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. Author manuscript; available in PMC: 2010 Feb 27.
Published in final edited form as: Dev Dyn. 2009 Jul;238(7):1638–1648. doi: 10.1002/dvdy.21970

Fig. 6.

Fig. 6

Loss of protein kinase C, iota (PrkCi) function causes formation of excess oligodendrocyte progenitor cells (OPCs) from pMN precursors. Panels show frames captured from time-lapse videos of wild-type and has−/− embryos carrying the Tg(olig2:egfp) reporter. Dorsal is up and time elapsed from beginning of imaging at 50 hours postfertilization (hpf) is indicated in upper right corners of panels. Brackets mark pMN precursor domain in ventral spinal cord. A: Wild-type embryo. Arrowheads mark OPCs migrating dorsally from the ventral pMN precursor domain. B: has−/− embryo. More OPCs (arrowheads) emerge from the pMN domain than in wild-type over a similar period of time. C: Quantification of dorsally migrating OPCs. Data were obtained from time-lapse movies of 6 wild-type and 5 has−/− embryos. Error bars represent SEM. Statistical significance was determined using Student’s t-test.