Gallus gallus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA210200 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Marek’s disease virus (MDV) is an oncovirus causing tumor disease known as Marek’s disease (MD) in chicken. Breeding of chickens genetically resistant to MD is considered a vital augment to better control MD. To find the mechanism underlying the genetic resistance to MD, a genomic structural variation, copy number variation (CNV), was examined in inbred MD-resistant and -susceptible chicken lines by using the comparative genomic hybridization (CGH) technique. A total of 45 copy number variation regions (CNVRs) were found spanning across 3,297,038 bp in length of the chicken genome in 4 lines of chickens. Ten CNVRs were selectively confirmed with quantitative real-time PCR. The comparison between the resistant and susceptible chicken lines revealed 28 differentially presented CNVRs, which are functionally involved in immune response, cell proliferation in midbrain, G-protein coupled receptor signaling pathway, and protein-glutamine gamma-glutamyltransferase activity. Two CNVRs that are related with MD-resistance and –susceptibility were also found transmitted to descendent recombinant congenic lines that differ in susceptibility to MD. A positive correlation was identified between the CNVRs and gene expression, indicating the importance of gene expression dosage in disease resistance. We also found the overlapping between the CNVR region and the Marek’s disease trait related quantitative trait loci (QTLs). In conclusion, our data provided additional information elucidating one of possible mechanisms underlying of genetic resistance to MD. The findings may eventually lead to better strategies for genetic improvement of resistance to MD in poultry. L63: highly resistant to MD; L72: highly susceptible to MD; RCS-L: moderate resistant to MD; RCS-M: moderate susceptible to MD
2012-09-01 | GSE38689 | GEO
Project description:Marekâs disease (MD) is an economically significant disease in chickens caused by the highly oncogenic Marekâs disease virus (MDV). Understanding the genes and biological pathways that confer MD genetic resistance should lead towards the development of more disease resistant commercial poultry flocks or improved MD vaccines. MDV Meq, a bZIP transcription factor, is largely attributed for viral oncogenicity though only a few host target genes have been described, which has impeded our understanding of MDV-induced tumorigenesis. Given the importance of Meq in MDV-induced pathogenesis, we explored the role of Meq in genetic resistance to MDV. Using global transcriptome analysis to compare the host response between birds challenge with either wild type MDV or a recombinant lacking Meq, we identified a number of specific genes and pathways associated with either MD resistance. Integrating prior information from ChIP-seq, microarray analysis, and SNPs exhibiting allele-specific expression (ASE) in response to MDV infection from two inbred layer lines that differ greatly in MD genetic resistance, we were able to provide a evidence for 35 genes that SNPs within transcription factor binding sites can affect transcription factor binding and gene expression in an allele-specific manner. Transcript profiling of CEF's (a chicken embryo fibroblast cell line) from MD susceptible and resistant lines using Affymetrix chicken GeneChips
2016-07-01 | E-GEOD-48453 | biostudies-arrayexpress
Project description:Marek’s disease (MD) is an economically significant disease in chickens caused by the highly oncogenic Marek’s disease virus (MDV). Understanding the genes and biological pathways that confer MD genetic resistance should lead towards the development of more disease resistant commercial poultry flocks or improved MD vaccines. MDV Meq, a bZIP transcription factor, is largely attributed for viral oncogenicity though only a few host target genes have been described, which has impeded our understanding of MDV-induced tumorigenesis. Given the importance of Meq in MDV-induced pathogenesis, we explored the role of Meq in genetic resistance to MDV. Using global transcriptome analysis to compare the host response between birds challenge with either wild type MDV or a recombinant lacking Meq, we identified a number of specific genes and pathways associated with either MD resistance. Integrating prior information from ChIP-seq, microarray analysis, and SNPs exhibiting allele-specific expression (ASE) in response to MDV infection from two inbred layer lines that differ greatly in MD genetic resistance, we were able to provide a evidence for 35 genes that SNPs within transcription factor binding sites can affect transcription factor binding and gene expression in an allele-specific manner.
2016-07-01 | GSE48453 | GEO
Project description:Chicken Marek’s disease (MD) is a unique naturally occurring model for human herpesvirus-induced lymphomas that over-express the “Hodgkin’s disease antigen” (TNFRSF-8; CD30) on the lymphoma’s neoplastically-transformed cells. We used transcriptomics, proteomics, computational systems biology and reductionist molecular biology to identify the differences between the CD30(hi) lymphoma cells and the non-transformed CD30(lo) MD lymphoma cells. We propose specific mechanisms of neoplastic transformation, genetic resistance to lymphomagenesis and impact of lymphoma microenvironment on CD30(hi) cell development. We demonstrate that: a) in situ, CD30(lo) cells are pre-neoplastic and we identify the proteome involved in transformation as well as potential mechanisms that may be controlled by MDV oncogene Meq; b) MD herpesvirus, (via its Meq oncogene) can drive a feed forward loop that induces CD30 transcription and overexpression, increased CD30 signaling, which then activates NFκB and, in turn, increases Meq transcription; c) Meq transcriptional repression or activation from the CD30 promoter generally correlates with a polymorphism in the CD30 promoter between MD-resistant and -susceptible chicken genotypes and so a herpesvirus has evolved to utilize NFκB as a direct transcriptional activator for its oncogene.
