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This Article Full Text Full Text (PDF) All Versions of this Article: 91/2/277    most recent expphysiol.2005.030767v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Haddad, G. G. Search for Related Content PubMed PubMed Citation Articles by Haddad, G. G. Related Collections Lectures Respiratory

¹ Departments of Pediatrics and Neuroscience, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0735, USA

Abstract

There have been extensive studies and experiments on cells, tissues and animals that are susceptible to low O₂, and many pathways have been discovered that can lead to injury in mammalian tissues. But other pathways that can help in the survival of low O₂ have also been discovered in these same tissues. It should be noted, however, that the mechanisms that can lead to better survival in susceptible mammalian tissues have quantitatively a ‘narrow range’ for recovery, since these tissues are inherently at risk. Another strategy for understanding the susceptibility of organisms is to learn about pathways used by anoxia-resistant animals. Approximately a decade ago, I and my co-workers discovered that one such animal, Drosophila melanogaster, is very tolerant of low O₂. Here, I detail some of the studies that we performed and the strategies that we developed to understand the mechanisms that underlie the fascinating resistance of Drosophila to measured partial pressure of O₂ of zero. We employed three ideas to try to address our questions: (1) mutagenesis screens to identify loss-of-function mutants; (2) microarrays on adapted versus naïve flies; and (3) studying cell biology and physiology of genes that seem important in flies and mammals. The hope is to learn from these studies about the fundamental basis of tolerance to the lack of O₂, and with this knowledge be able to develop better therapies for the future.

(Received 9 December 2005; accepted after revision 16 January 2006; first published online 23 January 2006)
Corresponding author G. G. Haddad: Department of Pediatrics, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0735, USA. Email: ghaddad{at}ucsd.edu

Experimental Biology, San Diego, CA, USA, April 2005.

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