First published online May 2, 2002; 10.1104/pp.001362
Plant Physiol, June 2002, Vol. 129, pp. 838-853
Heat Stress- and Heat Shock Transcription Factor-Dependent
Expression and Activity of Ascorbate Peroxidase in
Arabidopsis1
Irina I.
Panchuk,
Roman A.
Volkov, and
Friedrich
Schöffl*
Zentrum für Molekularbiologie der Pflanzen (Center of Plant
Molecular Biology), Allgemeine Genetik, Universität
Tübingen, 72076 Tübingen, Germany
To find evidence for a connection between heat stress
response, oxidative stress, and common stress tolerance, we studied the
effects of elevated growth temperatures and heat stress on the activity
and expression of ascorbate peroxidase (APX). We compared wild-type
Arabidopsis with transgenic plants overexpressing heat shock
transcription factor 3 (HSF3), which synthesize heat shock proteins and
are improved in basal thermotolerance. Following heat stress, APX
activity was positively affected in transgenic plants and correlated
with a new thermostable isoform, APXS. This enzyme was
present in addition to thermolabile cytosolic APX1, the prevalent
isoform in unstressed cells. In HSF3-transgenic plants,
APXS activity was detectable at normal temperature and
persisted after severe heat stress at 44°C. In nontransgenic plants,
APXS was undetectable at normal temperature, but could be
induced by moderate heat stress. The mRNA expression profiles of known and three new Apx genes were determined using real-time
PCR. Apx1 and Apx2 genes encoding
cytosolic APX were heat stress and HSF dependently expressed, but only
the representations of Apx2 mRNA met the criteria that
suggest identity between APXS and APX2: not expressed at
normal temperature in wild type, strong induction by heat stress, and
HSF3-dependent expression in transgenic plants. Our data suggest that
Apx2 is a novel heat shock gene and that the enzymatic
activity of APX2/APXS is required to compensate heat
stress-dependent decline of APX1 activity in the cytosol. The
functional roles of modulations of APX expression and the
interdependence of heat stress and oxidative stress response and
signaling mechanisms are discussed.
1
This work was supported in part by
Sonderforschungsbereich 446 University of Tübingen of the
Deutsche Forschungsgemeinschaft.
*
Corresponding author; e-mail
friedrich.schoeffl{at}zmbp.uni-tuebingen.de; fax
49-7071-29-5042.
© 2002 American Society of Plant Physiologists
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