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Chlamydomonas reinhardtii Hydin Is a Central Pair Protein Required for Flagellar Motility

Karl-Ferdinand Lechtreck and George B. Witman
The Journal of Cell Biology
Vol. 176, No. 4 (Feb. 12, 2007), pp. 473-482
Stable URL: http://www.jstor.org/stable/30049988
Page Count: 10
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Chlamydomonas reinhardtii Hydin Is a Central Pair Protein Required for Flagellar Motility
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Abstract

Mutations in Hydin cause hydrocephalus in mice, and HYDIN is a strong candidate for causing hydrocephalus in humans. The gene is conserved in ciliated species, including Chlamydomonas reinhardtii. An antibody raised against C. reinhardtii hydin was specific for an ∼540-kD flagellar protein that is missing from axonemes of strains that lack the central pair (CP). The antibody specifically decorated the C2 microtubule of the CP apparatus. An 80% knock down of hydin resulted in short flagella lacking the C2b projection of the C2 microtubule; the flagella were arrested at the switch points between the effective and recovery strokes. Biochemical analyses revealed that hydin interacts with the CP proteins CPC1 and kinesin-like protein 1 (KLP1). In conclusion, C. reinhardtii hydin is a CP protein required for flagellar motility and probably involved in the CP-radial spoke control pathway that regulates dynein arm activity. Hydrocephalus caused by mutations in hydin likely involves the malfunctioning of cilia because of a defect in the CP.

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