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C57BL\/6OlaHsd\u2010<jats:italic>Wld<jats:sup>S<\/jats:sup><\/jats:italic> (Wld<jats:sup>S<\/jats:sup>) mutant mice exhibit significant delays in WD. This results in considerably delayed Schwann cell and macrophage responses and thus in impaired nerve regenerations. In our previous work, thousands of genes were screened by DNA microarrays and over 700 transcripts were found to be differentially expressed in the injured sciatic nerve of Wld<jats:sup>S<\/jats:sup> compared with wild\u2010type (WT) mice. One of these transcripts, betacellulin (Btc), was selected for further analysis since it has yet to be characterized in the nervous system, despite being known as a ligand of the ErbB receptor family. We show that <jats:italic>Btc<\/jats:italic> mRNA is strongly upregulated in immature and dedifferentiated Sox2<jats:sup>+<\/jats:sup> Schwann cells located in the sciatic nerve distal stump of WT mice, but not Wld<jats:sup>S<\/jats:sup> mutants. Transgenic mice ubiquitously overexpressing Btc (Tg\u2010Btc) have increased numbers of Schmidt\u2010Lantermann incisures compared with WT mice, as revealed by Coherent anti\u2010Stokes Raman scattering (CARS). Tg\u2010Btc mice also have faster nerve conduction velocity. Finally, we found that deficiency in Btc reduces the proliferation of myelinating Schwann cells after sciatic nerve injury, while Btc overexpression induces Schwann cell proliferation and improves recovery of locomotor function. Taken together, these results suggest a novel regulatory role of Btc in axon\u2010Schwann cell interactions involved in myelin formation and nerve repair. 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