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Sensing and responding to hypoxia via HIF in model invertebrates


Gorr, T A; Gassmann, M; Wappner, P (2006). Sensing and responding to hypoxia via HIF in model invertebrates. Journal of Insect Physiology, 52(4):349-364.

Abstract

This past decade has brought considerable progress towards elucidating the molecular mechanisms of oxygen sensing pathways by which mammalian cells are able to detect and adjust, or succumb, to hypoxia. In contrast, far less is known about the protein and DNA constituents that endow many invertebrate species to withstand and recover from even more severe and prolonged O2 limitations. In spite of these differences in hypoxia tolerance, inadequacy in oxygen supply is, from mammals to insects to nematodes, signaled onto the DNA level predominantly by hypoxia-inducible factors (HIFs). Across the animal kingdom, HIF accumulates in hypoxic, but not normoxic, cells and functions in a remarkably conserved pathway. Using crustacean (Daphnia magna) and insect (Drosophila melanogaster) models, work by us and others has implicated HIF in restoring O2 delivery via stimulated hemoglobin synthesis (Daphnia) or tracheal remodeling (Drosophila). HIF is essential for these arthropods to adapt and survive during moderate O2 limitations. A similar life-preserving role for HIF-signaling in hypoxic, but not anoxic, environments had previously been established for another stress-tolerant invertebrate model, the nematode Caenorhabditis elegans. Exploring regulations of oxygen-dependent Daphnia and Drosophila genes in cell culture and in vivo have furthermore aided in uncovering novel HIF-targeting mechanisms that might operate to fine-tune the activity of this transcription factor under steadily hypoxic, rather than changing, oxygen tensions. We conclude our review with yet another addition to the growing list of HIF's many functions: the control of cellular growth during fly development.

This past decade has brought considerable progress towards elucidating the molecular mechanisms of oxygen sensing pathways by which mammalian cells are able to detect and adjust, or succumb, to hypoxia. In contrast, far less is known about the protein and DNA constituents that endow many invertebrate species to withstand and recover from even more severe and prolonged O2 limitations. In spite of these differences in hypoxia tolerance, inadequacy in oxygen supply is, from mammals to insects to nematodes, signaled onto the DNA level predominantly by hypoxia-inducible factors (HIFs). Across the animal kingdom, HIF accumulates in hypoxic, but not normoxic, cells and functions in a remarkably conserved pathway. Using crustacean (Daphnia magna) and insect (Drosophila melanogaster) models, work by us and others has implicated HIF in restoring O2 delivery via stimulated hemoglobin synthesis (Daphnia) or tracheal remodeling (Drosophila). HIF is essential for these arthropods to adapt and survive during moderate O2 limitations. A similar life-preserving role for HIF-signaling in hypoxic, but not anoxic, environments had previously been established for another stress-tolerant invertebrate model, the nematode Caenorhabditis elegans. Exploring regulations of oxygen-dependent Daphnia and Drosophila genes in cell culture and in vivo have furthermore aided in uncovering novel HIF-targeting mechanisms that might operate to fine-tune the activity of this transcription factor under steadily hypoxic, rather than changing, oxygen tensions. We conclude our review with yet another addition to the growing list of HIF's many functions: the control of cellular growth during fly development.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:05 Vetsuisse Faculty > Institute of Veterinary Physiology
04 Faculty of Medicine > Center for Integrative Human Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:April 2006
Deposited On:23 Mar 2009 17:27
Last Modified:05 Apr 2016 13:05
Publisher:Elsevier
ISSN:0022-1910
Publisher DOI:10.1016/j.jinsphys.2006.01.002
PubMed ID:16500673
Permanent URL: http://doi.org/10.5167/uzh-16055

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