4.5 Article

A glucose-starvation response governs endocytic trafficking and eisosomal retention of surface cargoes in budding yeast

期刊

JOURNAL OF CELL SCIENCE
卷 134, 期 2, 页码 -

出版社

COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.257733

关键词

Eisosomes; Endosomal trafficking; Glucose starvation; Membrane trafficking

资金

  1. Wellcome Trust
  2. Royal Society [204636/Z/16/Z]
  3. Engineering and Physical Sciences Research Council [EP/T002166/1]
  4. Biotechnology and Biological Sciences Research Council [BB/R001235/1]
  5. FP7 People: Marie-Curie Actions (ITN) [764591]
  6. Leverhulme Trust [RPG-2019-156/RPG-2017-340]
  7. University of York
  8. BBSRC [BB/R001235/1] Funding Source: UKRI
  9. EPSRC [EP/T002166/1] Funding Source: UKRI
  10. Marie Curie Actions (MSCA) [764591] Funding Source: Marie Curie Actions (MSCA)

向作者/读者索取更多资源

Eukaryotic cells adjust their metabolism in response to extracellular environment, with downregulation of surface cargo proteins under nutrient stress to enhance nutrient uptake. Glucose starvation triggers various transcriptional responses, including increased internalization and nutrient transport, enabling cells to persist and maximize nutrient uptake during starvation.
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.

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