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Chicken Spleen Tissues: MDV-infected vs non-infected in inbred lines 63, 72 & RCSM

ABSTRACT: 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.

ORGANISM(S): Gallus gallus

PROVIDER: GSE24017 | GEO | 2010/09/08

SECONDARY ACCESSION(S): PRJNA130257

REPOSITORIES: GEO

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Project description:Background: Marek’s disease (MD) is a highly contagious, lymphomatous disease of chickens induced by a herpesvirus, Marek’s disease virus (MDV) that is the cause of major annual losses to the poultry industry. MD pathogenesis involves multiple stages including an early cytolytic phase and latency, and transitions between these stages are governed by several host and environmental factors. The success of vaccination strategies has led to the increased virulence of MDV and selective breeding of naturally resistant chickens is seen as a viable alternative. While multiple gene expression studies have been performed in resistant and susceptible populations, little is known about the epigenetic effects of infection. Results: In this study, we investigated temporal chromatin signatures induced by MDV by analyzing early cytolytic and latent phases of infection in the bursa of Fabricius of MD-resistant and –susceptible birds. Major global variations in chromatin marks were observed at different stages of MD in the two lines. Differential H3K27me3 marks were associated with immune-related pathways, such as MAP kinase signaling, focal adhesion and neuroactive ligand receptor interaction, and suggested varying degrees of silencing in response to infection. Immune-related microRNAs, e.g. gga-miR-155 and gga-miR-10b, bore chromatin signatures, which suggested their contribution to MD-susceptibility. Finally, several members of the focal adhesion pathway, e.g. THBS4 and ITGA1, showed marked concordance between gene expression and chromatin marks indicating putative epigenetic regulation in response to MDV infection. Conclusions: Our comprehensive analysis of chromatin signatures, therefore, revealed further clues about the epigenetic effects of MDV infection although further studies are necessary to elucidate the functional implications of the observed variations in histone modifications. Total of 32 samples analyzed; 2 histone modifications - H3K4me3 and H3K27me3 x 2 chicken lines with varying resistance to MD - L63 and L72 x 2 time-points of disease progression - 5 and 10 days post infection x 2 conditions - infected and control x 2 biological replicates

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Chicken Spleen Tissues: MDV-infected vs non-infected in inbred lines 63, 72 & RCSM

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