Abstract Oligodendrocytes are the myelinating glia of the central nervous system and ensure rapid saltatory conduction. Shortage or loss of these cells leads to severe malfunctions as observed in human leukodystrophies and multiple sclerosis, and their replenishment by reprogramming or cell conversion strategies is an important research aim. Using a transgenic approach we increased levels of the transcription factor Sox10 throughout the mouse embryo and thereby prompted Fabp7-positive glial cells in dorsal root ganglia of the peripheral nervous system to convert into cells with oligodendrocyte characteristics including myelin gene expression. These rarely studied and poorly characterized satellite glia did not go through a classic oligodendrocyte precursor cell stage. Instead, Sox10 directly induced key elements of the regulatory network of differentiating oligodendrocytes, including Olig2, Olig1, Nkx2.2 and Myrf. An upstream enhancer mediated the direct induction of the Olig2 gene. Unlike Sox10, Olig2 was not capable of generating oligodendrocyte-like cells in dorsal root ganglia. Our findings provide proof-of-concept that Sox10 can convert conducive cells into oligodendrocyte-like cells in vivo and delineates options for future therapeutic strategies. Author Summary Developmental or acquired defects of oligodendrocytes or their myelin sheaths impairs saltatory nerve conduction in the central nervous system and thus leads to severe neurological diseases. Strategies to regenerate or replace these cells require a deeper understanding of the regulatory processes that underlie their generation during development. Here we show in a Sox10 overexpressing mouse model that increase of the levels of a single transcription factor during embryogenesis efficiently converts the already Sox10 expressing satellite glial cells of the peripheral nervous system into oligodendrocyte-like cells by a mechanism that does not simply recapitulate developmental oligodendrogenesis but involves direct Sox10-dependent induction of the oligodendroglial differentiation network. Our study identifies mechanisms that may help to convert other cell types into oligodendrocytes and thus prove eventually useful for therapies of myelin diseases.