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Cytokinesis is an essential step in neurogenesis, yet the mechanisms that control cytokinesis in the developing CNS are not well understood. The flathead ( fh) mutation in rat results in cytokinesis failure in neural progenitors followed by apoptosis and a dramatic reduction in CNS growth. Here we present evidence that the fh mutation is caused by a single base deletion in exon 1 of the gene encoding Citron-Kinase (CitronK). This base deletion causes a premature stop codon at the 27th codon in the N-terminal kinase domain of Citron-K, and Western blot and immunocytochemical analysis show that the Citron-K protein is absent in proliferative zones in fh/fh mutant embryos. We find that Citron-K protein is normally expressed along the ventricular zone (VZ) surface and localizes to cleavage furrows of both symmetrically and asymmetrically dividing progenitors. In addition, Citron-K colocalizes with RhoA at cleavage furrows in wild-type (wt) embryos, whereas RhoA expression is reduced at the VZ surface and is absent from many cytokinesis furrows in homozygous fh/fh mutants. These results, together with evidence from a recently described induced mutation in mice, indicate that the flathead mutation is in the Citron-K gene and that Citron-K may act with RhoA to ensure the progression of cytokinesis in neuronal progenitors.

Citron-Kinase, A Protein Essential to Cytokinesis in Neuronal Progenitors, Is Deleted in the FlatheadMutant Rat