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RNA-sequencing of CD4+ T cells from mice prior to and after infection with influenza virus, and that were exposed developmentally to vehicle or TCDD

ABSTRACT: RNA-sequencing of CD4+ T cells from mice prior to and after infection with influenza virus, and that were exposed developmentally to vehicle or TCDD

PROVIDER: PRJNA601990 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10910862.fastq.gz	Fastqsanger.gz
	SRR10910863.fastq.gz	Fastqsanger.gz
	SRR10910864.fastq.gz	Fastqsanger.gz
	SRR10910865.fastq.gz	Fastqsanger.gz
	SRR10910866.fastq.gz	Fastqsanger.gz

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RNA-sequencing of CD4+ T cells from mice prior to and after infection with influenza virus, and that were exposed developmentally to vehicle or TCDD

Project description:We used next generation RNAsequencing to identify how developmental exposure to TCDD alters gene expression in CD4+ T cells. Specifically, mice were developmentally exposed to vehicle or TCDD. At adulthood, CD4+ T cells were purified from peripheral lymph nodes of naive animals or the mediastinal lymph nodes of influenza A virus (IAV) infected mice (9 days post infection). RNA was isolated from these cells, and RNA-seq was performed. Gene expression analysis revealed developmental activation of the aryl hydrocarbon receptor with TCDD changes expression of genes that are involved in important CD4+ T cell functions.

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Whole Genome Bisulfite Sequencing of CD4+ T cells from mice developmentally exposed to vehicle or TCDD prior to and during influenza infection

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Whole Genome Bisulfite Sequencing of CD4+ T cells from mice developmentally exposed to vehicle or TCDD prior to and during influenza infection

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Project description:We used next generation RNAsequencing to identify how triggering the aryl hydrocarbon receptor (AHR) during development alters T cell gene expression. Specifically, mice were developmentally exposed to vehicle or the AHR agonist TCDD. At adulthood, mice were infected with influenza A virus. CD44hiCD4+ and CD44loCD4+ T cells were FACs purified from the mediastinal lymph nodes on day 9 post infection. RNA was isolated from these cells, and RNA-seq was performed. Gene expression analysis revealed developmental AHR activation durably changes the expression of genes involved in several important CD4+ T cell functions, including proliferation, differentiation, and metabolism.

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Project description:Adult zebrafish can completely regenerate their caudal fin following amputation. This complex process is initiated by the formation of an epithelial would cap over the amputation site by 12 hours post amputation (hpa). Once the cap is formed, mesenchymal cells proliferate and migrate from sites distal to the wound plane and accumulate under the epithelial cap forming the blastemal structure within 48 hpa. Blastemal cells proliferate and differentiate, replacing the amputated tissues, which are populated with angiogenic vessels and innervating nerves during the regenerative outgrowth phase which is completed around 14 days post amputation (dpa). Regenerative outgrowth does not occur in TCDD-exposed zebrafish. To identify the molecular pathways that are perturbed by TCDD exposure, male zebrafish were i.p. injected with 50 ng/g TCDD or vehicle and caudal fins were amputated. Regenerating fin tissue was collected at 1, 3 and 5 dpa for mRNA abundance analysis. Microarray analysis and quantitative real time PCR revealed that wound healing and regeneration alone altered the expression of nearly 900 genes by at least two fold between 1 and 5 dpa. TCDD altered the abundance of 370 genes at least two fold. Among these, several known aryl hydrocarbon responsive genes were identified in addition to several genes involved in extracellular matrix composition and metabolism. The profile of misexpressed genes is suggestive of impaired cellular differentiation and extracellular matrix composition potentially regulated by Sox9b. Keywords: Time course and TCDD exposure response

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