Olig1 function is required for oligodendrocyte differentiation in the mouse brain

Abstract

Oligodendrocyte differentiation and myelinationaretightly regulated processes orchestratedbyacomplex transcriptional network.Two bHLH transcription factors in this network, Olig1 and Olig2, are expressed exclusively by oligodendrocytes after late embryonic development. Although the role of Olig2 in the lineage is well established, the role of Olig1 is still unclear. The current studies analyzed the function of Olig1 in oligodendrocyte differentiation and developmental myelination in brain. Both oligodendrocyte progenitor cell commitment and oligodendrocyte differentiation were impaired inthe corpus callosum of Olig1-null mice, resulting inhypomyelination throughout adulthoodinthebrain.Asseeninpreviousstudies withthis mouse line,although there wasanearly myelination deficitinthe spinal cord, essentially full recovery with normal spinal cord myelination was seen. Intriguingly, this regional difference may be partially attributedtocompensatoryupregulationofOlig2protein expressioninthe spinalcord after Olig1 deletion,whichisnot seeninbrain.The current study demonstrates a unique role for Olig1 in promoting oligodendrocyte progenitor cell commitment, differentiation, and subsequent myelination primarily in brain, but not spinal cord.