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| Status |
Public on Feb 25, 2021 |
| Title |
Loss of Prdm12 during development, but not in mature nociceptors, causes defects in pain sensation. |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
Prdm12 is a key transcription factor in nociceptor neurogenesis. Mutations of Prdm12 cause Congenital Insensitivity to Pain (CIP) due to 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 found mostly unique changes in adult Prdm12 knockout DRGs compared to 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.
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| Overall design |
Bulk mRNA profiles of dorsal root ganglia (DRGs) from wild type (WT, n = 2) and Prdm12AvilERT2CKO (Mut, n = 2)
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| Contributor(s) |
Landy MA, Goyal M, Casey KM, Liu C, Lai HC |
| Citation(s) |
33789102 |
| Submission date |
Feb 24, 2021 |
| Last update date |
Apr 20, 2021 |
| Contact name |
Mark Landy |
| E-mail(s) |
mark.landy@utsouthwestern.edu
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| Organization name |
UT Southwestern Medical Center
|
| Lab |
Lai Lab
|
| Street address |
5323 Harry Hines Blvd
|
| City |
Dallas |
| State/province |
TX |
| ZIP/Postal code |
75390 |
| Country |
USA |
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| Platforms (1) |
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| Samples (4)
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| Relations |
| BioProject |
PRJNA704694 |
| SRA |
SRP307995 |
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