Previous reports, including transplantation experiments using dominant-negative inhibition of β1-integrin signaling in oligodendrocyte progenitor cells, suggested that β1-integrin signaling is required for myelination. Here, we test this hypothesis using conditional ablation of the β1-integrin gene in oligodendroglial cells during the development of the CNS. This approach allowed us to study oligodendroglial β1-integrin signaling in the physiological environment of the CNS, circumventing the potential drawbacks of a dominant-negative approach. We found that β1-integrin signaling has a much more limited role than previously expected. Although it was involved in stage-specific oligodendrocyte cell survival, β1-integrin signaling was not required for axon ensheathment and myelination per se. We also found that, in the spinal cord, remyelination occurred normally in the absence of β1-integrin. We conclude that, although β1-integrin may still contribute to other aspects of oligodendrocyte biology, it is not essential for myelination and remyelination in the CNS.