Plant Cell Advance Online Publication
Published on November 26, 2002; 10.1105/tpc.006981
Received August 9, 2002
Accepted September 17, 2002
OSM1/SYP61: A syntaxin protein in arabidopsis controls abscisic acid-mediated
and non-abscisic acid-mediated responses to abiotic stress
Jianhua Zhu 1, Zhizhong Gong 2, Changqing Zhang 2, Chun-Peng Song 2, Barbara Damsz 1, Günsu Inan 1, Hisashi Koiwa 3, Jian-Kang Zhu 2, Paul M. Hasegawa 1, and Ray A. Bressan 1*
1
Center for Plant Environmental Stress Physiology, Department of Horticulture and
Landscape Architecture, Purdue University, West Lafayette, Indiana 47907-1165
2
Department of Plant Sciences, University of Arizona, Tucson, Arizona 85721
3
Department of Horticultural Sciences, Texas A&M University, College Station,
Texas 77843-2133
* To whom correspondence should be addressed. E-mail: bressan{at}hort.purdue.edu.
To identify the genetic loci that control salt tolerance in higher plants, a large-scale
screen was conducted with a bialaphos marker-based T-DNA insertional collection
of Arabidopsis ecotype C24 mutants. One line, osm1 (for osmotic stress-sensitive
mutant), exhibited increased sensitivity to both ionic (NaCl) and nonionic (mannitol)
osmotic stress in a root-bending assay. The osm1 mutant displayed a more
branched root pattern with or without stress and was hypersensitive to inhibition
by Na+, K+, and Li+ but not Cs+. Plants
of the osm1 mutant also were more prone to wilting when grown with limited
soil moisture compared with wild-type plants. The stomata of osm1 plants
were insensitive to both ABA-induced closing and inhibition of opening compared with
wild-type plants. The T-DNA insertion appeared in the first exon of an open reading
frame on chromosome 1 (F3M18.7, which is the same as AtSYP61).
This insertion mutation cosegregated closely with the osm1 phenotype and
was the only functional T-DNA in the mutant genome. Expression of the OSM1
gene was disrupted in mutant plants, and abnormal transcripts accumulated. Gene complementation
with the native gene from the wild-type genome completely restored the mutant phenotype
to the wild type. Analysis of the deduced amino acid sequence of the affected gene
revealed that OSM1 is related most closely to mammalian syntaxins 6 and 10, which
are members of the SNARE superfamily of proteins required for vesicular/target membrane
fusions. Expression of the OSM1 promoter:: -glucuronidase gene in transformants
indicated that OSM1 is expressed in all tissues except hypocotyls and young
leaves and is hyperexpressed in epidermal guard cells. Together, our results demonstrate
important roles of OSM1/SYP61 in osmotic stress tolerance and in the ABA regulation
of stomatal responses.
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