Gallus gallus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA210197 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR924305.fastq.gz | Fastqsanger.gz | |||
| SRR924306.fastq.gz | Fastqsanger.gz | |||
| SRR924307.fastq.gz | Fastqsanger.gz | |||
| SRR924308.fastq.gz | Fastqsanger.gz | |||
| SRR924309.fastq.gz | Fastqsanger.gz |
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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.
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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
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Project description:Marek's disease lymphoma sequencing
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Project description:Chicken MarekM-bM-^@M-^Ys disease (MD) is a unique naturally occurring model for human herpesvirus-induced lymphomas that over-express the M-bM-^@M-^\HodgkinM-bM-^@M-^Ys disease antigenM-bM-^@M-^] (TNFRSF-8; CD30) on the lymphomaM-bM-^@M-^Ys 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 NFM-NM-:B 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 NFM-NM-:B as a direct transcriptional activator for its oncogene. A dual color, balanced design was carried on eight sorted lymphoma cells from white leghorn chickens infected with MDV GA/22 strain. Each of two sample types, CD30(hi) and CD30(lo) cells, includes four biological replicates for total RNA extraction and labeling. A Dye swap was used in four biological repeats of CD30(hi) to CD30(lo) cells comparison. Background subtracted signal intensities were collected from 4 arrays and normalized for data analysis.
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