Microsatellite markers associated with quantitative trait loci controlling antibody response to Escherichia coli and Salmonella enteritidis in young broilers

A unique resource population was produced to facilitate detection of microsatellite markers associated with quantitative trait loci controlling antibody (Ab) response in broiler chickens. Three F1 males were produced by mating two lines divergently selected on Ab response to Escherichia coli vaccina...

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Veröffentlicht in:Animal genetics 2002-12, Vol.33 (6), p.407-414
Hauptverfasser: Yunis, R., Heller, E. D., Hillel, J., Cahaner, A.
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Sprache:eng
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Zusammenfassung:A unique resource population was produced to facilitate detection of microsatellite markers associated with quantitative trait loci controlling antibody (Ab) response in broiler chickens. Three F1 males were produced by mating two lines divergently selected on Ab response to Escherichia coli vaccination. Each F1 male was mated with females from four genetic backgrounds: F1, high‐Ab line (HH), low‐Ab line and commercial line, producing three resource families, each with four progeny types. About 1700 chicks were immunized with E. coli and Salmonella enteritidis vaccines. Selective genotyping was conducted on the individuals with highest or lowest average Ab to E. coli and S. enteritidis within each progeny type in each sire family. Twelve markers were significantly associated with Ab to E. coli and six of them were also associated with Ab to S. enteritidis, mostly exhibiting a similar low effect (∼ 0.35 phenotypic SD) in all progeny types. Four markers exhibited a highly significant and much larger effect (∼1.7 SD), but only in progeny of females from the HH, suggesting that a backcross to the high parental line should be preferred over the commonly used F2 population. Results from two markers suggested a quantitative trait locus on chromosome 2 around 400 cM. The marker MCW0083, significant in two sire families, is closely linked to the bone morphogenetic protein 2 (BMP2) gene, known to be associated with the control of T‐cell transformation in humans.
ISSN:0268-9146
1365-2052
DOI:10.1046/j.1365-2052.2002.00890.x