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BioMed Central, BMC Biology, 1(14), 2016

DOI: 10.1186/s12915-016-0293-y

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

Journal article published in 2016 by Mingli Li ORCID, Jillian L. Lindblad, Ernesto Perez, Andreas Bergmann ORCID, Yun Fan
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Data provided by SHERPA/RoMEO

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 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. Conclusion In addition to a role of dAtg1 in autophagy and neuronal development, we report a third function of dAtg1 for AiP.