| Literature DB >> 32376681 |
Anja Beckers1, Christian Adis1, Karin Schuster-Gossler1, Lena Tveriakhina1, Tim Ott2, Franziska Fuhl2, Jan Hegermann3, Karsten Boldt4, Katrin Serth1, Ev Rachev1, Leonie Alten1, Elisabeth Kremmer5, Marius Ueffing4, Martin Blum6, Achim Gossler7.
Abstract
Cilia are complex cellular protrusions consisting of hundreds of proteins. Defects in ciliary structure and function, many of which have not been characterised molecularly, cause ciliopathies: a heterogeneous group of human syndromes. Here, we report on the FOXJ1 target gene Cfap206, orthologues of which so far have only been studied in Chlamydomonas and Tetrahymena In mouse and Xenopus, Cfap206 was co-expressed with and dependent on Foxj1 CFAP206 protein localised to the basal body and to the axoneme of motile cilia. In Xenopus crispant larvae, the ciliary beat frequency of skin multiciliated cells was enhanced and bead transport across the epidermal mucociliary epithelium was reduced. Likewise, Cfap206 knockout mice revealed ciliary phenotypes. Electron tomography of immotile knockout mouse sperm flagella indicated a role in radial spoke formation reminiscent of FAP206 function in Tetrahymena Male infertility, hydrocephalus and impaired mucociliary clearance of the airways in the absence of laterality defects in Cfap206 mutant mice suggests that Cfap206 may represent a candidate for the subgroup of human primary ciliary dyskinesias caused by radial spoke defects.Entities:
Keywords: Ciliary beat frequency; Hydrocephalus; Male infertility; Motile cilia; Mucus accumulation; Radial spoke defect
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Year: 2020 PMID: 32376681 DOI: 10.1242/dev.188052
Source DB: PubMed Journal: Development ISSN: 0950-1991 Impact factor: 6.862