To clarify the temporal window within which OLIG2-SETDB1 complex functions, various mouse models were generated to interrogate the repressive complex in different OL lineages. When the complex was disassembled in the OPCs of NG2-Cre; Setdb1F/F mice, myelination was substantially reduced in the cortex (Fig. 5e) and spinal cord (Supplementary Fig. 6f); and the abundance of CC1+ cells was diminished in the brain and spinal cord (Fig. 5f and Supplementary Fig. 6g, h). To disassemble the complex after iOLs generation, we generated Cnp-Cre; Setdb1F/F mice (Fig. 5g). These mutant mice survived indistinguishably as the control littermates (Fig. 5h). The number of Plp1+ cell was comparable between mutant and control mice (Supplementary Fig. 6i, j). Ultrastructure analyses of the optic nerves revealed that myelination and g-ratio of axons were also similar (Fig. 5i and Supplementary Fig. 6k). Consistently, MBP and CC1 immunostaining showed that mutant mice did not exhibit notable alternations in myelin (Supplementary Fig. 6l) and OLs at P15 (Fig. 5j and Supplementary Fig. 6m) and P60 (Supplementary Fig. 6n).
