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?7C, Suppl. Fig.?7B and 8), suggesting that the effect of gnl2 or ns depletion on EdU incorporation is cell-autonomous. Even in very large clones (>?300 cells), this difference was apparent Thymidine kinase ( Suppl. Figs.?7F and G). Interestingly, in the 2?ng gnl2 MO clones in WT retinae, there was no apparent difference in EdU intensity between transplanted and directly surrounding cells ( Suppl. Fig.?8F). Since we could not examine the EdU intensity of mutant cells in a WT environment, the cell-autonomous nature of the EdU intensity phenotype cannot be concluded with certainty. Nucleostemin has recently received a great deal of attention in the field of stem cells and cancer biology due to its role in maintenance of proliferation and its high expression in actively proliferating cells. However, the functions of the related protein Gnl2 have not been characterized in detail. We demonstrate that the depletion of either Gnl2 or NS in the retina results in the failure of cells to exit the cell cycle and subsequent delayed terminal differentiation. In contrast, premature cell cycle exit and neuronal differentiation takes place in the brain. These defects appear to be linked to the aberrant expression of specific cell cycle regulators and not to cell cycle arrest caused by the stabilization of p53. Partial redundancy between Gnl2 and NS was suggested by the synergistic worsening of the retinal differentiation MK-8776 cost phenotype in compound gnl2/ns mutants as compared to the respective single mutants. In general, the gnl2 phenotype regarding p53 stabilization and retinal Quizartinib concentration differentiation is more severe compared to the ns mutant phenotype. This difference could be due to differential expression of the two genes. This possibility is supported by the observation that ns expression is more restricted than that of gnl2 during early development (