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A glucose-starvation response governs endocytic trafficking and eisosomal retention of surface cargoes in budding yeast
Journal of Cell Science ( IF 4 ) Pub Date : 2021-01-25 , DOI: 10.1242/jcs.257733
Kamilla M E Laidlaw 1 , Daniel D Bisinski 1 , Sviatlana Shashkova 1, 2 , Katherine M Paine 1 , Malaury A Veillon 1 , Mark C Leake 1, 2 , Chris MacDonald 3
Affiliation  

Kamilla M. E. Laidlaw, Daniel D. Bisinski, Sviatlana Shashkova, Katherine M. Paine, Malaury A. Veillon, Mark C. Leake, and Chris MacDonald

Eukaryotic cells adapt their metabolism to the extracellular environment. Downregulation of surface cargo proteins in response to nutrient stress reduces the burden of anabolic processes whilst elevating catabolic production in the lysosome. We show that glucose starvation in yeast triggers a transcriptional response that increases internalisation from the plasma membrane. Nuclear export of the Mig1 transcriptional repressor in response to glucose starvation increases levels of the Yap1801 and Yap1802 clathrin adaptors, which is sufficient to increase cargo internalisation. Beyond this, we show that glucose starvation results in Mig1-independent transcriptional upregulation of various eisosomal factors. These factors serve to sequester a portion of nutrient transporters at existing eisosomes, through the presence of Ygr130c and biochemical and biophysical changes in Pil1, allowing cells to persist throughout the starvation period and maximise nutrient uptake upon return to replete conditions. This provides a physiological benefit for cells to rapidly recover from glucose starvation. Collectively, this remodelling of the surface protein landscape during glucose starvation calibrates metabolism to available nutrients.

This article has an associated First Person interview with the first author of the paper.



中文翻译:

葡萄糖饥饿反应控制出芽酵母中表面货物的内吞运输和 eisosomal 保留

Kamilla ME Laidlaw、Daniel D. Bisinski、Sviatlana Shashkova、Katherine M. Paine、Malaury A. Veillon、Mark C. Leake 和 Chris MacDonald

真核细胞使它们的新陈代谢适应细胞外环境。响应营养压力的表面货物蛋白的下调减少了合成代谢过程的负担,同时提高了溶酶体中的分解代谢产生。我们表明酵母中的葡萄糖饥饿会触发转录反应,从而增加质膜的内化。响应葡萄糖饥饿的 Mig1 转录抑制因子的核输出增加了 Yap1801 和 Yap1802 网格蛋白接头的水平,这足以增加货物的内化。除此之外,我们表明葡萄糖饥饿导致各种 eisosomal 因子的独立于 Mig1 的转录上调。这些因素有助于将一部分营养转运蛋白隔离在现有的 eisosomes 中,通过 Ygr130c 的存在以及 Pil1 中的生化和生物物理变化,允许细胞在整个饥饿期间持续存在,并在恢复到充足条件时最大限度地吸收营养。这为细胞从葡萄糖饥饿中快速恢复提供了生理益处。总的来说,葡萄糖饥饿期间表面蛋白质景观的这种重塑将新陈代谢校准为可用的营养物质。

本文与该论文的第一作者进行了相关的第一人称采访。

更新日期:2021-02-01
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