Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.
Subscribe

Logo for

Mol. Biol. Cell 21 (1): 212-217

Copyright © 2010 by The American Society for Cell Biology.

Hydrogen Sulfide Increases Hypoxia-inducible Factor-1 Activity Independently of von Hippel–Lindau Tumor Suppressor-1 in C. elegans

Mark W. Budde, and Mark B. Roth

Division of Basic Sciences, Fred Hutchinson Cancer Research Center; and Molecular and Cellular Biology Program, University of Washington, Seattle, WA 98109

Received for publication March 11, 2009. Revision received October 9, 2009. Accepted for publication October 23, 2009.

Monitoring Editor: William P. Tansey

Abstract: Rapid alteration of gene expression in response to environmental changes is essential for normal development and behavior. The transcription factor hypoxia-inducible factor (HIF)-1 is well known to respond to alterations in oxygen availability. In nature, low oxygen environments are often found to contain high levels of hydrogen sulfide (H2S). Here, we show that Caenorhabditis elegans can have mutually exclusive responses to H2S and hypoxia, both involving HIF-1. Specifically, H2S results in HIF-1 activity throughout the hypodermis, whereas hypoxia causes HIF-1 activity in the gut as judged by a reporter for HIF-1 activity. C. elegans require hif-1 to survive in room air containing trace amounts of H2S. Exposure to H2S results in HIF-1 nuclear localization and transcription of HIF-1 targets. The effects of H2S on HIF-1 reporter activity are independent of von Hippel–Lindau tumor suppressor (VHL)-1, whereas VHL-1 is required for hypoxic regulation of HIF-1 reporter activity. Because H2S is naturally produced by animal cells, our results suggest that endogenous H2S may influence HIF-1 activity.

This was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E09-03-0199) on November 4, 2009.

Address correspondence to: Mark B. Roth (mroth{at}fhcrc.org).

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Hydrogen Sulfide Stimulates Ischemic Vascular Remodeling Through Nitric Oxide Synthase and Nitrite Reduction Activity Regulating Hypoxia-Inducible Factor-1{alpha} and Vascular Endothelial Growth Factor-Dependent Angiogenesis.
S. C. Bir, G. K. Kolluru, P. McCarthy, X. Shen, S. Pardue, C. B. Pattillo, and C. G. Kevil (2012)
JAHA 1, e004093
   Abstract »    Full Text »    PDF »
Physiological Implications of Hydrogen Sulfide: A Whiff Exploration That Blossomed.
R. Wang (2012)
Physiol Rev 92, 791-896
   Abstract »    Full Text »    PDF »
The Response of Caenorhabditis elegans to Hydrogen Sulfide and Hydrogen Cyanide.
M. W. Budde and M. B. Roth (2011)
Genetics 189, 521-532
   Abstract »    Full Text »    PDF »

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882