Location: Location not imported yet.Title: Comparison and contrast of genes and biological pathways responding to Marek’s disease virus infection using allele-specific expression and differential expression in broiler and layer chickens) Author
|Black Pyrkosz, Alexis|
Submitted to: Biomed Central (BMC) Genomics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/21/2013
Publication Date: 1/30/2013
Publication URL: http://handle.nal.usda.gov/10113/57046
Citation: Perumbakkam, S., Muir, W.M., Black Pyrkosz, A.A., Okimoto, R., Cheng, H.H. 2013. Comparison and contrast of genes and biological pathways responding to Marek’s disease virus infection using allele-specific expression and differential expression in broiler and layer chickens. Biomed Central (BMC) Genomics. 14:64. Available: http://www.biomedcentral.com/content/pdf/1471-2164-14-64.pdf. Interpretive Summary: Marek’s disease (MD), a T cell lymphoma of chickens caused by the Marek’s disease virus (MDV), is a very serious problem to the poultry industry. Enhancing MD genetic resistance through genetic markers is an attractive solution to augment current MD vaccines as it avoids the need to exposure elite flocks to a hazardous pathogen. Using genomic techniques, we were able to identify candidate markers in genes that respond to MDV infection in both experimental layers (egg type) and commercial broilers (meat type). This information and accompanying genetic markers can allow scientists to evaluate the contribution of each towards disease resistance.
Technical Abstract: Marek’s disease (MD) is a commercially important neoplastic disease of chickens caused by the Marek’s disease virus (MDV), a naturally occurring oncogenic alphaherpesvirus. Enhancing MD genetic resistance is desirable to augment current vaccines and other MD control measures. High throughput sequencing was used to profile splenic transcriptomes from individual F1 progeny infected with MDV at 4 days of age from both outbred broilers (meat-type) and inbred layer (egg-type) chicken lines that differed in MD genetic resistance. The resulting information was used to identify SNPs, genes, and biological pathways exhibiting allele-specific expression (ASE) in response to MDV infection in each type of chicken. In addition, we compared and contrasted the results of pathway analyses (ASE and differential expression (DE)) between chicken types to help inform on the biological response to MDV infection. With 7 individuals per line and treatment group providing high power, we identified 6,132 single nucleotide polymorphisms (SNPs) in 4,768 genes and 4,528 SNPs in 3,718 genes in broilers and layers, respectively that exhibited ASE in response to MDV infection. Furthermore, 548 and 434 genes in broilers and layers, respectively, were found to show DE following MDV infection. Comparing the datasets, only 72 SNPs and 850 genes for ASE and 20 genes for DE were common between the two bird types. Although the chicken types used in this study were genetically different, at the pathway level, both TLR receptor and JAK/STAT signaling pathways were enriched as well as exhibiting a high proportion of ASE genes, especially at the beginning of both above mentioned regulatory pathways. RNA sequencing with adequate biological replicates is a powerful approach to identify high confidence SNPs, genes, and pathways that are associated with transcriptional response to MDV infection. In addition, the SNPs exhibiting ASE in response to MDV infection provide a strong foundation for determining the extent to which variation in expression influences MD incidence plus yield genetic markers for genomic selection. However, given the paucity of overlap among ASE SNP sets (broilers vs. layers), it is likely that separate screens need to be incorporated for each population. Finally, comparison of gene lists obtained between these two diverse chicken types indicate the TLR and JAK/STAT signaling are conserved when responding to MDV infection and may be altered by selection of genes exhibiting ASE found at the start of each pathway.