ArticleCell communication and signaling : CCS2026
AlphaFold3-based modeling uncovers the dynamic structural interface between full-length IAP antagonists and DIAP1 for apoptosis regulation in Drosophila.
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Apoptosis in Drosophila is governed by caspases, inhibitor of apoptosis proteins (IAPs), and IAP antagonists. Using AlphaFold3, we modeled full-length 3D structures of the IAP antagonists Reaper, Hid, Grim, Sickle, and Jafrac2, as well as DIAP1 and dBruce, and their binary and higher-order complexes. We predict a paradoxical role for the N-terminal methionine of Reaper in stabilizing Reaper/Hid complexes and inhibiting DIAP1 binding. Our models reveal that Reaper uniquely engages both BIR1 and BIR2 domains of DIAP1, guided by α-helical residues in its backbone, while all other IAP antagonists preferentially target BIR2. Higher-order assemblies show how Reaper and Hid as well as Reaper and Grim cooperatively engage DIAP1 and allosterically modulate its E3 ligase activity. We present the first full-length model of dBruce and its inhibitory interaction with Rpr. These findings provide a comprehensive structural framework for apoptosis regulation in Drosophila, and offer new insights into conserved mechanisms of caspase control and IAP antagonism across species.
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