| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2048508 | FEBS Letters | 2012 | 7 Pages |
Ycf1p function is regulated by casein kinase 2αα, Cka1p, via phosphorylation of Ser251. Cka1p-mediated phosphorylation of Ycf1p is attenuated in response to high salt stress. Previous results from our lab suggest a role for Ycf1p in cellular resistance to salt stress. Here, we show that Ycf1p plays an important role in cellular resistance to salt stress by maintaining the cellular redox balance via glutathione recycling. Our results suggest that during acute salt stress increased Sod1p, Sod2p and Ctt1p activity is the main compensatory for the loss in Ycf1p function that results from reduced Ycf1p-dependent recycling of cellular GSH levels.
► Ycf1p plays a role in normal basal growth glutathione (GSH) recycling. ► ycf1Δ cells have reduced GSH recycling and a reduced [GSH]/[GSSG] ratio. ► Reduced GSH recycling in ycf1Δ cells induces Sod1p, Sod2p, and Ctt1p activity.
