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

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

PROVIDER: PRJNA699162 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13617969.fastq.gz	Fastqsanger.gz
	SRR13617970.fastq.gz	Fastqsanger.gz
	SRR13617971.fastq.gz	Fastqsanger.gz
	SRR13617972.fastq.gz	Fastqsanger.gz
	SRR13617973.fastq.gz	Fastqsanger.gz

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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

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

Project description:Loss of Prdm12 induces gene deregulation in mature dorsal root ganglia neurons of adult mice

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Identification by RNAsequencing of deregulated genes due to the loss of Prdm12 in dorsal root ganglia of mice in inflammatory condition

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Identification by RNA-seq of Prdm12 regulated genes in trigeminal ganglia of adult mice

Project description:Loss of Prdm12 induces gene deregulation in mature trigeminal ganglia of adult mice

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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.

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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 of adult mice

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

| PRJNA758262 | ENA

Dorsal root ganglia(DRG) proteomic analysis

Project description:Complete annotation mice dorsal root ganglia proteome

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Analysis of the consequences of the constitutive loss of Prdm12 in developing trigeminal ganglia

Project description:Prdm12 is required to repress visceral markers in developing trigeminal ganglia

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Expression data from FACS purified nociceptor neurons from peripheral sensory ganglia

Project description:The goal of this study was to analyze global gene expression in specific populations of nociceptor sensory neurons, the neurons that detect damaging/noxious stimuli. The dorsal root ganglia (DRG), trigeminal ganglia, and nodose ganglia are anatomically distinct peripheral sensory ganglia that contain nociceptors which innervate skin, gut, lungs, and other distinct organ tissues. We used flow cytometry to purify nociceptors from these ganglia and profiled their global gene expression signatures to compare gene expression between these different anatomically distinct nociceptors. Nav1.8-Cre were bred with Rosa26-TdTomato to generate Nav1.8-Cre/R26-TdTomato reporter progeny, where all peripheral nociceptor neurons are genetically marked with red fluroescence due to specific expression of the TTX- resistant sodium channel Nav1.8. Lumbar region dorsal root ganglia (DRG), trigeminal ganglia, and nodose ganglia were dissected from mice (3 mice were pooled/sample). Highly red fluorescent neurons were Facs purified, RNA extracted, and processed for microarray analysis.

2013-08-28 | E-GEOD-46546 | biostudies-arrayexpress

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