![]() ![]() Phospho-histone-3 antibody staining suggested that the cell cycle is delayed in the mutant embryo. In situ hybridization of notch1b and deltaa also showed fewer neural stem cells that give rise to fewer but bigger neuronal precursors. In situ hybridization of markers expressed in neural precursors and blood cells showed that, in general, mutant embryos have bigger and fewer cells. We found that the earliest visible mutant phenotype was a darkening of the head caused by the appearance of apoptotic cells in the brain. In situ hybridization of cyclin B1 revealed that the mRNA is absent in the mutant embryo by gastrulation. Sequencing showed a transition (C139→T) that caused a nonsense mutation in exon 2 of the cyclin B1 gene. The spr mutation mapped to the cyclin B1 gene. Here we show that the zebrafish specter (spr) mutant is mutation in the cyclin B1 gene, a gene necessary for the G2 to M transition of the cell cycle. Cell division is controlled by genes that regulate the cell cycle. ![]()
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