ABI1 did not have any apparent effect. Moreover, transgenic plants overexpressing abi1-1 were blocked in the induction of ABA-responsive genes; however, overexpression of ABI1 did not affect gene expression. Taken together, our results demonstrate that abi1-1 is likely to be a dominant negative mutation and ABI1 likely acts downstream of cADPR in the ABA-signaling pathway. Our results on ABI1 overexpression in Arabidopsis are not compatible with a negative regulatory role of this phosphatase in ABA responses.