The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
Mutations in Hydin impair ciliary motility in mice
Open accessAbstract
Chlamydomonas reinhardtii hydin is a central pair protein required for flagellar motility, and mice with Hydin defects develop lethal hydrocephalus. To determine if defects in Hydin cause hydrocephalus through a mechanism involving cilia, we compared the morphology, ultrastructure, and activity of cilia in wild-type and hydin mutant mice strains. The length and density of cilia in the brains of mutant animals is normal. The ciliary axoneme is normal with respect to the 9 + 2 microtubules, dynein arms, and radial spokes but one of the two central microtubules lacks a specific projection. The hydin mutant cilia are unable to bend normally, ciliary beat frequency is reduced, and the cilia tend to stall. As a result, these cilia are incapable of generating fluid flow. Similar defects are observed for cilia in trachea. We conclude that hydrocephalus in hydin mutants is caused by a central pair defect impairing ciliary motility and fluid transport in the brain.
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Flagellar motility is required for the viability of the bloodstream trypanosome
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Metadata
- Authors
- Lechtreck, K.-F., Delmotte, P., Robinson, M. L., Sanderson, M. J., & Witman, G. B.
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2008-02-04
- Volume
- 180
- Issue
- 3
- Pages
- 633-643
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W1967146176
- Cited by
- 278
- References
- 47
- FWCI
- 11.60
- Type
- journal article
- Language
- en
- Open access
- green
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