Single nuclei RNA sequencing of mouse dorsal root, nodose, and trigeminal ganglia from humanized JAK1 gain-of-function mice

Janus kinase 1 (JAK1) critically mediates downstream signaling from a variety of immune receptors. Gain-of-function mutations in JAK1 in humans lead to immune dysregulation and exaggerated type 2 immune responses, including atopic dermatitis. We have previously shown that JAK1 expressed in neurons mediates cytokine-enhanced itch signaling in atopic dermatitis. We generated a novel mouse expressing human JAK1 with the gain-of-function mutation p.A634D. To better understand how enhanced JAK1 signaling my impact sensory neurons, we performed single nuclei RNA sequencing on different sensory ganglia from JAK1 gain-of-function mice and littermate controls. 10-12-week-old C57BL6 mice heterozygous for an allele where the mouse Jak1 gene was replaced by human JAK1 with the p.A634D mutation, or homozygous for wild type mouse Jak1, were used. Thoracic dorsal root ganglia, nodose ganglia, and trigeminal ganglia were dissociated into single nuclei preps and sequenced using the 10X Genomics multiome pipeline.