Developmental Cell
Volume 35, Issue 5, 7 December 2015, Pages 584-599
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Article
Role for Lipid Droplet Biogenesis and Microlipophagy in Adaptation to Lipid Imbalance in Yeast

https://doi.org/10.1016/j.devcel.2015.11.010Get rights and content
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Highlights

  • Phospholipid imbalance results in morphology defects of ER and mitochondria

  • Excess lipids stimulate lipid droplet (LD) biogenesis at ER aggregates

  • LDs are associated with damaged proteins and are degraded in the vacuole

  • LD delivery to vacuole requires ESCRT proteins and a regulator of ESCRT Ylr312p

Summary

The immediate responses to inhibition of phosphatidylcholine (PC) biosynthesis in yeast are altered phospholipid levels, slow growth, and defects in the morphology and localization of ER and mitochondria. With chronic lipid imbalance, yeast adapt. Lipid droplet (LD) biogenesis and conversion of phospholipids to triacylglycerol are required for restoring some phospholipids to near-wild-type levels. We confirmed that the unfolded protein response is activated by this lipid stress and find that Hsp104p is recruited to ER aggregates. We also find that LDs form at ER aggregates, contain polyubiquitinated proteins and an ER chaperone, and are degraded in the vacuole by a process resembling microautophagy. This process, microlipophagy, is required for restoration of organelle morphology and cell growth during adaptation to lipid stress. Microlipophagy does not require ATG7 but does requires ESCRT components and a newly identified class E VPS protein that localizes to ER and is upregulated by lipid imbalance.

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Present address: Department of Neuroscience, Howard Hughes Medical Institute, University of Wisconsin, Madison, WI 53705, USA