Nuclear receptor DHR96 acts as a sentinel for low cholesterol concentrations in Drosophila melanogaster.
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ABSTRACT: All eukaryotic cells have to maintain cholesterol concentrations within defined margins in order to function normally. Perturbing cholesterol homeostasis can result in a wide range of cellular and systemic defects, including cardiovascular diseases, as well as Niemann-Pick and Tangier diseases. Here, we show that DHR96 is indispensable for mediating the transcriptional response to dietary cholesterol and that it acts as a key regulator of the Niemann-Pick type C gene family, as well as of other genes involved in cholesterol uptake, metabolism, and transport. DHR96 mutants are viable and phenotypically normal on a standard medium but fail to survive on diets that are low in cholesterol. DHR96 mutants have aberrant cholesterol levels, demonstrating a defect in maintaining cholesterol homeost
SUBMITTER: Bujold M
PROVIDER: S-EPMC2812236 | biostudies-literature | 2010 Feb
REPOSITORIES: biostudies-literature
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