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A Snf1-related nutrient-responsive kinase antagonizes endocytosis in yeast.
PLOS Genetics ( IF 4.0 ) Pub Date : 2020-03-19 , DOI: 10.1371/journal.pgen.1008677
Jessica M Tumolo 1 , Nathaniel L Hepowit 1 , Samika S Joshi 1 , Jason A MacGurn 1
Affiliation  

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.

中文翻译:

Snf1相关的营养响应激酶拮抗酵母菌的内吞作用。

响应于变化的环境条件来调节内吞作用,以调节质膜(PM)蛋白质组成,以实现最佳的细胞生长。涉及货物捕获和分类,膜雕刻和变形以及囊切的蛋白质网络已被很好地表征,但对感知细胞外信号并传递信号以触发特定货物的内吞作用的网络知之甚少。Hal4和Hal5是酵母Snf1相关的激酶,以前有报道通过未知的机制调节营养物质转运蛋白的稳定性。在这里,我们证明Hal4和Hal5的失活会激活许多不同种类的PM蛋白的内吞作用,包括Art1介导的和Art1独立的胞吞事件。在没有Hal4的情况下对Hal5的急性抑制会触发快速的内吞作用,提示Hal激酶在胞吞反应上游的营养感知继电器中发挥作用。有趣的是,Hal5定位于PM,但响应特定营养物的刺激而从细胞表面移开。我们建议Hal5充当PM蛋白稳定性的营养响应性调节剂,拮抗内吞作用,并在营养限度条件下促进PM内吞货物的稳定性。
更新日期:2020-04-06
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