First published online October 15, 2002; 10.1104/pp.009480
Plant Physiol, November 2002, Vol. 130, pp. 1276-1287
Localization, Ion Channel Regulation, and Genetic Interactions
during Abscisic Acid Signaling of the Nuclear mRNA Cap-Binding
Protein, ABH11
Véronique
Hugouvieux,
Yoshiyuki
Murata,2
Jared J.
Young,
June M.
Kwak,
Daniel Z.
Mackesy, and
Julian I.
Schroeder*
Division of Biology, Cell, and Developmental Biology Section, and
Center for Molecular Genetics, University of California San Diego,
9500 Gilman Drive, La Jolla, California 92093-0116
Abscisic acid (ABA) regulates developmental processes and
abiotic stress responses in plants. We recently characterized a new
Arabidopsis mutant, abh1, which shows ABA-hypersensitive
regulation of seed germination, stomatal closing, and cytosolic calcium
increases in guard cells (V. Hugouvieux, J.M. Kwak, J.I. Schroeder
[2001] Cell 106: 477-487). ABH1 encodes the large
subunit of a dimeric Arabidopsis mRNA cap-binding complex and in
expression profiling experiments was shown to affect mRNA levels of a
subset of genes. Here, we show that the dimeric ABH1 and AtCBP20
subunits are ubiquitously expressed. Whole-plant growth phenotypes of
abh1 are described and properties of ABH1 in guard cells
are further analyzed. Complemented abh1 lines expressing
a green fluorescent protein-ABH1 fusion protein demonstrate that
ABH1 mainly localizes in guard cell nuclei. Stomatal apertures were
smaller in abh1 compared with wild type (WT) when plants
were grown at 40% humidity, and similar at 95% humidity. Correlated
with stomatal apertures from plants grown at 40% humidity, slow anion
channel currents were enhanced and inward potassium channel currents
were decreased in abh1 guard cells compared with WT. Gas
exchange measurements showed similar primary humidity responses in
abh1 and WT, which together with results from
abh1/abi1-1 double-mutant analyses suggest that
abh1 shows enhanced sensitivity to endogenous ABA.
Double-mutant analyses of the ABA-hypersensitive signaling mutants,
era1-2 and abh1, showed complex genetic
interactions, suggesting that ABH1 and ERA1 do not modulate the same
negative regulator in ABA signaling. Mutations in the RNA-binding
protein sad1 showed hypersensitive ABA-induced stomatal
closing, whereas hyl1 did not affect this response.
These data provide evidence for the model that the mRNA-processing proteins ABH1 and SAD1 function as negative regulators in guard cell
ABA signaling.
1
This research was supported by the National
Institutes of Health (grant no. R01GM60396-01), by the Torrey
Mesa Research Institute/University of California Biostar
(grant), in part by the National Science Foundation (grant no.
MCB 0077791 to J.I.S.), and by the Human Frontier Science Program
Organization (fellowship to J.M.K.).
2
Present address: Department of Agriculture, Okayama
University, Tsushima-Naka, Okayama 700-8530, Japan.
*
Corresponding author; e-mail julian{at}biomail.ucsd.edu;
fax 858-534-7108.
© 2002 American Society of Plant Biologists
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