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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

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

PROVIDER: PRJNA758271 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15652000.fastq.gz	Fastqsanger.gz
	SRR15651981.fastq.gz	Fastqsanger.gz
	SRR15651982.fastq.gz	Fastqsanger.gz
	SRR15651983.fastq.gz	Fastqsanger.gz
	SRR15651984.fastq.gz	Fastqsanger.gz

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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 dorsal root ganglia of adult mice

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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.

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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.

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

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

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

Project description:Analysis of the consequences of the constitutive loss of Prdm12 in developing trigeminal ganglia

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2015-11-04 | GSE64551 | GEO