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J Cell Biol. 2007 Feb 12;176(4):403-4.

Hydin seek: finding a function in ciliary motility.

Author information

1
Department of Biological Sciences, Dartmouth College, Hanover, NH 03755, USA. elizabeth.f.smith@dartmouth.edu

Abstract

One of the most surprising discoveries in cell biology in the past 5-10 years is the number of diverse human diseases that result from defects in ciliary assembly and/or motility, so-called ciliopathies (Badano, J.L., N. Mitsuma, P.L. Beales, and N. Katsanis. 2006. Annu. Rev. Genomics Hum. Genet. 7:125-148). The results presented by Lechtreck and Witman (see p. 473 of this issue) provide yet another example of how work in the model organism Chlamydomonas reinhardtii can reveal important insights into the underlying mechanisms of ciliary assembly/function and the diseases associated with defects in these organelles. By taking advantage of the wide array of experimental approaches C. reinhardtii offers, Lechtreck and Witman determined the precise axonemal location of hydin, a protein that, when mutated, causes hydrocephalus, and defined a unique role for hydin in ciliary motility.

PMID:
17296793
PMCID:
PMC2063975
DOI:
10.1083/jcb.200701113
[Indexed for MEDLINE]
Free PMC Article
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