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首页> 外文期刊>PLoS Genetics >A Snf1-related nutrient-responsive kinase antagonizes endocytosis in yeast
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A Snf1-related nutrient-responsive kinase antagonizes endocytosis in yeast

机译：与酵母中的SNF1相关的营养反应激酶拮抗内吞作用

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Endocytosis is regulated in response to changing environmental conditions to adjust plasma membrane (PM) protein composition for optimal cell growth. Protein networks involved in cargo capture and sorting, membrane sculpting and deformation, and vesicle scission have been well-characterized, but less is known about the networks that sense extracellular cues and relay signals to trigger endocytosis of specific cargo. Hal4 and Hal5 are yeast Snf1-related kinases that were previously reported to regulate nutrient transporter stability by an unknown mechanism. Here we demonstrate that loss of Hal4 and Hal5 activates endocytosis of many different kinds of PM proteins, including Art1-mediated and Art1-independent endocytic events. Acute inhibition of Hal5 in the absence of Hal4 triggers rapid endocytosis, suggesting that Hal kinases function in a nutrient-sensing relay upstream of the endocytic response. Interestingly, Hal5 localizes to the PM, but shifts away from the cell surface in response to stimulation with specific nutrients. We propose that Hal5 functions as a nutrient-responsive regulator of PM protein stability, antagonizing endocytosis and promoting stability of endocytic cargos at the PM in nutrient-limiting conditions.
机译：响应于改变环境条件来调节血浆膜（PM）蛋白质组合物以获得最佳细胞生长的调节内吞作用。涉及货物捕获和分类，膜雕刻和变形的蛋白质网络以及囊泡群体的特征在于，但是较少关于感测细胞外提示和继电器信号以触发特定货物的内吞作用的网络知之甚少。 HAL4和HAL5是先前通过未知机制调节营养转运蛋白稳定性的酵母SNF1相关激酶。在这里，我们证明了HAL4和HAL5的丧失激活了许多不同种类的PM蛋白的内吞作用，包括ART1介导和ART1-Inderynocytic事件。急性抑制HAL5在没有HAL4触发快速内吞作用，表明HAL激酶在内吞反应的上游营养传感继电器中起作用。有趣的是，HAL5定位于PM，但响应于具有特定营养素的刺激而远离细胞表面。我们提出了HAL5作为PM蛋白质稳定性的营养响应性调节剂，拮抗内吞作用，促进PM在营养限制条件下的内吞作用的稳定性。

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