Presentation
Nociceptors are specialized sensory neurons that protect organism from dangers by elicitating pain and driving avoidance. Nociceptors can however be sensitized under pathological conditions such as inflammation, leading to chronic pain. Prdm12 is a conserved epigenetic regulator that we showed to be critical for the survival of developing nociceptors. Our recent data indicate that in adulthood, Prdm12 does not control nociceptor survival anymore, but still contribute to the control of gene expression and increases their sensitivity in inflammatory conditions. In this project, to better understand the role and mechanism of action of Prdm12 in nociceptor sensitization, we will study the consequences of its gain of function in nociception and identify its direct transcriptional targets and potential interactors. Besides, we will also test the hypothesis that alterations in Prdm12 expression may contribute to the nociceptor loss observed in the pain insensitive naked mole rat.
Promoters
- Eric Bellefroid, Developmental Genetics Laboratory, ULB
- Ewan St. John Smith, Sensory Neurophysiology and Pain Laboratory, University of Cambridge