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Vol. 12, Issue 2, 297-308, February 2001
*Department of Molecular Biology, and §McDermott
Center for Human Growth and Development and Center for Biomedical
Inventions, University of Texas Southwestern Medical Center, Dallas,
Texas 75390-9148
Mitochondrial dysfunction can lead to diverse cellular and
organismal responses. We used DNA microarrays to characterize the transcriptional responses to different mitochondrial perturbations in
Saccharomyces cerevisiae. We examined
respiratory-deficient petite cells and respiratory-competent wild-type
cells treated with the inhibitors of oxidative phosphorylation
antimycin, carbonyl cyanide m-chlorophenylhydrazone, or
oligomycin. We show that respiratory deficiency, but not inhibition of
mitochondrial ATP synthesis per se, induces a suite of genes associated
with both peroxisomal activities and metabolite-restoration
(anaplerotic) pathways that would mitigate the loss of a complete
tricarboxylic acid cycle. The array data suggested, and direct
microscopic observation of cells expressing a derivative of green
fluorescent protein with a peroxisomal matrix-targeting signal
confirmed, that respiratory deficiency dramatically induces peroxisome
biogenesis. Transcript profiling of cells harboring null alleles of
RTG1, RTG2, or RTG3, genes known to
control signaling from mitochondria to the nucleus, suggests that there
are multiple pathways of cross-talk between these organelles in yeast.
Online version of this article contains video
material and is available at www.molbiolcell.org.
Present addresses:
Aventis Pharmaceuticals, Inc.,
Cambridge Genomics Center, Cambridge, MA 02139.
Molecular Staging, Inc., Guilford, CT 06437.
Corresponding author. E-mail address:
butow{at}swmed.edu.
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