William R. Renthal

The paper shows that somatosensory neuron repertoires in mammals diversify through changes to conserved neuron types, enabling adaptation to different habitats and body forms.

The paper identifies compartment-specific translational programs in sensory neuron axons using spatial translatomics and shows that RNA-binding proteins guide mRNA sorting to establish molecular identities.

The paper creates a canine dorsal root ganglion cell atlas, identifies cell subtypes, and compares them across species to inform pain research.

The paper identifies cis-regulatory elements for targeted gene delivery to nociceptors using multi-omic profiling and develops a sequence-based model to design synthetic enhancers.

The paper identifies OSMR and SST as molecular markers for human dermal sleeping nociceptors, providing new therapeutic targets for neuropathic pain.

This paper constructs a human dorsal root ganglion reference atlas, identifying 22 neuronal subtypes and 10 non-neuronal cell types, and reveals functional differences between human and mouse DRG neurons.

The paper identifies a specific subtype of injured C-fibre nociceptors in neuromas that drive chronic spontaneous neuropathic pain in mice.

This study optimizes MERFISH protocols to improve RNA imaging performance in cell culture and tissue samples.

The paper compares the transcriptome of a human sensory neuron-derived cell line with primary and iPSC-derived sensory neurons to assess its utility as a human model for nociceptive signaling.

This study demonstrates the use of lipid nanoparticles to deliver siRNA to dorsal root ganglion neurons, effectively silencing TRPV1 and reducing pain-related behaviors.

The paper builds harmonized cross-species cell atlases of DRG and TG, identifies 29 cell types across 6 species, and shows transcriptomic similarities and differences in sensory neurons.

This study shows that activity-induced phosphorylation of MeCP2 is critical for retinogeniculate synapse maturation during early postnatal development.

The paper shows that Schwann cell loss causes demyelination and transcriptional reprogramming in specific sensory neurons, suggesting a non-cell autonomous response to axon-Schwann cell interaction loss.

The paper shows that peripheral sensory neurons undergo consistent transcriptional changes after axonal injury, which promote regeneration but also suppress cell identity, with Atf3 playing a key role.