Mapping QTL affecting resistance to Mareks disease in an F6 advanced intercross population of commercial layer chickensReportar como inadecuado

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BMC Genomics

, 10:20

First Online: 14 January 2009Received: 14 October 2008Accepted: 14 January 2009


BackgroundMarek-s disease MD is a T-cell lymphoma of chickens caused by the Marek-s disease virus MDV, an oncogenic avian herpesvirus. MD is a major cause of economic loss to the poultry industry and the most serious and persistent infectious disease concern. A full-sib intercross population, consisting of five independent families was generated by crossing and repeated intercrossing of two partially inbred commercial White Leghorn layer lines known to differ in genetic resistance to MD. At the F6 generation, a total of 1615 chicks were produced 98 to 248 per family and phenotyped for MD resistance measured as survival time in days after challenge with a very virulent plus vv+ strain of MDV.

ResultsQTL affecting MD resistance were identified by selective DNA pooling using a panel of 15 SNPs and 217 microsatellite markers. Since MHC blood type BT is known to affect MD resistance, a total of 18 independent pool pairs were constructed according to family × BT combination, with some combinations represented twice for technical reasons. Twenty-one QTL regions QTLR affecting post-challenge survival time were identified, distributed among 11 chromosomes GGA1, 2, 3, 4, 5, 8, 9, 15, 18, 26 and Z, with about two-thirds of the MD resistance alleles derived from the more MD resistant parental line. Eight of the QTLR associated with MD resistance, were previously identified in a backcross BC mapping study with the same parental lines. Of these, 7 originated from the more resistant line, and one from the less resistant line.

ConclusionThere was considerable evidence suggesting that MD resistance alleles tend to be recessive. The width of the QTLR for these QTL appeared to be reduced about two-fold in the F6 as compared to that found in the previous BC study. These results provide a firm basis for high-resolution linkage disequilibrium mapping and positional cloning of the resistance genes.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2164-10-20 contains supplementary material, which is available to authorized users.

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Autor: Eliyahu M Heifetz - Janet E Fulton - Neil P O-Sullivan - James A Arthur - Hans Cheng - Jing Wang - Morris Soller - Jack


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