The thoroughbred (TB) horse is one of the oldest breeds of domestic animals, with pedigree records spanning three centuries. Because the population is essentially closed, there is concern about loss of genetic variation. Here we report two parallel analyses. In the first, genetic variation in the current population is measured using data from 13 microsatellite loci in 211 horses with relationships calculated based on allele sharing. In the second analysis, pedigree information is used to calculate genetic relationships between animals based on shared ancestry. These two measures of relationship are compared and shown to be closely related. Together, they provide an estimate of the amount of genetic variation which existed in founder animals. This study confirms the narrow genetic base of the breed and provides comprehensive analysis of contributions of founder animals. Seventy-eight percent of alleles in the current population are derived from 30 founders, 27 of these male. Ten founder females account for 72% of maternal lineages, while one founder stallion is responsible for 95% of paternal lineages.
Mitochondrial DNA (mtDNA) D-loop sequences (381 bp) from 100 thoroughbreds in 19 of the most common matrilineal female families were used to reconstruct a founder female population for the thoroughbred ( approximately 1650-1750 AD). Seventeen haplotypes were found to have contributed to the 19 female lineages. In order to place the reconstructed founder population in wider historical context, we examined, using both single strand conformation polymorphism and direct sequence analysis, variation in a 343 bp mtDNA fragment in that population and 13 other horse populations of disparate provenance. Interpopulation diversity analyses revealed no significant difference in variation between the thoroughbred founder population and the 13 other diverse horse populations and suggested a non-random partitioning of diversity among geographically diverse horse populations. Within thoroughbreds, almost half of the female families, which are each considered from pedigrees to have matrilines converging to one of>30 historically recognized female ancestors, contained sequences which were inconsistent with common descent. Examination of the anomalies in the context of pedigree records suggests the majority might be best explained as confusion of mares at the foundation stages, although some could have some bearing on more recent (19th century - 1980) lineages. We have used this combination of molecular and historical information to identify some of the founder dams and to make new interpretations about the early history of the thoroughbred.
Thoroughbred horses have been bred exclusively for racing in England since Tudor times and thoroughbred horse racing is now practised in over 40 countries and involves more than half-a-million horses worldwide. The genetic origins of the thoroughbred go back largely to horses imported from the Middle East and North Africa to England in the late seventeenth and early eighteenth centuries. Since the establishment of the Stud Book in 1791, the population has been effectively closed to outside sources, and over 80% of the thoroughbred population's gene pool derives from 31 known ancestors from this early period. Despite intense directional selection, especially on the male side, and the generally high heritabilities of various measures of racing performance, winning times of classic races have not improved in recent decades. One possible explanation for this is that additive genetic variance in performance may have been exhausted in the face of strong selection. To test this, we have estimated the genetic trend in performance over the period 1952-77 using TIMEFORM handicap ratings which are based entirely on the horse's own performance, and express its racing merit as a weight in pounds which the compilers believe the horse should carry in an average free-handicap race. These ratings take into account such factors as the firmness of the ground, the distance and the level of the competition. Our results indicate that the failure of winning times to improve is not due to insufficient genetic variance in the thoroughbred population as a whole.
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