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首页> 外文期刊>Journal of cellular physiology. >AMPKa promotes basal autophagy induction in Dictyostelium discoideum
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AMPKa promotes basal autophagy induction in Dictyostelium discoideum

机译：AMPKa促进基底自噬诱导

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Autophagy is a degradation process, wherein long-lived proteins, damaged organelles, and protein aggregates are degraded to maintain cellular homeostasis. Upon starvation, 5'-AMP-activated protein kinase (AMPK) initiates autophagy. We show that ampkα~- cells exhibit 50% reduction in pinocytosis and display defective phagocytosis. Re-expression of AMPKa in ampkα~-cells co-localizes with red fluorescence protein-tagged bacteria. The ampkα~- cells show reduced cell survival and autophagic flux under basal and starvation conditions. Co-immunoprecipitation studies show conservation of the AMPK-ATG1 axis in basal autophagy. Computational analyses suggest that the N-terminal region of DdATG1 is amenable for interaction with AMPK. Furthermore, β-actin was found to be a novel interacting partner of AMPK, attributed to the alteration in macropinocytosis and phagocytosis in the absence of AMPK. Additionally, ampkα~- cells exhibit enhanced poly-ubiquitinated protein levels and allied large ubiquitin-positive protein aggregates. Our findings suggest that AMPK provides links among pinocytosis, phagocytosis, autophagy, and is a requisite for basal autophagy in Dictyostelium.
机译：自噬是一个退化的过程,其中长寿蛋白质,受损的细胞器蛋白质总量是退化的维护细胞内稳态。5 ' -AMP-activated蛋白激酶(AMPK)发起自噬。减少胞饮和显示缺陷吞噬作用。ampkα-肽硝唑与红色荧光protein-tagged细菌。减少细胞生存和自噬流量基底和饥饿条件。Co-immunoprecipitation研究显示保护基底AMPK-ATG1轴的自噬。计算分析表明,氨基端DdATG1是经得起检验的与AMPK的交互。发现一种新的互动伙伴AMPK,归因于macropinocytosis的变更缺乏AMPK和吞噬作用。此外,ampkα~ -细胞表现出增强的poly-ubiquitinated蛋白质水平和盟军大型ubiquitin-positive蛋白质聚合。研究结果表明,AMPK提供之间的联系胞饮,吞噬作用,自噬,是一个必要的基底自噬在盘基网柄菌。

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