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J. Biol. Chem., Vol. 276, Issue 10, 7593-7601, March 9, 2001
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From the Department of Molecular, Cellular, and Developmental
Biology, University of Colorado, Boulder, Colorado 80309-0347
Eucaryotic cells contain at least two general
classes of oxygen-regulated nuclear genes: aerobic genes
and hypoxic genes. Hypoxic genes are induced
upon exposure to anoxia while aerobic genes are
down-regulated. Recently, it has been reported that induction of some
hypoxic nuclear genes in mammals and yeast requires mitochondrial respiration and that cytochrome-c oxidase
functions as an oxygen sensor during this process. In this study, we
have examined the role of the mitochondrion and
cytochrome-c oxidase in the expression of yeast
aerobic nuclear COX genes. We have found that
the down-regulation of these genes in anoxic cells is reflected in
reduced levels of their subunit polypeptides and that
cytochrome-c oxidase subunits I, II, III, Vb, VI, VII, and VIIa are present in promitochondria from anoxic cells. By using nuclear
cox mutants and mitochondrial rho0
and mit
Effects of Anoxia and the Mitochondrion on Expression of
Aerobic Nuclear COX Genes in Yeast
EVIDENCE FOR A SIGNALING PATHWAY FROM THE MITOCHONDRIAL GENOME
TO THE NUCLEUS*
, and
mutants, we have found that neither
respiration nor cytochrome-c oxidase is required for the
down-regulation of these genes in cells exposed to anoxia but that a
mitochondrial genome is required for their full expression under both
normoxic and anoxic conditions. This requirement for a mitochondrial
genome is unrelated to the presence or absence of a functional
holocytochrome-c oxidase. We have also found that the
down-regulation of these genes in cells exposed to anoxia and the
down-regulation that results from the absence of a mitochondrial genome
are independent of one another. These findings indicate that the
mitochondrial genome, acting independently of respiration and oxidative
phosphorylation, affects the expression of the aerobic nuclear
COX genes and suggest the existence of a signaling pathway
from the mitochondrial genome to the nucleus.
*
This work was supported by National Institutes of Health
Grants HL63324 and GM30228.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by a National Institutes of Health postdoctoral fellowship.
§
To whom correspondence should be addressed. Tel.: 303-493-3823;
Fax: 303-492-8783; E-mail: Poyton@spot.Colorado.EDU.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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