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Plant Physiol, April 2000, Vol. 122, pp. 1099-1108
The Expression of Small Heat Shock Proteins in Seeds Responds to
Discrete Developmental Signals and Suggests a General Protective Role
in Desiccation Tolerance1
Nadja
Wehmeyer and
Elizabeth
Vierling*
Department of Biochemistry (N.W., E.V.) and Department of Molecular
and Cellular Biology (E.V.), University of Arizona, Tucson, Arizona
85721
To learn more about the function and
regulation of small heat shock proteins (sHSPs) during seed
development, we studied sHSP expression in wild-type and seed
maturation mutants of Arabidopsis by western analysis and using an
HSP17.4 promoter-driven  -glucuronidase (GUS) reporter gene in
transgenic plants. In the absence of stress, GUS activity increases
during development until the entire embryo is stained before
desiccation. Heat-stressed embryos stained for GUS at all stages,
including early stages that showed no detectable HSP17.4::GUS
activity without heat. Examination of HSP17.4 expression in seeds of
the transcriptional activator mutants abi3-6,
fus3-3 (AIMS no. CS8014/N8014), and
lec1-2 (AIMS no. CS2922/N2922) showed that protein and
HSP17.4::GUS activity were highly reduced in fus3-3 and lec1-2 and undetectable in
abi3-6 seeds. In contrast, heat-stressed
abi3-6, fus3-3, and lec1-2
seeds stained for GUS activity throughout the embryo. These data
indicate that there is distinct developmental and stress regulation of
HSP17.4, and imply that ABI3 activates HSP17.4 transcription during
development. Quantitation of sHSP protein in desiccation-intolerant
seeds of abi3-6, fus3-3,
lec1-2, and line24 showed that all had
<2% of wild-type HSP17.4 levels. In contrast, the
desiccation-tolerant but embryo-defective mutants emb266
(AIMS no. CS3049/N3049) and lec2-1 (AIMS no.
CS2728/N2728) had wild-type levels of HSP17.4. These data correlate a
reduction in sHSPs with desiccation intolerance and suggest that sHSPs
have a general protective role throughout the seed.
1
This work was supported by the U.S. Department
of Agriculture National Research Initiative Competitive Grants Program
(grant no. 96-35100-3232) and by University of Arizona Hatch Funds to E.V.
*
Corresponding author; e-mail vierling{at}u.arizona.edu; fax
520-621-3709.
© 2000 American Society of Plant Physiologists
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