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N-cadherin and Slit2/3/Robo interactions provide the outward force to drive collective Schwann cell migration during nerve regeneration, identifying a dual role for N-cadherin in both adhesion and repulsion processes during Schwann cell collective migration.

Glial TDP-43 regulates splicing and expression of neurofascin and is required for proper assembly and maintenance of paranodal axoglial junctions.

High PI3K-Akt-mTORC1 activity inhibits Schwann cell differentiation, while after onset of myelination, residual PI3K-Akt-mTORC1 activity promotes myelin growth.

Close examination of lanceolate mechanosensory complexes has revealed clues about the ways that sensory nerves detect the movement of hairs and shown than terminal Schwann cells are needed to maintain and regenerate these intricate structures.

A genetic strategy reveals that the perisynaptic glial response to neural activity in one population of these glia regulates postsynaptic function and therefore muscle fatigue.

GDNF receptor-expressing mesenchymal progenitor subpopulation within skeletal muscle responds to peripheral nerve injury by sensing GDNF and secreting BDNF, thereby directly promoting nerve regeneration through facilitating remyelination by Schwann cells.

Establishing transcriptional profiles of nerve-inhabitant cells as resource to foster the fundamental understanding of peripheral nerves.

Neural tube-associated boundary caps are heterogeneous with a non-neural crest-derived subpopulation that may originate from the developing meninges, which gives rise to derivatives that migrate along nerves to detach and differentiate into skin mural cells.

Distinctive microenvironments within demyelinated white matter determine fate decisions of adult oligodendrocyte progenitor cells.

Myelin generation during development and nerve regeneration is guaranteed by responsive backup circuits that coordinate class IIa HDACs to repress the expression of negative regulators of myelination and permit Schwann cell differentiation in response to cAMP.