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

## TL;DR

Deleting a gene that regulates phospholipid production in yeast changes a protein's modification, possibly affecting cell function.

## Contribution

Shows that lipid biosynthesis disruption alters protein modification, not degradation, in yeast ER.

## Key findings

- INO4 deletion does not destabilize Sbh1 or Cue1 proteins.
- Sbh1 shows altered electrophoretic mobility in ino4Δ yeast.
- Phospholipid changes may affect post-translational modifications.

## Abstract

We recently discovered that disrupting phospholipid biosynthesis by eliminating the Ino2/4 transcriptional regulator impairs endoplasmic reticulum (ER)-associated degradation (ERAD) in
Saccharomyces cerevisiae
, 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,
INO4
deletion does not destabilize Sbh1 or Cue1. However, we observed altered electrophoretic mobility of Sbh1 in
ino4
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.