Genetics. Published Articles Ahead of Print: September 15, 2006, Copyright © 2006
doi:10.1534/genetics.106.061390


A more recent version of this article appeared on November 1, 2006.

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Glyceraldehyde-3-phosphate dehydrogenase mediates anoxia response and survival in Caenorhabditis elegans

Alexander R Mendenhall 1, Bobby LaRue 1 and Pamela A Padilla 1*

1 University of North Texas

* To whom correspondence should be addressed. E-mail: ppadilla{at}unt.edu.

Submitted on June 17, 2006
Revised on August 21, 2006
Accepted on 22 August 2006


Abstract

Oxygen deprivation has a role in the pathology of many human diseases thus it is of interest to understand the genetic and cellular responses to hypoxia or anoxia in oxygen deprivation tolerant organisms such as Caenorhabditis elegans. In C. elegans the DAF-2/DAF-16 pathway, an IGF-1/insulin-like signaling pathway, is involved with dauer formation, longevity and stress resistance. In this report we compared the response wild- type and daf-2(e1370) animals have to anoxia. Unlike wild-type animals, the daf-2(e1370) animals have an enhanced anoxia-survival phenotype in that they survive long-term anoxia and high-temperature anoxia, do not accumulate significant tissue damage in either of these conditions and are motile after 24 hrs of anoxia. RNA interference was used to screen DAF-16 regulated genes that suppress the daf-2(e1370) enhanced anoxia-survival phenotype. We identified gpd-2 and gpd-3; two nearly identical genes in an operon that encode the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase. We found that not only is the daf-2(e1370) enhanced anoxia phenotype dependent upon gpd-2/3 but the motility of animals exposed to brief periods of anoxia is prematurely arrested in gpd-2/3(RNAi) and daf-2 (e1370);gpd-2/3(RNAi) animals. These data suggest that gpd-2/3 may serve a protective role in tissue exposed to oxygen deprivation.

Key Words: C. elegans, Oxygen deprivation, anoxia, dauer pathway, glycolysis