The abstract is read at the publisher; the summary is JClub's.
Phosphorylation-site mutations in Cmk2p in budding yeast differentially control calcium-induced steady-state expression of slow- and fast-migrating Cmk2, with S445 blocking both.
- Why it matters: Calcium signaling regulation in yeast depends on Cmk2p, but how specific post-translational modification residues tune its steady-state levels under calcium stress is unclear.
- What they did: The study mutated 15 posttranslational modification residues in Cmk2p (14 phosphorylated, one ubiquitinylated) and measured steady-state expression of SM-Cmk2 and FM-Cmk2 under calcium stress.
- The result: K173 ubiquitinylation altered steady-state level independent of calcium stress, while Y353/S354, S371/S379, S433, S445, and S406 each selectively blocked or reduced SM-Cmk2 and/or FM-Cmk2 expression, implying site-specific roles in stability during calcium stress.
The findingWhy it mattersWhat they didThe result
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