Journal article
Drosophila VHL tumor-suppressor gene regulates epithelial morphogenesis by promoting microtubule and aPKC stability
S Duchi, L Fagnocchi, V Cavaliere, A Hsouna, G Gargiulo, T Hsu
Development | COMPANY OF BIOLOGISTS LTD | Published : 2010
DOI: 10.1242/dev.042804
Abstract
Mutations in the human von Hippel-Lindau (VHL) genes are the cause of VHL disease, which displays multiple benign and malignant tumors. The VHL gene has been shown to regulate angiogenic potential and glycolic metabolism via its E3 ubiquitin ligase function against the alpha subunit of hypoxia-inducible factor (HIF). However, many other HIF-independent functions of VHL have been identified and recent evidence indicates that the canonical function cannot fully explain the VHL mutant cell phenotypes. Many of these functions have not been verified in genetically tractable systems. Using an established follicular epithelial model in Drosophila, we show that the Drosophila VHL gene is involved in..
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Awarded by National Institute of General Medical Sciences
Funding Acknowledgements
We thank W. M. Deng (Florida State University), D. Grifoni (University of Bologna), T. Schupbach (Princeton University) and A. Wodarz (Georg-August-University Gottingen) for generous gifts of antibodies and fly stocks. K. Lavenburg contributed to the initial cloning of the Drosophila VHL genomic sequence for subsequent mutagenesis. The work was supported by grants from the National Institutes of Health (PO1CA78582 and RO1CA109860) to T. H., a grant from the University of Bologna (RFO 2007) to G. G. and V. C. and a Marco Polo Fellowship from the University of Bologna to S. D. Deposited in PMC for release after 12 months.