Developmental regulatory mechanisms for peripheral nervous system formation appear to be conserved in ascidians despite extensive genomic divergence after 390 MY of separate evolution.

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

A comprehensive compendium of myelin proteins in the peripheral nervous system has been created, alongside a method to address molecular diversity of myelin sheaths in health and disease.

A protein called Megf8 regulates the activity of key signaling molecules involved in the development of the peripheral nervous system.

Precise spatiotemporal optogenetic activation of ERK and AKT signaling pathways reveals neural repair mechanisms of the peripheral and central nervous systems in live Drosophila larvae.

Dynamic early clusters of nodal proteins in peripheral nerves represent a neurofascin-dependent developmental stage of node assembly during myelination that precedes heminode formation.

In the peripheral nervous system, the large GTPase dynamin 2 is required for Schwann cell survival, developmental radial sorting of axons, myelination, and myelin maintenance.

Unbiased computational integration of single-cell- and human genetics data shows that susceptibility to obesity is driven by a broad set of neuronal populations across the brain.

Pre-migratory and early migratory neural crest cells in zebrafish are transcriptionally diverse, with some cells expressing genes associated with differentiated derivatives while still in the neural tube.

mTORC1 and c-Jun are implicated in a possible mechanism causing myelin loss downstream of mitochondrial dysfunction in Schwann cells.