Loss of Prdm12 during development, but not in mature nociceptors, causes defects in pain sensation

Mark A. Landy, Megan Goyal, Katherine M. Casey, Chen Liu, Helen C. Lai

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


Prdm12 is a key transcription factor in nociceptor neurogenesis. Mutations of Prdm12 cause congenital insensitivity to pain (CIP) from failure of nociceptor development. However, precisely how deletion of Prdm12 during development or adulthood affects nociception is unknown. Here, we employ tissue- and temporal-specific knockout mouse models to test the function of Prdm12 during development and in adulthood. We find that constitutive loss of Prdm12 causes deficiencies in proliferation during sensory neurogenesis. We also demonstrate that conditional knockout from dorsal root ganglia (DRGs) during embryogenesis causes defects in nociception. In contrast, we find that, in adult DRGs, Prdm12 is dispensable for most pain-sensation and injury-induced hypersensitivity. Using transcriptomic analysis, we find mostly unique changes in adult Prdm12 knockout DRGs compared with embryonic knockout and that PRDM12 is likely a transcriptional activator in the adult. Overall, we find that the function of PRDM12 changes over developmental time.

Original languageEnglish (US)
Article number108913
JournalCell Reports
Issue number13
StatePublished - Mar 30 2021


  • DRG
  • Prdm12
  • behavior
  • congenital insensitivity to pain
  • mouse
  • nociceptors
  • pain
  • painlessness
  • sensory neurogenesis

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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