Bunched, the Drosophila Homolog of the Mammalian Tumor Suppressor TSC-22, Promotes Cellular Growth

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Bunched, the Drosophila Homolog of the Mammalian Tumor Suppressor TSC-22, Promotes Cellular Growth

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Title: Bunched, the Drosophila Homolog of the Mammalian Tumor Suppressor TSC-22, Promotes Cellular Growth
Author: Gluderer, Silvia; Oldham, Sean; Rintelen, Felix; Sulzer, Andrea; Schütt, Corina; Wu, Xiaodong; Hafen, Ernst; Stocker, Hugo; Raftery, Laurel Anne

Note: Order does not necessarily reflect citation order of authors.

Citation: Gluderer, Silvia, Sean Oldham, Felix Rintelen, Andrea Sulzer, Corina Schütt, Xiaodong Wu, Laurel A. Raftery, Ernst Hafen, and Hugo Stocker. 2008. Bunched, the homolog of the mammalian tumor suppressor TSC-22, promotes cellular growth. BMC Developmental Biology 8: 10.
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Abstract: Background: Transforming Growth Factor-β1 stimulated clone-22 (TSC-22) is assumed to act as a negative growth regulator and tumor suppressor. TSC-22 belongs to a family of putative transcription factors encoded by four distinct loci in mammals. Possible redundancy among the members of the TSC-22/Dip/Bun protein family complicates a genetic analysis. In Drosophila, all proteins homologous to the TSC-22/Dip/Bun family members are derived from a single locus called bunched (bun). Results: We have identified bun in an unbiased genetic screen for growth regulators in Drosophila. Rather unexpectedly, bun mutations result in a growth deficit. Under standard conditions, only the long protein isoform BunA – but not the short isoforms BunB and BunC – is essential and affects growth. Whereas reducing bunA function diminishes cell number and cell size, overexpression of the short isoforms BunB and BunC antagonizes bunA function. Conclusion: Our findings establish a growth-promoting function of Drosophila BunA. Since the published studies on mammalian systems have largely neglected the long TSC-22 protein version, we hypothesize that the long TSC-22 protein is a functional homolog of BunA in growth regulation, and that it is antagonized by the short TSC-22 protein.
Published Version: doi://10.1186/1471-213X-8-10
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2253523/pdf/
http://www.biomedcentral.com/1471-213X/8/10
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:4817300

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