Autophagy-independent function of Atg1 for apoptosis-induced compensatory proliferation.
Autophagy-independent function of Atg1 for apoptosis-induced compensatory proliferation.
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DOI：
10.1186/s12915-016-0293-y
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发表时间：
2016-08-19
期刊：
影响因子：
5.4
通讯作者：
Fan Y
中科院分区：
文献类型：
--
作者：
Li M;Lindblad JL;Perez E;Bergmann A;Fan Y
ATG 1属于Uncoordinated-51-like kinase蛋白家族。这个家族的成员最好的特点是在宏观自噬和神经元发育的作用。凋亡诱导的增殖（Apoptosis-induced proliferation，AiP）是一种半胱天冬酶（caspase）介导的JNK依赖性过程，参与了大量应激诱导的凋亡细胞丢失后的组织修复和再生。在某些情况下，AiP可能导致组织过度生长，从而导致癌症。在这里，我们表明，Atg 1在果蝇（dAtg 1）有一个以前未被认识到的功能，再生和过度生长促进AiP在眼睛和翅膀的成虫盘。dAtg 1在JNK活性的遗传下游起作用，并由JNK活性转录诱导，并且它是JNK依赖性的有丝分裂原（如AiP的Wingless）产生所必需的。有趣的是，dAtg 1在AiP中的这种功能与其在自噬和神经元发育中的作用无关。除了dAtg 1在自噬和神经元发育中的作用外，我们还报告了dAtg 1对AiP的第三种功能。本文的在线版本（doi：10.1186/s12915-016-0293-y）包含补充材料，可供授权用户使用。
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. 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. In addition to a role of dAtg1 in autophagy and neuronal development, we report a third function of dAtg1 for AiP. The online version of this article (doi:10.1186/s12915-016-0293-y) contains supplementary material, which is available to authorized users.
影响因子：
2.8
作者：
Ahantarig A;Chadwell LV;Terrazas IB;Garcia CT;Nazarian JJ;Lee HK;Lundell MJ;Cassill JA
通讯作者：
Cassill JA