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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

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

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Occupancy and transcriptional profile of Prdm12 in posteriorized neural tissue

2015-11-04 | GSE64551 | GEO

Nociceptor translational profiling reveals the RagA-mTORC1 network as a critical generator of neuropathic pain

Project description:Pain sensing neurons, nociceptors, are key drivers of neuropathic pain. We used translating ribosome affinity purification (trap) to comprehensively characterize up- and down-regulated mRNA translation in Scn10a-positive nociceptors in chemotherapy-induced neuropathic pain. We provide evidence that an underlying mechanism driving these changes in gene expression is a sustained mTORC1 activation driven by MNK1-eIF4E signaling. RagA, a GTPase controlling mTORC1 activity, is identified as a novel target of MNK1-eIF4E signaling, demonstrating a new link between these distinct signaling pathways. Neuropathic pain and RagA translation are strongly attenuated by genetic ablation of eIF4E phosphorylation, MNK1 elimination or treatment with the MNK inhibitor eFT508. We reveal a novel translational circuit for the genesis of neuropathic pain with important implications for next generation neuropathic pain therapeutics.

2018-08-01 | GSE113941 | 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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