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Updated: Apr 25, 2026

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation
Published on: March 5, 2018
A mitochondrial-associated link between an effector caspase and autophagic flux
Lindsay DeVorkin1, Sharon M Gorski1
1The Genome Sciences Centre; BC Cancer Agency; Vancouver, BC Canada; Department of Molecular Biology and Biochemistry; Simon Fraser University; Burnaby, BC Canada.
Abstract:
It has become evident that caspases function in nonapoptotic cellular processes in addition to the canonical role for caspases in apoptotic cell death. We recently demonstrated that the Drosophila effector caspase Dcp-1 localizes to the mitochondria and positively regulates starvation-induced autophagic flux during mid-oogenesis. Loss of Dcp-1 leads to elongation of the mitochondrial network, increased levels of the adenine nucleotide translocase sesB, increased ATP levels, and a reduction in autophagy. We found that sesB is a negative regulator of autophagic flux, and Dcp-1 interacts with sesB in a nonproteolytic manner to regulate its stability, uncovering a novel mechanism of mitochondrial associated, caspase-mediated regulation of autophagy in vivo.
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