Please use this identifier to cite or link to this item:
Scopus Web of Science® Altmetric
Type: Journal article
Title: Buffy, a Drosophila Bcl-2 protein, has anti-apoptotic and cell cycle inhibitory functions
Author: Quinn, L.
Coombe, M.
Mills, K.
Daish, T.
Colussi, P.
Kumar, S.
Richardson, H.
Citation: The EMBO Journal, 2003; 22(14):3568-3579
Publisher: Oxford Univ Press
Issue Date: 2003
ISSN: 0261-4189
Statement of
Leonie Quinn, Michelle Coombe, Kathryn Mills, Tasman Daish, Paul Colussi, Sharad Kumar and Helena Richardson
Abstract: Bcl-2 family proteins are key regulators of apoptosis. Both pro-apoptotic and anti-apoptotic members of this family are found in mammalian cells, but only the pro-apoptotic protein Debcl has been characterized in Drosophila. Here we report that Buffy, the second Drosophila Bcl-2-like protein, is a pro-survival protein. Ablation of Buffy by RNA interference leads to ectopic apoptosis, whereas overexpression of buffy results in the inhibition of developmental programmed cell death and γ irradiation-induced apoptosis. Buffy interacts genetically and physically with Debcl to suppress Debcl-induced cell death. Genetic interactions suggest that Buffy acts downstream of Rpr, Grim and Hid, and upstream of the apical caspase Dronc. Furthermore, overexpression of buffy inhibits ectopic cell death in diap1 (th5) mutants. Taken together these data suggest that Buffy can act downstream of Rpr, Grim and Hid to block caspase-dependent cell death. Overexpression of Buffy in the embryo results in inhibition of the cell cycle, consistent with a G1/early-S phase arrest. Our data suggest that Buffy is functionally similar to the mammalian pro-survival Bcl-2 family of proteins.
Keywords: apoptosis, cell survival, Drosophila, programmed cell death, RNA interference, TUNEL
Description: © by the European Molecular Biology Organization
DOI: 10.1093/emboj/cdg355
Published version:
Appears in Collections:Aurora harvest
Medicine publications

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.