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Yorkie Growth-Promoting Activity Is Limited by Atg1-Mediated Phosphorylation.
Developmental Cell ( IF 11.8 ) Pub Date : 2020-02-04 , DOI: 10.1016/j.devcel.2020.01.011
Lauren K Tyra 1 , Nilay Nandi 1 , Charles Tracy 1 , Helmut Krämer 2
Affiliation  

The expression of multiple growth-promoting genes is coordinated by the transcriptional co-activator Yorkie with its major regulatory input provided by the Hippo-Warts kinase cascade. Here, we identify Atg1/ULK1-mediated phosphorylation of Yorkie as an additional inhibitory input independent of the Hippo-Warts pathway. Two serine residues in Yorkie, S74 and S97, are Atg1/ULK1 consensus target sites and are phosphorylated by ULK1 in vitro, thereby preventing its binding to Scalloped. In vivo, gain of function of Atg1, or its activator Acinus, caused elevated Yorkie phosphorylation and inhibited Yorkie's growth-promoting activity. Loss of function of Atg1 or Acinus raised expression of Yorkie target genes and increased tissue size. Unlike Atg1's role in autophagy, Atg1-mediated phosphorylation of Yorkie does not require Atg13. Atg1 is activated by starvation and other cellular stressors and therefore can impose temporary stress-induced constraints on the growth-promoting gene networks under the control of Hippo-Yorkie signaling.

中文翻译:

约克生长促进活性受Atg1介导的磷酸化作用的限制。

多个促生长基因的表达由转录共激活因子Yorkie和Hippo-Warts激酶级联反应提供的主要调控输入进行协调。在这里,我们确定约克的Atg1 / ULK1介导的磷酸化是独立于Hippo-Warts途径的其他抑制输入。Yorkie中的两个丝氨酸残基S74和S97是Atg1 / ULK1共有靶位点,并且在体外被ULK1磷酸化,从而阻止了其与扇贝的结合。在体内,Atg1或其激活物Acinus的功能获得导致约克磷酸化升高,并抑制了约克的促生长活性。Atg1或Acinus的功能丧失会提高Yorkie靶基因的表达并增加组织大小。与Atg1在自噬中的作用不同,Atg1介导的Yorkie磷酸化不需要Atg13。
更新日期:2020-02-07
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