Here we describe one mutation, vu166, which causes a reduction of oligodendrocytes. We Veratramine determined that the vu166 allele is a nonsense mutation of pescadillo, which has been implicated in ribosome biogenesis. Our analysis indicates that the oligodendrocyte deficit of pes mutant larvae results from disruption of cell cycle progression among neural precursors. In addition, we found that OPCs fail to migrate normally in mutant embryos as a consequence of an altered cellular environment and that oligodendrocytes express abnormally low levels of myelin genes in mutant larvae, raising the possibility that Pes function is necessary for oligodendrocyte differentiation. Although the apparent reduction of reaction product could result from decreased probe penetration in mutant larvae, a sox2 RNA probe detected higher levels of gene expression in mutants than in wild-type. By finding the period of time that it took for cells to become labeled with PH-3, we calculated the time it took them to progress from S-phase to mitosis. In light of this information and the known role of pes in regulating S-phase progression in yeast, we predicted that the delay in cell cycle progression in mutant zebrafish is due to a failure to progress through S-phase. To test this possibility, we conducted a second BrdU pulse-chase experiment in which we first pulsed cells and then, at varying time-points, pulsed them with the thymidine analog EdU and fixed them immediately. Cells that co-labeled were during the initial pulse and had not yet exited it by the start of the second pulse. By three hours after the initial pulse, the majority of the cells in wild-type spinal cords had progressed through S-phase. In contrast, only about four percent of the cells in mutant spinal cords had exited S-phase. Therefore, loss of pes function impairs the ability of spinal cord precursors to progress through S phase. These data indicate that spinal cord precursors in pes mutant larvae failed to progress through the cell cycle at their normal rates, therefore, one possible explanation for the transient deficit of OPCs is that spinal cord cells are maintained as precursors at the expense of Halothane specified cell types.