Abstract：
:CEP63 is a centrosomal protein that facilitates centriole duplication and is regulated by the DNA damage response. Mutations in CEP63 cause Seckel syndrome, a human disease characterized by microcephaly and dwarfism. Here we demonstrate that Cep63-deficient mice recapitulate Seckel syndrome pathology. The attrition of neural progenitor cells involves p53-dependent cell death, and brain size is rescued by the deletion of p53. Cell death is not the result of an aberrant DNA damage response but is triggered by centrosome-based mitotic errors. In addition, Cep63 loss severely impairs meiotic recombination, leading to profound male infertility. Cep63-deficient spermatocytes display numerical and structural centrosome aberrations, chromosome entanglements and defective telomere clustering, suggesting that a reduction in centrosome-mediated chromosome movements underlies recombination failure. Our results provide novel insight into the molecular pathology of microcephaly and establish a role for the centrosome in meiotic recombination.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Marjanović M,Sánchez-Huertas C,Terré B,Gómez R,Scheel JF,Pacheco S,Knobel PA,Martínez-Marchal A,Aivio S,Palenzuela L,Wolfrum U,McKinnon PJ,Suja JA,Roig I,Costanzo V,Lüders J,Stracker THdoi
10.1038/ncomms8676subject
Has Abstractpub_date
2015-07-09 00:00:00pages
7676issn
2041-1723pii
ncomms8676journal_volume
6pub_type
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