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首页> 外文期刊>Development >C-elegans PTEN and AMPK block neuroblast divisions by inhibiting a BMP-insulin-PP2A-MAPK pathway
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C-elegans PTEN and AMPK block neuroblast divisions by inhibiting a BMP-insulin-PP2A-MAPK pathway

机译：C-elegans PTER和AMPK通过抑制BMP-Insulin-PP2A-MAPK途径来阻断神经细胞分裂

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摘要

Caenorhabditis elegans that hatch in the absence of food stop their postembryonic development in a process called L1 arrest. Intriguingly, we find that the postembryonic Q neuroblasts divide and migrate during L1 arrest in mutants that have lost the energy sensor AMP-activated protein kinase (AMPK) or the insulin/IGF-1 signaling (IIS) negative regulator DAF-18/PTEN. We report that DBL-1/BMP works upstream of IIS to promote agonistic insulin-like peptides during L1 arrest. However, the abnormal Q cell divisions that occur during L1 arrest use a novel branch of the IIS pathway that is independent of the terminal transcription factor DAF-16/FOXO. Using genetic epistasis and drug interactions we show that AMPK functions downstream of, or in parallel with DAF-18/PTEN and IIS to inhibit PP2A function. Further, we show that PP2A regulates the abnormal Q cell divisions by activating the MPK-1/ERK signaling pathway via LIN-45/RAF, independently of LET-60/RAS. PP2A acts as a tumor suppressor in many oncogenic signaling cascades. Our work demonstrates a new role for PP2A that is needed to induce neuroblast divisions during starvation and is regulated by both insulin and AMPK.
机译：在没有食物的情况下孵化的皮卡腊肠杆菌在一个名为L1逮捕的过程中停止他们的后宫内发育。有趣的是，我们发现后后型Q神经细胞在L1停滞期间分裂和迁移，突变体损失能量传感器AMP活化蛋白激酶（AMPK）或胰岛素/ IGF-1信号传导（IIS）负调节剂DAF-18 / PTON。我们认为DBL-1 / BMP在IIS的上游工作，以在L1逮捕期间促进激动的胰岛素样肽。然而，在L1逮捕期间发生的异常Q细胞分裂使用IIS途径的新型分支，其独立于终端转录因子DAF-16 / FOXO。使用遗传外观和药物相互作用，我们表明AMPK在下游或与DAF-18 / PTEN和IIS平行的AMPK功能，以抑制PP2A功能。此外，我们表明PP2A通过独立于Let-60 / RA来激活MPK-1 / ERK信号通路来调节异常Q细胞分割。 PP2A在许多致癌信号级联中用作肿瘤抑制剂。我们的工作表明，PP2A的新作用是在饥饿期间诱导神经细胞分裂所需的pp2a，并由胰岛素和安培调节。

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