Abstract
We performed a genome-wide linkage and quantitative trait locus (QTL) analysis to confirm the existence of QTL affecting Rous Sarcoma Virus (RSV) induced tumor regression, and to estimate their effects on phenotypic variance in an F2 resource population. The F2 population comprised 158 chickens obtained by crossing tumor regressive White Leghorn (WL) and tumor progressive Rhode Island Red (RIR) lines was measured for tumor formation after RSV inoculation. Forty-three tumor progressive and 28 tumor regressive chickens were then used for genome-wide linkage and QTL analysis using a total of 186 microsatellite markers. Microsatellite markers were mapped on 20 autosomal chromosomes. A significant QTL was detected with marker LEI0258 located within the MHC B region on chromosome 16. This QTL had the highest F ratio (9.8) and accounted for 20.1% of the phenotypic variation. Suggestive QTL were also detected on chromosomes 4, 7 and 10. The QTL on chromosome 4 were detected at the 1% chromosome-wide level explaining 17.5% of the phenotypic variation, and the QTLs on chromosome 7 and 10 were detected at the 5% chromosome-wide level and explained 11.1% and 10.5% of the phenotypic variation, respectively. These results indicate that the QTLs in the non-MHC regions play a significant role in RSV-induced tumor regression. The present study constitutes one of the first preliminary reports in domestic chickens for QTLs affecting RSV-induced tumor regression outside the MHC region. I .
Highlights
Genetic control of disease resistance is one of the most important targets for breeding schemes in the future
The objective of the present study was to confirm the existence of non-major histocompatibility complex (MHC) quantitative trait locus (QTL) affecting Rous Sarcoma Virus (RSV)-induced tumor regression, and to estimate their effect on phenotypic variance using an F2 resource population generated by crossing a tumor regressive White Leghorn (WL) line and a tumor progressive Rhode Island Red (RIR) line
Bates et al (1998) and Elleder et al (2004) reported that the tva gene coding for viral receptor on chromosome 28 determines the susceptibility of chicken cells to the subgroup A avian sarcoma and leukosis viruses (ASLV-A)
Summary
Genetic control of disease resistance is one of the most important targets for breeding schemes in the future. Infectious diseases are associated with substantial costs and losses in commercial meat and egg production in chickens. It has been suggested that continuous successful selection for rapid growth and/or more egg production has resulted in the loss of disease resistance and overall immunocompetence (Knap and Bishop, 2000; McKay et al, 2000). Genetic methods for improving disease resistance are Recently, the availability of informative DNA markers such as microsatellites and development of statistical methods have made it possible to dissect complex quantitative traits. The identification and utilization of QTL provide the potential for more rapid genetic improvement in selection programs, in difficult-to-measure and troublesome traits such as disease resistance
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