A genome-wide RNAi screen reveals multiple regulators of caspase activation.
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Apoptosis is an evolutionally conserved cellular suicide mechanism that can be activated in response to a variety of stressful stimuli. Increasing evidence suggests that apoptotic regulation relies on specialized cell death signaling pathways and also integrates diverse signals from additional regulatory circuits, including those of cellular homeostasis. We present a genome-wide RNA interference screen to systematically identify regulators of apoptosis induced by DNA damage in Drosophila melanogaster cells. We identify 47 double- stranded RNA that target a functionally diverse set of genes, including several with a known function in promoting cell death. Further characterization uncovers 10 genes that influence caspase activation upon the removal of Drosophila inhibitor of apoptosis 1. This set includes the Drosophila initiator caspase Dronc and, surprisingly, several metabolic regulators, a candidate tumor suppressor, Charlatan, and an N-acetyltransferase, ARD1. Importantly, several of these genes show functional conservation in regulating apoptosis in mammalian cells. Our data suggest a previously unappreciated fundamental connection between various cellular processes and caspase-dependent cell death.
RNA, Small Interfering
bcl-2 Homologous Antagonist-Killer Protein
bcl-2-Associated X Protein
Inhibitor of Apoptosis Proteins
N-Terminal Acetyltransferase A
N-Terminal Acetyltransferase E
Published Version (Please cite this version)10.1083/jcb.200708090
Publication InfoYi, Caroline H; Sogah, Dodzie K; Boyce, Michael; Degterev, Alexei; Christofferson, Dana E; & Yuan, Junying (2007). A genome-wide RNAi screen reveals multiple regulators of caspase activation. The Journal of cell biology, 179(4). pp. 619-626. 10.1083/jcb.200708090. Retrieved from https://hdl.handle.net/10161/19702.
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Michael Scott Boyce
Associate Professor of Biochemistry
The Boyce Lab studies mammalian cell signaling through protein glycosylation. For the latest news, project information and publications from our group, please visit our web site at http://www.boycelab.org or follow us on Twitter at https://twitter.com/BoyceLab.
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