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Marek's disease virus infection induces widespread differential chromatin marks in inbred chicken lines.

ABSTRACT: BACKGROUND: Marek's disease (MD) is a neoplastic disease in chickens caused by the MD virus (MDV). Successful vaccine development against MD has resulted in increased virulence of MDV and the understanding of genetic resistance to the disease is, therefore, crucial to long-term control strategies. Also, epigenetic factors are believed to be one of the major determinants of disease response. RESULTS: Here, we carried out comprehensive analyses of the epigenetic landscape induced by MDV, utilizing genome-wide histone H3 lysine 4 and lysine 27 trimethylation maps from chicken lines with varying resistance to MD. Differential chromatin marks were observed on genes previously implicated in the disease such as MX1 and CTLA-4 and also on genes reported in other cancers including IGF2BP1 and GAL. We detected bivalent domains on immune-related transcriptional regulators BCL6, CITED2 and EGR1, which underwent dynamic changes in both lines as a result of MDV infection. In addition, putative roles for GAL in the mechanism of MD progression were revealed. CONCLUSION: Our results confirm the presence of widespread epigenetic differences induced by MD in chicken lines with different levels of genetic resistance. A majority of observed epigenetic changes were indicative of increased levels of viral infection in the susceptible line symptomatic of lowered immunocompetence in these birds caused by early cytolytic infection. The GAL system that has known anti-proliferative effects in other cancers is also revealed to be potentially involved in MD progression. Our study provides further insight into the mechanisms of MD progression while revealing a complex landscape of epigenetic regulatory mechanisms that varies depending on host factors.

SUBMITTER: Mitra A

PROVIDER: S-EPMC3505159 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature

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Marek's disease virus infection induces widespread differential chromatin marks in inbred chicken lines.

Mitra Apratim A Luo Juan J Zhang Huanming H Cui Kairong K Zhao Keji K Song Jiuzhou J

BMC genomics 20121016

<h4>Background</h4>Marek's disease (MD) is a neoplastic disease in chickens caused by the MD virus (MDV). Successful vaccine development against MD has resulted in increased virulence of MDV and the understanding of genetic resistance to the disease is, therefore, crucial to long-term control strategies. Also, epigenetic factors are believed to be one of the major determinants of disease response.<h4>Results</h4>Here, we carried out comprehensive analyses of the epigenetic landscape induced by M ...[more]

PMID: 23072359

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Project description:Campylobacteriosis is the leading foodborne bacterial diarrheal illness in many countries, with up to 80% of human cases attributed to the avian reservoir. The only control strategies currently available are stringent on-farm biosecurity and carcass treatments. Heritable differences in the resistance of chicken lines to Campylobacter colonization have been reported and resistance-associated quantitative trait loci are emerging, although their impact on colonization appears modest. Recent studies indicated a protective role of the microbiota against colonization by Campylobacter in chickens. Furthermore, in murine models, differences in resistance to bacterial infections can be partially transferred between lines by transplantation of gut microbiota. In this study, we investigated whether heritable differences in colonization of inbred chicken lines by Campylobacter jejuni are associated with differences in cecal microbiota. We performed homologous and heterologous cecal microbiota transplants between line 61 (resistant) and line N (susceptible) by orally administering cecal contents collected from 3-week-old donors to day-of-hatch chicks. Recipient birds were challenged (day 21) with C. jejuni 11168H. In birds given homologous microbiota, the differential resistance of lines to C. jejuni colonization was reproduced. Contrary to our hypothesis, transfer of cecal microbiota from line 61 to line N significantly increased C. jejuni colonization. No significant difference in the overall composition of the cecal microbial communities of the two lines was identified, although line-specific differences for specific operational taxonomic units were identified. Our data suggest that while heritable differences in avian resistance to Campylobacter colonization exist, these are not explained by significant variation in the cecal microbiota.IMPORTANCE Campylobacter is a leading cause of foodborne diarrheal disease worldwide. Poultry are a key source of human infections, but there are currently few effective measures against Campylobacter in poultry during production. One option to control Campylobacter may be to alter the composition of microbial communities in the avian intestines by introducing beneficial bacteria, which exclude the harmful ones. We previously described two inbred chicken lines which differ in resistance to intestinal colonization by Campylobacter Here, we investigated the composition of the microbial communities in the gut of these lines and whether transferring gut bacteria between the resistant and susceptible lines alters their resistance to Campylobacter No major differences in microbial populations were found, and resistance or susceptibility to colonization was not conferred by transferring gut bacteria between lines. The data suggest that gut microbiota did not play a role in resistance to Campylobacter colonization, at least in the lines used.

Project description:Heat stress results in reduced productivity, anorexia, and mortality in chickens. The objective of the study was to identify genes and signal pathways associated with heat stress and Newcastle disease virus (NDV) infection in the liver of chickens through RNA-seq analysis, using two highly inbred chicken lines (Leghorn and Fayoumi). All birds were held in the same environment until 14 days of age. On day 14, half the birds were exposed to 38 °C with 50% relative humidity for 4 h, then 35 °C until the end of the experiment. The remaining birds were kept at 25 °C throughout the experiment. The heat-treated birds were inoculated at 21 days of age with 107 EID50 (One EID50 unit is the amount of virus that will infect 50 percent of inoculated embryos) NDV La Sota strain to investigate the effects of both heat stress and NDV infection. Physiological parameters were recorded as blood phenotypes at three stages: acute heat (AH), chronic heat (CH1), and chronic heat combined with NDV infection (CH&NDV), at 4 h, 7 days, and 10 days post-initiation of heat treatment, respectively. Our previous work revealed that the heat-resilient Fayoumi line maintained a more stable acid-base balance in their blood compared to the Leghorn line. Liver samples were harvested on both AH and CH&NDV to characterize the transcriptome profiles of these two inbred lines. Both genetic lines and treatments had large impact on the liver transcriptome. Fayoumi birds had more differentially expressed genes (DEGs) than Leghorn birds for both treatments. Metabolic and immune-related genes were on the DEG list, with Fayoumi having more immune-related DEGs than Leghorns, which was confirmed by gene functional enrichment analysis. Weighted correlation network analysis (WGCNA) indicated that the driver genes such as Solute Carrier Family genes could be very important for stabilizing the acid-base balance in Fayoumi birds during heat stress. Therefore, candidate genes such solute carrier family genes could be potential genetic targets that are regulated by Fayoumis to maintain physical hemostasis under heat stress. Differential gene expression showed that Leghorns mainly performed metabolic regulation in response to heat stress and NDV infection, while Fayoumis regulated both immune and metabolic functions. This study provides novel insights and enhances our understandings of liver response to heat stress of heat resilient and susceptible inbred chicken lines.

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Marek's disease virus infection induces widespread differential chromatin marks in inbred chicken lines.

Publications

Marek's disease virus infection induces widespread differential chromatin marks in inbred chicken lines.

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