Drosophila homologs of baculovirus inhibitor of apoptosis proteins function to block cell death
Abstract
Apoptotic cell death is a mechanism by which organisms eliminate superfluous or harmful cells. Expression of the cell death regulatory protein REAPER (RPR) in the developing Drosophila eye results in a small eye owing to excess cell death. We show that mutations in thread (th) are dominant enhancers of RPR-induced cell death and that th encodes a protein homologous to baculovirus inhibitors of apoptosis (IAPs), which we call Drosophila IAP1 (DIAP1). Overexpression of DIAP1 or a related protein, DIAP2, in the eye suppresses normally occurring cell death as well as death due to overexpression of rpr or head involution detective. IAP death-preventing activity localizes to the N-terminal baculovirus IAP repeats, a motif found in both viral and cellular proteins associated with death prevention.
Additional Information
© 1995 Published by Elsevier Inc. Received 14 November 1995, Revised 8 December 1995, Available online 14 April 2004. We would like to thank T. Wolff and H. Chang for an enormous amount of help generating the data and figures presented. We also thank T. Wolff and M. Therrien for comments on drafts of the manuscript and members of the Rubin lab for useful discussions during this work. In addition, we thank J. A. Kennison for providing extensive information on the genetics of the 72D region and for generously providing us with unpublished deficiencies and mutants in this region, the Bloomington Stock Center for providing a collection of chromosomal deficiencies, L. K. Miller for providing CplAP prior to publication, H. Steller for providing GMR-hid flies, and M. Rothe and D. Goeddel for communicating results and providing reagents prior to publication. We also thank T. Laverty for analysis of polytene chromosomes, C. Harmon for help with database analysis, D. Davis for help with scanning electron microscopy, and N. Solomon for much help with sequencing and analysis. B. A. H. is supported by an American Cancer Society fellowship (California division). D. A. W. is supported by a Helen Hay Whitney postdoctoral fellowship. G. M. R. is a Howard Hughes Medical Institute Investigator.Additional details
- Eprint ID
- 102895
- Resolver ID
- CaltechAUTHORS:20200428-154514541
- American Cancer Society, California Division
- Helen Hay Whitney Foundation
- Howard Hughes Medical Institute (HHMI)
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2020-04-28Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field