Loss of transcriptional regulator of phospholipid biosynthesis alters post-translational modification of Sec61 translocon beta subunit Sbh1 in .

We recently discovered that disrupting phospholipid biosynthesis by eliminating the Ino2/4 transcriptional regulator impairs endoplasmic reticulum (ER)-associated degradation (ERAD) in , but the mechanism is unclear. Phosphatidylcholine deficiency has been reported to accelerate degradation of Sec61 translocon beta subunit Sbh1 and ERAD cofactor Cue1. Here, we found that, unlike targeted phosphatidylcholine depletion, deletion does not destabilize Sbh1 or Cue1. However, we observed altered electrophoretic mobility of Sbh1 in Δ yeast, consistent with phospholipid-responsive post-translational modification. A better understanding of the molecular consequences of disrupted lipid homeostasis could lead to enhanced treatments for conditions associated with perturbed lipid biosynthesis.