Autophagy-independent function of Atg1 for apoptosis-induced compensatory proliferation

BMC Biology

Research Article

Andreas Bergmann¹  Ernesto Perez¹  Jillian L. Lindblad¹  Mingli Li²  Yun Fan² 

[1] Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, 364 Plantation Street, LRB419, 01605, Worcester, MA, USA;University of Birmingham, School of Biosciences, Edgbaston, B15 2TT, Birmingham, UK;

关键词: Apoptosis-induced proliferation;    Atg1;    ULK1/2;    Autophagy;    Jun-N-terminal kinase signaling;   

DOI  :  10.1186/s12915-016-0293-y

 received in 2016-05-15, accepted in 2016-08-08,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundATG1 belongs to the Uncoordinated-51-like kinase protein family. Members of this family are best characterized for roles in macroautophagy and neuronal development. Apoptosis-induced proliferation (AiP) is a caspase-directed and JNK-dependent process which is involved in tissue repair and regeneration after massive stress-induced apoptotic cell loss. Under certain conditions, AiP can cause tissue overgrowth with implications for cancer.ResultsHere, we show that Atg1 in Drosophila (dAtg1) has a previously unrecognized function for both regenerative and overgrowth-promoting AiP in eye and wing imaginal discs. dAtg1 acts genetically downstream of and is transcriptionally induced by JNK activity, and it is required for JNK-dependent production of mitogens such as Wingless for AiP. Interestingly, this function of dAtg1 in AiP is independent of its roles in autophagy and in neuronal development.ConclusionIn addition to a role of dAtg1 in autophagy and neuronal development, we report a third function of dAtg1 for AiP.

【 授权许可】

CC BY   
© Li et al. 2016