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Structural organization of the intermediate and light chain complex of Chlamydomonas ciliary I1 dynein.

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PKA, PP1, and DC1 phosphorylation mediate alcohol-induced ciliary dysfunction in Chlamydomonas reinhardtii.

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Characterization of a new oda3 allele, oda3-6, defective in assembly of the outer dynein arm-docking complex in Chlamydomonas reinhardtii.

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Related Experiment Video

Updated: Apr 18, 2026

Observation of the Ciliary Movement of Choroid Plexus Epithelial Cells Ex Vivo
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Alcohol-induced ciliary dysfunction targets the outer dynein arm.

Fan Yang1, Jacqueline Pavlik2, Laura Fox3

  • 1University of Mississippi Medical Center, Department of Biochemistry, Jackson, Mississippi;

American Journal of Physiology. Lung Cellular and Molecular Physiology
|January 18, 2015
PubMed
Summary

Alcohol abuse impairs cilia function by affecting motor proteins. This study in Chlamydomonas reveals alcohol targets outer dynein arm components, impacting ciliary beat frequency and suggesting DCC1

Keywords:
alcoholciliadyneinethanol

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Biophysics

Background:

  • Alcohol abuse is linked to increased pulmonary infections due to impaired mucociliary clearance.
  • Alcohol affects mammalian airway cilia motility by altering axonemal protein phosphorylation.
  • Cilia are highly conserved, suggesting conserved mechanisms for alcohol-induced ciliary dysfunction (AICD).

Purpose of the Study:

  • To investigate the precise effects of alcohol on ciliary dynein activity in Chlamydomonas.
  • To identify axonemal phosphoproteins altered by alcohol exposure.
  • To elucidate the conserved mechanisms of alcohol-induced ciliary dysfunction.

Main Methods:

  • Utilized the model organism Chlamydomonas for experimental advantages.
  • Analyzed ciliary motility in live cells and reactivated cell models.
  • Employed informative mutant strains, including those lacking specific heavy-chain motor domains.
  • Used a phospho-threonine-specific antibody to assess protein phosphorylation states.

Main Results:

  • Alcohol significantly inhibits ciliary motility in Chlamydomonas.
  • Alcohol impacts the activity of the outer dynein arm, specifically the β- and γ-heavy chains.
  • Alcohol exposure reduces ciliary beat frequency.
  • The phosphorylation state of DCC1, part of the outer dynein arm-docking complex, is altered by alcohol and correlates with AICD.

Conclusions:

  • Alcohol targets specific outer dynein arm components, contributing to ciliary dysfunction.
  • DCC1 is implicated in an alcohol-sensitive mechanism controlling outer dynein arm activity.
  • These findings in Chlamydomonas provide insights into conserved mechanisms of alcohol-induced ciliary dysfunction relevant to human health.