RT Journal Article
SR Electronic
T1 Bab2 activates JNK signaling to reprogram <em>Drosophila</em> wing disc development
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.12.30.424794
DO 10.1101/2020.12.30.424794
A1 Yunpo Zhao
A1 Jianli Duan
A1 Alexis Dziedziech
A1 Sabrina Büttner
A1 Ylva Engström
YR 2020
UL http://biorxiv.org/content/early/2020/12/30/2020.12.30.424794.abstract
AB In response to cellular stress and damage, certain tissues are able to regenerate and to restore tissue homeostasis. In Drosophila imaginal wing discs, dying cells express mitogens that induce compensatory proliferation in the surrounding tissue. Here we report that high levels of the BTB/POZ transcription factor Bab2 in the posterior compartment of wing discs activates c-Jun N-terminal kinase (JNK) signaling and local, cell-autonomous apoptotic cell death. This in turn triggered the upregulation of the Dpp mitogen and cellular proliferation in the anterior compartment in a JNK-dependent manner. In the posterior compartment, however, dpp expression was suppressed, most likely by direct transcriptional repression by Bab2. This dual-mode of JNK-signaling, autocrine pro-apoptotic signaling and paracrine pro-proliferative signaling, led to opposite effects in the two compartments and reprogramming of the adult wing structure. We establish Bab2 as a regulator of wing disc development, with the capacity to reprogram development via JNK activation in a cell-autonomous and non-cell-autonomous manner.Summary statement Zhao et al. shows that the BTB/POZ transcription factor Bab2 is a potent activator of JNK signaling, apoptosis and compensatory proliferation, thereby driving both pro-tumorigenic and anti-tumorigenic processes.