Impairment of RPN4, a transcription factor, induces ER stress and lipid abnormality in Saccharomyces cerevisiae.

Accumulation of misfolded/unfolded proteins in the endoplasmic reticulum (ER) induces ER stress. The transcription factor RPN4 {"Regulatory Particle Non-ATPase"} regulates protein homeostasis by degrading proteins that elude proper folding or assembly via the proteasomal degradation pathway. Here, we studied the lipid alterations exerted by Saccharomyces cerevisiae to mitigate (ER) stress during adaptive responses in rpn4∆ cells.

Endoplasmic reticulum stress and calcium imbalance are involved in cadmium-induced lipid aberrancy in Saccharomyces cerevisiae.

The endoplasmic reticulum is the key organelle which controls protein folding, lipid biogenesis, and calcium (Ca(2+)) homeostasis. Cd exposure in Saccharomyces cerevisiae activated the unfolded protein response and was confirmed by the increased Kar2p expression. Cd exposure in wild-type (WT) cells increased PC levels and the PC biosynthetic genes.