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Title: Genome-wide histone modification profile induced by MDV in MD-resistant and -susceptible chickens

item LUO, JUAN - University Of Maryland
item MITRA, APRATIM - University Of Maryland
item TIAN, FEI - China Agricultural University
item Zhang, Huanmin
item CHANG, SHUANG - Michigan State University
item CUI, KAIRONG - National Institutes Of Health (NIH)
item ZHAO, KEJI - National Institutes Of Health (NIH)
item KRAUSE, MICHAEL - National Institutes Of Health (NIH)
item Cheng, Hans
item SONG, JIUZHOU - University Of Maryland

Submitted to: Annual International Plant & Animal Genome Conference
Publication Type: Abstract Only
Publication Acceptance Date: 12/15/2010
Publication Date: 1/19/2011
Citation: Luo, J., Mitra, A., Tian, F., Zhang, H., Chang, S., Cui, K., Zhao, K., Krause, M., Cheng, H.H., Song, J. 2011. Genome-wide histone modification profile induced by MDV in MD-resistant and -susceptible chickens. Plant and Animal Genome XIX Conference, January 15-19, 2011, San Diego, California. Paper No. 578.

Interpretive Summary:

Technical Abstract: Marek’s disease (MD) is a lymphoproliferative disease in chicken caused by oncogenic Marek’s disease virus (MDV). MD is characterized by infiltration of proliferating lymphoid cells in organs, such as peripheral nerve, skin, muscle, liver, spleen, heart, kidney, gonads and proventriculus. Epigenetic modifications such DNA methylation, histone modification and some non-coding RNAs are mitotically or meiotically heritable gene expression changes that do alter the underlying DNA sequences. Epigenetic factors are believed to play important roles in tumorigenesis in mammals with increasing evidence for viruses as environmental agents especially in humans. The goal of our research is to explore the histone modification profiles induced by MDV in two chicken lines that are relatively resistant (Line 63) or highly susceptible (Line 72) to MD. We hope to identify changes of specific histone modifications that differentiate the two chicken lines for MD resistance. These changes may provide clues that lead to the identification of causal genes or pathways responsible for genetic resistance to tumorigenesis.