Autophagy-independent function of Atg1 for apoptosis-induced compensatory proliferation. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Li, Mingli; Lindblad, Jillian; Perez, Ernesto; Bergmann, Andreas; Fan, Yun
• Is Part Of: BMC biology. Volume 14:Issue 1(2016)
• Page Start: 1
• Page End: 15
• Publication Date: 2016-12
• Subjects: Apoptosis-induced proliferation -- Atg1 -- ULK1/2 -- Autophagy -- Jun-N-terminal kinase signaling; Biology -- Periodicals; Medical sciences -- Periodicals; Biomedical Research -- Periodicals; 570.5
• DOI: 10.1186/s12915-016-0293-y
• Languages: English
• ISSNs: 1741-7007

Abstract

Abstract Background ATG1 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. Results Here, we show thatAtg1 inDrosophila (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 ofdAtg1 in AiP is independent of its roles in autophagy and in neuronal development. Conclusion In addition to a role ofdAtg1 in autophagy and neuronal development, we report a third function ofdAtg1 for AiP.