PubMed ID
17296796
UMMS Affiliation
Department of Cell Biology
Date
2-14-2007
Document Type
Article
Subjects
Animals; Chlamydomonas reinhardtii; DNA-Binding Proteins; Down-Regulation; Flagella; Fungal Proteins; Hydrocephalus; Locomotion; Microfilament Proteins; Microtubule-Associated Proteins; Microtubules; Mutation; Protozoan Proteins
Disciplines
Life Sciences | Medicine and Health Sciences
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 approximately 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.
Rights and Permissions
Citation: J Cell Biol. 2007 Feb 12;176(4):473-82. Link to article on publisher's site