TL;DR
It is found that the endogenous UPR that precedes meiosis in budding yeast is required for gamete production but diverges dramatically from previously defined UPR outputs, with only a few characterized UPR targets induced, and mildly.
DCP2, encoding a major mRNA decapping enzyme, is identified as a previously unrecognized ISR-induced transcript and it is shown that translational induction of DCP2 depends on an overlapping ORF whose conserved 3′ region, corresponding to a ribosome pausing site, acts as a potent inhibitory element.
This study identifies the ER-anchored transcription factor NAC089 as an ER-phagy receptor acting downstream of the ADP-ribosylation factor (ARF)-like (ARL) GTPase ARLA1A under carbon starvation and demonstrates that active ARLA1A inhibits ER phagy by negatively regulating NAC089.
Findings support a central role for lipid homeostasis in ER functional regulation and suggest that membrane lipid composition contributes to the coordination of ERSU, UPR, and ERAD during ER inheritance under stress.
These findings identify ER-to-Golgi trafficking proteins as cargo-selective regulators that link secretory-pathway demand to adaptive UPR.
Together, the findings establish hY3 as a ribosome-bound regulator of translation and stress responses, positioning it as a determinant of cell fate under metabolic stress.
The results situate Dhh1 and Pat1 as central regulators of the translational response to iron starvation, coordinating both repression of initiation and downstream reinitiation events.
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