W762
NGS Analysis Identified Differentially Expressed Coding and microRNA Genes in ALV-like Spontaneous Tumors Potentially Contributing to Tumorigenicity in Susceptible Chickens

Date: Saturday, January 14, 2017
Time: 11:40 AM
Room: Sunset - Meeting House
Huanmin Zhang , USDA-ARS, Avian Disease & Oncology Laboratory, East Lansing, MI
Kunzhe Dong , USDA-ARS, Avian Disease & Oncology Laboratory, East Lansing, MI
Shuang Chang , Shandong Agricultural University, Tai'an, China
Qingmei Xie , South China Agricultural University, Guangzhou, China
Jody Mays , USDA-ARS, Avian Disease & Oncology Laboratory, East Lansing, MI
Tamer Mansour , Michigan State University, East Lansing, MI
Brian Schutte , Michigan State University, East Lansing, MI
Henry Hunt , USDA-ARS, Avian Disease & Oncology Laboratory, East Lansing, MI
Aly Fadly , USDA-ARS, Avian Disease & Oncology Laboratory, East Lansing, MI
It is documented that some experimental and commercial lines of chickens develop spontaneous ALV-like tumors. It is also documented that MDV-2 or ALV-E or both escalate the incidence of such tumors. In one ADOL chicken line, known as rapid feathering susceptible (RFS), the observed tumor incidence was 9% in control RFS versus 14%, 17% and 42% in MDV-2, ALV-E, and MDV-2 plus ALV-E infected groups, respectively. To investigate the possible genetic and epigenetic mechanism underlying the tumorigenesis enhanced by MDV-2 plus ALV-E infection, total RNA samples were extracted from 6 spontaneous bursa tumors of MDV-2 and ALV-E infected and 3 normal bursae of young RFS birds. Analyses of the deep sequence data of mRNA and small RNA resulted in 1,981 and 50 of differentially expressed genes (DEGs) (FDR <0.05 and Fold change >2) and microRNAs (miRNAs) (P value <0.01), respectively, between the tumors and normal bursa samples. The DEGs and the target genes of the differentially expressed miRNAs are enriched in key pathways, including Wnt signaling pathway, MAPK signaling pathway and mTOR signaling pathway, which have been shown to implicate in a wide range of human tumors. The findings of this study provided the first piece of genomic evidence in elucidating the tumorigenic mechanism of ALV-like tumors attributable to genetics and epigenetics of the susceptible chickens.