Drosophila p53 Upregulates VDAC Gene Expression That Is Linked to Apoptosis

摘要

p53 is a representative tumor suppressor whose dysfunction is a major cause of human cancer syndrome. Upon activation by various cellular stresses, p53 transactivates downstream target genes as a sequence-specific transcription factor, regulating cellcycle and apoptosis. The signaling pathway leading to apoptosis via the mitochondria is triggered by binding of the Bcl-2 family such as Bcl-2, Bax and Bak to voltage dependent anion channel (VDAC), and this interaction forms large pore in the mitochondria membrane and triggers cytochrome c release. In this study, we investigated the effect of Drosophila p53 (dp53) on VDAC gene expression. Our results indicate that overexpression of dp53 under specific GAL4 drivers induces severe morphological and developmental defects and dp53-mediated apoptosis may occur via VDAC gene upregulation.