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

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

PROVIDER: PRJNA704694 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13779900.fastq.gz	Fastqsanger.gz
	SRR13779897.fastq.gz	Fastqsanger.gz
	SRR13779898.fastq.gz	Fastqsanger.gz
	SRR13779899.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Project description: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.

2021-02-25 | GSE167468 | GEO

Identification by RNA-seq of Prdm12 regulated genes in dorsal root ganglia nociceptors of adult mice

Project description:Loss of Prdm12 increases formalin induced inflammatory pain by remodeling gene expression in mature nociceptors

2022-01-25 | GSE166062 | GEO

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

Project description: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.

| S-EPMC8048104 | biostudies-literature

Prdm12 modulates pain-related behavior by remodeling gene expression in mature nociceptors.

Project description:AbstractPrdm12 is a conserved epigenetic transcriptional regulator that displays restricted expression in nociceptors of the developing peripheral nervous system. In mice, Prdm12 is required for the development of the entire nociceptive lineage. In humans, PRDM12 mutations cause congenital insensitivity to pain, likely because of the loss of nociceptors. Prdm12 expression is maintained in mature nociceptors suggesting a yet-to-be explored functional role in adults. Using Prdm12 inducible conditional knockout mouse models, we report that in adult nociceptors Prdm12 is no longer required for cell survival but continues to play a role in the transcriptional control of a network of genes, many of them encoding ion channels and receptors. We found that disruption of Prdm12 alters the excitability of dorsal root ganglion neurons in culture. Phenotypically, we observed that mice lacking Prdm12 exhibit normal responses to thermal and mechanical nociceptive stimuli but a reduced response to capsaicin and hypersensitivity to formalin-induced inflammatory pain. Together, our data indicate that Prdm12 regulates pain-related behavior in a complex way by modulating gene expression in adult nociceptors and controlling their excitability. The results encourage further studies to assess the potential of Prdm12 as a target for analgesic development.

| S-EPMC9341233 | biostudies-literature

Proteomics on Nav1.8-positive nociceptors of mouse DRG

Project description:Nociceptors play an essential role in both acute pain and chronic pain conditions. In this study, we examined the proteome of mouse dorsal root ganglia and compared NaV1.8Cre+/-; ROSA26-flox-stop-flox-DTA (Diphtheria toxin fragment A) mutant mice (NaV1.8Cre-DTA), in which NaV1.8-positive neurons (mainly nociceptors) in dorsal root ganglia (DRG) were ablated, with respective littermate wildtype controls.

2022-10-03 | PXD034447 | Pride

Occupancy and transcriptional profile of Prdm12 in posteriorized neural tissue

Project description:V1 interneurons are a class of inhibitory neurons that play an essential role in vertebrate locomotion; however, the factors contributing to their specification are poorly understood. Morphological and molecular evidence suggest that the zinc finger transcription factor Prdm12 may play a role in promoting V1 interneurons while repressing V2 and V0 fates. Here, we performed RNAseq on Xenopus laevis ectoderm converted to posteriorized neural tissue (with noggin and retinoic acid) in the presence or absence of a series of Prdm12 constructs (wild-type Prdm12, Prdm12-VP16, and Prdm12-engrailed-repressor). We also performed ChIPseq on a Prdm12-FLAG in wild-type or posteriorized neuralized (with noggin and retinoic acid) X. laevis ectoderm. Taken together, these data demonstrate Prdm12's genomic targets and their downstream transcription. X. laevis embryos were injected with mRNAs encoding prdm12 constructs, along with the bmp inhibitor noggin. Presumptive ectoderm (neuralized by noggin) was dissected and treated with retinoic acid. Samples were then processed into RNAseq libraries or prdm12-FLAG was immunoprecipitated and its targets sequenced. Background was input prior to IP.

2015-11-04 | E-GEOD-64551 | biostudies-arrayexpress

Comparison of human PRDM12 mutants D31Y and E172D with wildtype fibroblasts

Project description:Fibroblasts from PRDM12 patients and unaffected wildtype relatives were cultured until near confluency. The transcriptional profile of those cells was determined by mRNA sequencing and uncovered differential expression in several known pain and neurodevelopmental genes.

2015-06-03 | GSE61600 | GEO

Identification by RNA-seq of Prdm12 regulated genes in dorsal root ganglia nociceptors of adult mice

Project description:Identification by RNA-seq of Prdm12 regulated genes in dorsal root ganglia nociceptors of adult mice

| PRJNA699162 | ENA

Occupancy and transcriptional profile of Prdm12 in posteriorized neural tissue

2015-11-04 | GSE64551 | GEO

Multi-Omics Analysis Unveils Nsun5-Mediated Molecular Alterations in the Somatosensory Cortex and its Impact on Pain Sensation

Project description:Nsun5 assumes a pivotal role in the regulation of RNA methylation, and its deficiency has been linked to the advancement of hepatocellular carcinoma, gliomas, tetralogy of Fallot, cognitive deficits in Williams–Beuren syndrome (WBS), and brain development. This underscores Nsun5's significant involvement in the nervous system. In this study, we present evidence of Nsun5's influence on the structure of the primary somatosensory cortex. Through comprehensive multi-omics analyses, we unveil a spectrum of systematically altered genes and proteins, collectively engaged in the orchestration of translation, neurotransmitter metabolism, nerve conduction, synaptic transmission, and other functions. Notably, there are discernible changes in molecules associated with pain sensation, strongly indicating that Nsun5 deficiency undermines pain-related behavior. This investigation establishes a clear link between Nsun5 deficiency and molecular as well as morphological transformations within the primary somatosensory cortex, thereby confirming its role in impairing pain sensation.

2024-07-05 | PXD053689 |

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