Finding. Take lipid droplets away from yeast and the mitochondrial proteome twitches. One of the proteins that falls is Ylr001c, now Vlf1. It is glycosylated, it lives in the vacuole, it touches the autophagic lipase Atg15, and it is a dose-dependent brake on lipophagy. No Vlf1, more fat eating; too much Vlf1, less. Mitochondria reported the lipid-droplet emergency. The vacuole holds the new regulator.
Why this paper matters
LD–mitochondria–vacuole traffic is one homeostasis loop. A mitochondrial-fraction screen that yields a vacuolar lipophagy factor is exactly how those loops get named. Rapamycin sensitivity plus Atg15 binding puts Vlf1 on the autophagy hardware, not only on a localization blot.
What they actually measured
Mito proteomes of LD-null cells, Vlf1 localization/glycosylation, rapamycin, Atg15 interaction, autophagy/lipophagy versus expression.
How to read the score
Around 70. Discovery route is mitochondrial; function is vacuolar lipophagy. Score 70.
What to do with it
If you work on lipophagy, LDs, or yeast autophagy, add Vlf1 next to Atg15. If you came for OXPHOS, keep the mito-proteome-of-LD-loss table and move on. The directional implication is that LD failure is written on mitochondria, and one of the downregulated names is a vacuolar lipophagy brake.