National Institute of Biological Sciences, Beijing 102206, China.
National Institute of Biological Sciences, Beijing 102206, China; Tsinghua Institute of Multidisciplinary Biomedical Research, Tsinghua University, Beijing 100084, China.
Cell Rep. 2021 Mar 23;34(12):108875. doi: 10.1016/j.celrep.2021.108875.
The maintenance of mitochondrial homeostasis requires PTEN-induced kinase 1 (PINK1)-dependent mitophagy, and mutations in PINK1 are associated with Parkinson's disease (PD). PINK1 is also downregulated in tumor cells with PTEN mutations. However, there is limited information concerning the role of PINK1 in tissue growth and tumorigenesis. Here, we show that the loss of pink1 caused multiple growth defects independent of its pathological target, Parkin. Moreover, knocking down pink1 in muscle cells induced hyperglycemia and limited systemic organismal growth by the induction of Imaginal morphogenesis protein-Late 2 (ImpL2). Similarly, disrupting PTEN activity in multiple tissues impaired systemic growth by reducing pink1 expression, resembling wasting-like syndrome in cancer patients. Furthermore, the re-expression of PINK1 fully rescued defects in carbohydrate metabolism and systemic growth induced by the tissue-specific pten mutations. Our data suggest a function for PINK1 in regulating systemic growth in Drosophila and shed light on its role in wasting in the context of PTEN mutations.
线粒体动态平衡的维持需要 PTEN 诱导的激酶 1(PINK1)依赖性的线粒体自噬,而 PINK1 的突变与帕金森病(PD)有关。PTEN 突变的肿瘤细胞中 PINK1 的表达也下调。然而,关于 PINK1 在组织生长和肿瘤发生中的作用的信息有限。在这里,我们表明,pink1 的缺失导致了多种生长缺陷,与它的病理性靶标 Parkin 无关。此外,在肌肉细胞中敲低 pink1 通过诱导 Imaginal morphogenesis protein-Late 2 (ImpL2) 引起高血糖和全身性生长受限。同样,在多种组织中破坏 PTEN 活性通过降低 pink1 的表达来损害全身性生长,类似于癌症患者的消耗综合征。此外,PINK1 的重新表达完全挽救了由组织特异性 pten 突变引起的碳水化合物代谢和全身性生长缺陷。我们的数据表明 PINK1 在调控果蝇的全身生长中具有功能,并揭示了其在 PTEN 突变背景下消耗中的作用。