2012-03-15 | GSE28034 | GEO
Project description:Marek’s disease (MD) is an economically significant disease in chickens caused by the highly oncogenic Marek’s disease virus (MDV). A major unanswered question is the mechanism of MDV-induced tumor formation. Meq, a bZIP transcription factor discovered in the 1990s, is critically involved in viral oncogenicity but only a few of its host target genes have been described impeding our understanding of MDV-induced tumorigenesis. Using ChIP-seq and microarray analysis, a high confidence list of Meq-binding sites in the chicken genome and a global transcriptome of Meq-responsive genes was generated. Meq binding sites were found to be enriched in the promoter regions of up-regulated genes, but not in those of down-regulated genes. ChIP-seq was also performed for c-Jun, a known heterodimeric partner of Meq. Close location of binding sites of Meq and c-Jun was noted, suggesting cooperativity between these two factors in modulating transcription. Pathway analysis indicated that Meq transcriptionally regulates many genes that are part of several signaling pathways include the ERK/MAPK, Jak-STAT, and ErbB pathways that are critical for oncogenesis and/or include signaling mediators involved in apoptosis. Meq activates oncogenic signaling cascades by transcriptionally activating major kinases in the ERK/MAPK pathway and simultaneously repressing phosphatases, as verified using inhibitors of MEK and ERK1/2 in a cell proliferation assay. This study provides significant insights into the mechanistic basis of Meq-dependent cell transformation.
2016-07-01 | GSE48451 | GEO
Project description:Marek’s disease (MD) is an economically significant disease in chickens caused by the highly oncogenic Marek’s disease virus (MDV). A major unanswered question is the mechanism of MDV-induced tumor formation. Meq, a bZIP transcription factor discovered in the 1990s, is critically involved in viral oncogenicity but only a few of its host target genes have been described impeding our understanding of MDV-induced tumorigenesis. Using ChIP-seq and microarray analysis, a high confidence list of Meq-binding sites in the chicken genome and a global transcriptome of Meq-responsive genes was generated. Meq binding sites were found to be enriched in the promoter regions of up-regulated genes, but not in those of down-regulated genes. ChIP-seq was also performed for c-Jun, a known heterodimeric partner of Meq. Close location of binding sites of Meq and c-Jun was noted, suggesting cooperativity between these two factors in modulating transcription. Pathway analysis indicated that Meq transcriptionally regulates many genes that are part of several signaling pathways include the ERK/MAPK, Jak-STAT, and ErbB pathways that are critical for oncogenesis and/or include signaling mediators involved in apoptosis. Meq activates oncogenic signaling cascades by transcriptionally activating major kinases in the ERK/MAPK pathway and simultaneously repressing phosphatases, as verified using inhibitors of MEK and ERK1/2 in a cell proliferation assay. This study provides significant insights into the mechanistic basis of Meq-dependent cell transformation.
2013-05-31 | GSE47191 | GEO
Project description:Genome-wide copy number variant analysis in inbred lines of chickens with different susceptibility to Marek’s disease
| PRJNA168441 | ENA
Project description:Transcriptional profiling of chicken spleen tissues from Marek's disease virus (MDV) infected and non-infected control individuals from three inbred chicken lines 63, 72, RCSM with varying disease resistance characteristics. Line 63 is highly resistant; line 72 is highly susceptible; and line RCSM has intermediate resistance. Our goal was to investigate the genetic basis of systemic variation in disease resistance in these genetically similar individuals. Three time points were chosen at different stages of disease progression - 5 days post-infection (dpi) - early cytolytic phase; 10 dpi - latent phase; and 21 dpi - late cytolytic phase with 4 replicates at each stage.
2010-09-08 | GSE24017 | GEO
Project description:MarekM-bM-^@M-^Ys disease (MD) is an economically significant disease in chickens caused by the highly oncogenic MarekM-bM-^@M-^Ys disease virus (MDV). A major unanswered question is the mechanism of MDV-induced tumor formation. Meq, a bZIP transcription factor discovered in the 1990s, is critically involved in viral oncogenicity but only a few of its host target genes have been described impeding our understanding of MDV-induced tumorigenesis. Using ChIP-seq and microarray analysis, a high confidence list of Meq-binding sites in the chicken genome and a global transcriptome of Meq-responsive genes was generated. Meq binding sites were found to be enriched in the promoter regions of up-regulated genes, but not in those of down-regulated genes. ChIP-seq was also performed for c-Jun, a known heterodimeric partner of Meq. Close location of binding sites of Meq and c-Jun was noted, suggesting cooperativity between these two factors in modulating transcription. Pathway analysis indicated that Meq transcriptionally regulates many genes that are part of several signaling pathways include the ERK/MAPK, Jak-STAT, and ErbB pathways that are critical for oncogenesis and/or include signaling mediators involved in apoptosis. Meq activates oncogenic signaling cascades by transcriptionally activating major kinases in the ERK/MAPK pathway and simultaneously repressing phosphatases, as verified using inhibitors of MEK and ERK1/2 in a cell proliferation assay. This study provides significant insights into the mechanistic basis of Meq-dependent cell transformation. Transcript profiling of DF-1 (a chicken embryo fibroblast cell line) and Meq-DF-1 clone 5G (DF-1 stably expressing Meq driven by the CMV promoter) using Affymetrix chicken GeneChips
2013-05-31 | E-GEOD-47191 | biostudies-arrayexpress
Project description:Copy number variation in two inbred chicken lines
| PRJNA280243 | ENA