Eukaryotic Cell
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Eukaryotic Cell, October 2008, p. 1795-1808, Vol. 7, No. 10
1535-9778/08/$08.00+0     doi:10.1128/EC.00160-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Anoxia-Induced Suspended Animation in Budding Yeast as an Experimental Paradigm for Studying Oxygen-Regulated Gene Expression{triangledown}

Kin Chan1,2 and Mark B. Roth2*

Molecular and Cellular Biology Program, University of Washington, Seattle, Washington 98195,1 Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 981092

Received 8 May 2008/ Accepted 6 August 2008

A lack of oxygen can force many organisms to enter into recoverable hypometabolic states. To better understand how organisms cope with oxygen deprivation, our laboratory previously had shown that when challenged with anoxia, both the nematode Caenorhabditis elegans and embryos of the zebrafish Danio rerio enter into suspended animation, in which all life processes that can be observed by light microscopy reversibly halt pending the restoration of oxygen (P. A. Padilla and M. B. Roth, Proc. Natl. Acad. Sci. USA 98:7331-7335, 2001, and P. A. Padilla, T. G. Nystul, R. A. Zager, A. C. Johnson, and M. B. Roth, Mol. Biol. Cell 13:1473-1483, 2002). Here, we show that both sporulating and vegetative cells of the budding yeast Saccharomyces cerevisiae also enter into a similar state of suspended animation when made anoxic on a nonfermentable carbon source. Transcriptional profiling using cDNA microarrays and follow-on quantitative real-time PCR analysis revealed a relative derepression of aerobic metabolism genes in carbon monoxide (CO)-induced anoxia when compared to nitrogen (N2) gas-induced anoxia, which is consistent with the known oxygen-mimetic effects of CO. We also found that mutants deleted for components of the mitochondrial retrograde signaling pathway can tolerate prolonged exposure to CO but not to N2. We conclude that the cellular response to anoxia is dependent on whether the anoxic gas is an oxygen mimetic and that the mitochondrial retrograde signaling pathway is functionally important for mediating this response.

* Corresponding author. Mailing address: 1100 Fairview Avenue North A3-015, Seattle, WA 98109. Phone: (206) 667-5602. Fax: (206) 667-5939. E-mail: mroth{at}fhcrc.org

{triangledown} Published ahead of print on 15 August 2008.

Eukaryotic Cell, October 2008, p. 1795-1808, Vol. 7, No. 10
1535-9778/08/$08.00+0     doi:10.1128/EC.00160-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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