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Brain Res Mol Brain Res. 1997 Jun;46(1-2):325-8.

Anoxia regulates gene expression in the central nervous system of Drosophila melanogaster.

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Department of Pediatrics (Section of Respiratory Medicine), Yale University School of Medicine, New Haven, CT 06520-8064, USA.


We took advantage of the Drosophila melanogaster's extraordinary resistance to anoxia to study the molecular mechanisms underlying this phenomenon. We analyzed mRNA expression of heat shock proteins (HSP) (HSP26 and HSP70), ubiquitins (UB) (UB3 and UB4), cytochrome oxidase I (COXI) and superoxide dismutase (SOD) using slot blot analysis. The expression of HSP genes, especially HSP70, was remarkably up-regulated (up to a thousand-fold) while those of UB4 and COXI were down-regulated (10-60%) in response to the anoxic stress. The expression of UB3 gene was up-regulated by 1.5x and the expression of SOD gene was not significantly affected. In response to heat shock stress, the expression of HSP genes increased by up to several thousand-fold, the expression of UB genes increased modestly (23-91%) but the expression of SOD and COXI genes was reduced by 25%. Furthermore, the expression patterns of HSP genes under anoxia and heat shock were clearly different. The expression of HSP genes peaked by 15 min into anoxia and then declined but stayed above baseline. In contrast, their expression increased as a function of time during heat exposure. From these results, we conclude that: (1) different forms of stress regulates gene expression in different ways; (2) anoxia differentially regulates gene expression; and (3) the up-regulation of HSP70 and down-regulation of UB4 by anoxia are consistent with the idea that Drosophila melanogaster resist anoxia, at least in part, by protecting proteins against degradation.

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