Fig. 4. Haploinsufficiency of Sox10 affects glial fate acquisition but not survival of neural crest cells. Undifferentiated p75-positive cells isolated from DRG of wild-type and Sox10^+/– mutant E13 embryos (A-D) were incubated at clonal density either in differentiation medium (‘no add’) or in differentiation medium supplemented with NRG1 (+NRG1). Wild-type cells produced mainly O4-positive glia-containing clones (E). Neurofilament-positive cells were not observed in either wild-type or in Sox10^+/– clones (H-J). Sox10^+/– clones contained no O4-positive cells (F,G). (N,O) Quantitative analysis (see legend to Fig. 3K). ‘Death’ indicates loss of clones. Note that glial fate specification is impaired in both conditions while cell death in Sox10^+/– mutant cells is similar to wild-type cells. NRG1 is acting as a survival factor for Sox10^+/– mutant cells and wild-type cells, independently of fate decisions. In both conditions a glial to non-neural cell fate switch was observed in the Sox10^+/– experiments. (N) represents the data of four independent experiments and (O) the data of three independent experiments. Fifty clones were scored per experiment.