The NAB-Brk signal bifurcates at JNK to independently induce apoptosis and compensatory proliferation.

ABSTRACT: Apoptosis operates to eliminate damaged or potentially dangerous cells. This loss is often compensated by extra proliferation of neighboring cells. Studies in Drosophila imaginal discs suggest that the signal for the additional growth emanates from the dying cells. In particular, it was suggested that the initiator caspase Dronc mediates compensatory proliferation (CP) through Dp53 in wing discs. However, the exact mechanism that governs this CP remained poorly understood. We have previously shown that elimination of misspecified cells due to reduced Dpp signaling is achieved by the interaction of the co-repressor NAB with the transcriptional repressor Brk, which in turn induces Jun N-terminal kinase-dependent apoptosis. Here, we performed a systematic in vivo loss- and gain-of-function an

SUBMITTER: Suissa Y 

PROVIDER: S-EPMC3083146 | biostudies-literature | 2011 Apr

REPOSITORIES: biostudies-literature