Transcriptional profiling of the innate immune response in bovine cells
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ABSTRACT:
PROVIDER: PRJNA767623 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16132441_1.fastq.gz | Fastqsanger.gz | |||
| SRR16132441_2.fastq.gz | Fastqsanger.gz | |||
| SRR16132442_1.fastq.gz | Fastqsanger.gz | |||
| SRR16132442_2.fastq.gz | Fastqsanger.gz | |||
| SRR16132443_1.fastq.gz | Fastqsanger.gz |
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Project description:Cattle are an important livestock species, and understanding the genomic architecture of agriculturally relevant traits such as disease susceptibility is of major interest in the bovine research community. Lineage-specific transposable elements (TEs) are a source of interferon-gamma (IFNG)-inducible regulatory elements that control human immune genes, but this possibility has been largely unexplored in other species that harbor distinct transposon landscapes, including cattle. We conducted transcriptomic and epigenomic profiling of the IFNG response in bovine cells, and found that ruminant-specific TEs are a major source of IFNG-inducible enhancer elements that shape bovine innate immune responses. CRISPR knockout experiments established that key immune genes including bovine IFNAR2 and IL2RB are regulated by TEs in MDBKs. Together with previous work in human cells, our findings demonstrate that lineage-specific TEs have been independently co-opted to regulate IFNG-inducible gene expression in at least two mammalian lineages. Therefore, TE co-option may mediate parallel evolutionary rewiring of mammalian immune regulation.
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Project description:Cattle are an important livestock species, and understanding the genomic architecture of agriculturally relevant traits such as disease susceptibility is of major interest in the bovine research community. Lineage-specific transposable elements (TEs) are a source of interferon-gamma (IFNG)-inducible regulatory elements that control human immune genes, but this possibility has been largely unexplored in other species that harbor distinct transposon landscapes, including cattle. We conducted transcriptomic and epigenomic profiling of the IFNG response in bovine cells, and found that ruminant-specific TEs are a major source of IFNG-inducible enhancer elements that shape bovine innate immune responses. CRISPR knockout experiments established that key immune genes including bovine IFNAR2 and IL2RB are regulated by TEs in MDBKs. Together with previous work in human cells, our findings demonstrate that lineage-specific TEs have been independently co-opted to regulate IFNG-inducible gene expression in at least two mammalian lineages. Therefore, TE co-option may mediate parallel evolutionary rewiring of mammalian immune regulation.
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Project description:Cattle are an important livestock species, and understanding the genomic architecture of agriculturally relevant traits such as disease susceptibility is of major interest in the bovine research community. Lineage-specific transposable elements (TEs) are a source of interferon-gamma (IFNG)-inducible regulatory elements that control human immune genes, but this possibility has been largely unexplored in other species that harbor distinct transposon landscapes, including cattle. We conducted transcriptomic and epigenomic profiling of the IFNG response in bovine cells, and found that ruminant-specific TEs are a major source of IFNG-inducible enhancer elements that shape bovine innate immune responses. CRISPR knockout experiments established that key immune genes including bovine IFNAR2 and IL2RB are regulated by TEs in MDBKs. Together with previous work in human cells, our findings demonstrate that lineage-specific TEs have been independently co-opted to regulate IFNG-inducible gene expression in at least two mammalian lineages. Therefore, TE co-option may mediate parallel evolutionary rewiring of mammalian immune regulation.
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Project description:The innate immune signaling pathway plays a crucial role in the recognition and early response to pathogens associated with disease. Genetic analysis has been unable to completely account for individual variability in the strength of the innate immune response. The aim of this study was to determine the role of the epigenetic markers (DNA methylation or histone acetylation) in controlling bovine gene expression in relation to the response to lipopolysaccharide (LPS). To determine the impact epigenetics may have in controlling innate immunity, dermal fibroblasts from fifteen dairy heifers having previously displayed a differential response to LPS were exposed to 5-aza-2M-bM-^@M-^Y-deoxyctidine (AZA) and trichostatin A (TSA); de-methylating and hyper-acetylating agents, respectively. The AZA-TSA Fibroblast cultures (n=3) were examined under either control conditions or for gene expression following epigenetic modification with the de-methylating agent 5-aza-2'-deoxycytidine and hyper-acetylation agent trichostatin-A. Finally, expression was investigated for responsiveness to lipopolysaccharide (LPS)
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Project description:The innate immune signaling pathway plays a crucial role in the recognition and early response to pathogens associated with disease. Genetic analysis has been unable to completely account for individual variability in the strength of the innate immune response. The aim of this study was to determine the role of the epigenetic markers (DNA methylation or histone acetylation) in controlling bovine gene expression in relation to the response to lipopolysaccharide (LPS). To determine the impact epigenetics may have in controlling innate immunity, dermal fibroblasts from fifteen dairy heifers having previously displayed a differential response to LPS were exposed to 5-aza-2’-deoxyctidine (AZA) and trichostatin A (TSA); de-methylating and hyper-acetylating agents, respectively. The AZA-TSA
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Project description:The innate immune system provides the first response to pathogen infection and orchestrates the activation of the adaptive immune system. Though a large component of the innate immune response is common to all infections, pathogen-specific innate immune responses have been documented as well. The innate immune response is thought to be especially critical for fighting infection with Mycobacterium tuberculosis (MTB), the causative agent of tuberculosis (TB). While TB can be a deadly disease, only 5-10% of individuals infected with MTB develop active disease, and this inter-individual variation is, at least partly, heritable. Studies of inter-individual variation in the innate immune response to MTB infection may therefore shed light on the genetic basis for variation in susceptibility to TB. Yet, to date, we still do not know which properties of the innate immune response are specific to MTB infection and which represent a general response to pathogen infection. To begin addressing this gap, we infected macrophages with eight different bacterial pathogens, including different MTB strains and related mycobacteria, and studied the transcriptional response to infection. We found that although the gene expression changes were largely consistent across the bacterial infection treatments, we were able to identify a novel subset of genes whose regulation was affected specifically by infection with mycobacteria. Genetic variants that are associated with regulatory differences in these genes should be considered candidate loci for explaining inter-individual susceptibility TB. RNA-seq of monocyte-derived macrophages isolated from 6 healthy European males at 4, 18, and 48 hours post-infection with the following 8 bacteria: Mycobacterium tuberculosis (MTB) H37Rv, Mycobacterium tuberculosis GC1237, MTB GC1237, bacillus Calmette-Guérin (BCG), Mycobacterium smegmatis, Yersinia pseudotuberculosis, Salmonella typhimurium, and Staphylococcus epidermidis. table-s1.txt is a tab-delimited text file that contains the batch-corrected log2 counts per million for each of the 156 samples, as well as the Ensembl gene ID and gene name. BCG = bacillus Calmette-Guérin GC = Mycobacterium tuberculosis GC1237 Rv = Mycobacterium tuberculosis (MTB) H37Rv Rv+ = heat-inactivated MTB H37Rv Salm = Salmonella typhimurium Smeg = Mycobacterium smegmatis Staph = Staphylococcus epidermidis Yers = Yersinia pseudotuberculosis
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