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Mitochondrial Contribution to the Anoxic Ca2+ Signal
in Maize Suspension-Cultured Cells1
Chalivendra C. Subbaiah*,
Douglas S. Bush2, and
Martin
M. Sachs
Department of Crop Sciences, University of Illinois, Urbana,
Illinois 61801 (C.C.S., M.M.S.); Department of Biological Sciences,
Rutgers University, Newark, New Jersey 07102 (D.S.B.); and United States
Department of Agriculture/Agricultural Research Service, Plant
Physiology and Genetics Research Unit, Urbana, Illinois 61801 (M.M.S.)
Anoxia
induces a rapid elevation of the cytosolic Ca2+
concentration ([Ca2+]cyt) in maize
(Zea mays L.) cells, which is caused by the release of
the ion from intracellular stores. This anoxic Ca2+ release
is important for gene activation and survival in
O2-deprived maize seedlings and cells. In this study we
examined the contribution of mitochondrial Ca2+ to the
anoxic [Ca2+]cyt elevation in maize cells.
Imaging of intramitochondrial Ca2+ levels showed that a
majority of mitochondria released their Ca2+ in response to
anoxia and took up Ca2+ upon reoxygenation. We also
investigated whether the mitochondrial Ca2+ release
contributed to the increase in
[Ca2+]cyt under anoxia. Analysis of the
spatial association between anoxic [Ca2+]cyt
changes and the distribution of mitochondrial and other intracellular Ca2+ stores revealed that the largest
[Ca2+]cyt increases occurred close to
mitochondria and away from the tonoplast. In addition,
carbonylcyanide p-trifluoromethoxyphenyl hydrazone
treatment depolarized mitochondria and caused a mild elevation of
[Ca2+]cyt under aerobic conditions but
prevented a [Ca2+]cyt increase in response to
a subsequent anoxic pulse. These results suggest that mitochondria play
an important role in the anoxic elevation of
[Ca2+]cyt and participate in the signaling of
O2 deprivation.
1
This work was supported by a grant from the
National Research Initiative Competitive Grants Program, U.S.
Department of Agriculture (no. 96-35100-3143 to M.M.S. and C.C.S.) and
by a National Science Foundation grant (no. DCB-9206692 to D.S.B.).
2
Present address: Department of Biological
Sciences, University of California, Santa Barbara, CA 93106-0001.
*
Corresponding author; e-mail subbaiah{at}uiuc.edu; fax
1-217-333-6064.
Plant Physiol. (1998) 118: 759-771
Copyright Clearance Center: 0032-0889/98/118//13
© 1998 American Society of Plant Physiologists
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