Figure 2. A putative mechanism for Ypt-dependent regulation of HAC1 stability. Under normal growth conditions, Ypts mediate vesicle-assisted trafficking of unspliced HAC1 away from the ER and the ER-localized Ire1/Ada5 complex to prevent unnecessary activation of the UPR. HAC1 degradation may also be happening directly adjacent to the ER. Ypt GTPases ‘communicate’ with each other via interactions with common protein factors (e.g., GEFs, effectors, etc. not shown) and may utilize this crosstalk to direct HAC1 localization in proximity to RNA decay factors for degradation. Additional adaptor proteins linking the HAC1 RNA to the lipid membrane of the vesicle or mediating the Ypt-RNA interactions may be present but are not shown for simplicity. The HAC1 RNA is depicted as a squiggly line. EE, early endosomes; LE, late endosomes; ER, endoplasmic reticulum; PM, plasma membrane.