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Ciliary beat frequency is controlled by a dynein light chain phosphorylation
P Satir1, K Barkalow, T Hamasaki
1Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Biophysical Journal
|April 1, 1995
Summary
Cyclic AMP-dependent phosphorylation of a 29-kDa axonemal polypeptide (p29) boosts swimming speed in Paramecium and microtubule movement. This suggests p29 regulates outer arm dynein, controlling ciliary beat frequency.
Area of Science:
- Cell Biology
- Biochemistry
- Biophysics
Background:
- Ciliary and flagellar motility are crucial for cellular function.
- Dynein motor proteins drive the movement of cilia and flagella.
- Regulation of dynein activity is essential for controlling motility.
Purpose of the Study:
- To investigate the role of a 29-kDa axonemal polypeptide (p29) in regulating motility.
- To determine the effect of cAMP-dependent phosphorylation on p29 activity.
- To elucidate the mechanism by which p29 influences ciliary beat frequency.
Main Methods:
- Utilized permeabilized Paramecium models.
- Measured in vitro microtubule translocation velocity using purified dynein.
- Developed a quantitative model relating translocation velocity to beat frequency.
Main Results:
- cAMP-dependent phosphorylation of p29 significantly increased Paramecium swimming speed.
- Phosphorylated p29 enhanced the in vitro translocation velocity of microtubules by dynein.
- A direct quantitative relationship was established between microtubule velocity and ciliary beat frequency.
Conclusions:
- The 29-kDa axonemal polypeptide (p29) functions as a regulatory light chain for outer arm dynein.
- p29 plays a critical role in the cAMP-mediated control of ciliary beat frequency.
- This finding provides insight into the molecular mechanisms governing ciliary motility.