ArticleAlcohol (Fayetteville, N.Y.)2019
PKA, PP1, and DC1 phosphorylation mediate alcohol-induced ciliary dysfunction in Chlamydomonas reinhardtii.
Article in Alcohol (Fayetteville, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Isoform-specific phosphorylation of axonemal dynein heavy chains.Molecular biology of the cell · 2025Article
- FromiScience · 2024Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Excessive alcohol consumption impairs mucociliary clearance, in part, by compromising ciliary movement. Our previous study found alcohol reduces ciliary beat frequency in Chlamydomonas through a mechanism that involves the β and γ heavy chains of the outer dynein arm (ODA). Moreover, we identified DC1, a subunit of the ODA-docking complex (ODA-DC), as the first ciliary target for alcohol. DC1 phosphorylation is alcohol sensitive and correlates with alcohol-induced ciliary dysfunction (AICD). Furthermore, DC1 phosphorylation is disrupted in the absence of the central pair and ODA. These results implicate a role for DC1 phosphorylation in regulating the ODA activity and mediating AICD. In our current study, we identified four alcohol-sensitive phosphosites in DC1: S33, T73, T351, and S628. Mutations of these sites rescue the assembly of the ODA-DC and ODA, resulting in wild-type swimming velocities. When cells were challenged with alcohol, we determined that three sites, S33, T351, and S628, are critical for mediating the ciliary slowing effects of alcohol. This result is consistent with our pharmacological studies, which reveal that both PP1 and PKA activities are required for AICD.
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