Chlamydomonas reinhardtii hydin is a central pair protein required for flagellar motility

Citations Over TimeTop 10% of 2007 papers

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.

Related Papers

• → Alpha-tubulin acetylase activity in isolated Chlamydomonas flagella.(1985)60 cited
• → Chlamydomonas as a model system to study cilia and flagella using genetics, biochemistry, and microscopy(2024)16 cited
• → Chlamydomonas reinhardtii: Biological Rationale for Genomics1(2000)20 cited
• → Defects in the ratio of the dynein isoform, DHC11 in the long-flagella mutants of Chlamydomonas reinhardtii(2016)3 cited
• → Μελέτη της βιοαποικοδόμησης φαινολικών ενώσεων από μικροοργανισμούς(2018)