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by JW Equine © Visit jwequine.com for more information & articles by Judy Wardrope Thoroughbred stallions have long been ranked according to their results at stud. Separate rankings are made based on the accomplishments of direct offspring on the Leading Sires list and for the offspring of a stallion's daughters on the Leading Broodmare Sires roster. If you noticed that not all top sires become top broodmare sires and not all top broodmare sires were previously listed as top sires, you were not alone. Dr. Doug Antczak, a speaker at this year's Horse Breeders and Owners Conference, made the same observation. In his presentation, Dr. Antczak offered a possible explanation for this - a phenomenon he calls the Maternal-Grandsire Effect. Despite high expectations and top quality mates, Dr. Antczak found it curious that some stallions were not nearly as successful as sires as they were as broodmare sires and cited Secretariat, Buckpasser, Key To The Mint, and Graustark as examples. In essence, these stallions, although not total failures at stud, were much better at siring the dams of stakes winners than they were at siring stakes winners or sons who sired stakes winners. Could it be that whatever "added performance" genes this type of stallion was passing to his offspring were only being exhibited when his daughters reproduced? So it seemed, as it was the offspring of daughters by these stallions that appeared to benefit most. This skipping of a generation is not peculiar to thoroughbreds; other breeds also have stallions that are either noted for their maternal grand-get or are seldom seen in the ancestry of a top competition horse through a son. Given his background and his research associations, Dr. Antczak was in an ideal position to look for an explanation for what students of pedigree and thoroughbred breeders have known for some time - some stallions exert their greatest influence through the progeny of their daughters. Dr. Antczak is a professor of Equine Medicine and Immunology at Cornell University's College of Veterinary Medicine in Ithaca, New York plus the Director of the James A. Baker Institute for Animal Health. His list of credentials is extensive, but for the purposes of this article we will take heed of his role in connection with the international collaboration known as "The Horse Genome Project". This project encompasses the work of some 70 scientists from 25 labs in 20 countries who are all sharing in the creation of a map of the total genetic code, or genome, (60,000 to 80,000 genes that are found on the 64 chromosomes) of the horse. Gene maps can be utilized to reveal some of the complexities associated with the heredity of performance, disease and other traits. It was just a couple of years ago that the Horse Genome Project got a boost when it was found that much of the previous research on other mammalian gene mapping projects, including the extensive research regarding humans, relates to the horse. (About 85% of genes are shared among mammals. e.g. Human chromosome number 8 equates to chromosome number 9 in the horse and human chromosome 6 equates to horse chromosome 20.) It is hoped that the project will identify some of the genes responsible for a host of equine diseases and disorders. The future may even bring tests to diagnose afflictions the likes of COPD (chronic obstructive pulmonary disease or heaves), wobbles, strangles, swayback as well as other developmental bone and muscle diseases. This is not futuristic science fiction; genetic tests already exist to identify Severe Combined Immunodeficiency Disease (SCID) in Arabians, Lethal White Disease in Overo Paints and Hyperkalemic Periodic Paralysis (HYPP) in Quarter Horses. Obviously, the study of genetics has expanded far past the basic premise that offspring get two copies of their genes, half from the father and the other half from the mother. The Maternal-Grandsire Effect theory that Dr. Antczak spoke about at the conference, took shape based on the findings of separate research projects by Dr. W. R. "Twink" Allen in the late 1960's and Dr. Azim Surani in 1986. Dr. Allen found that there was a hormone that is normally found at high levels in pregnant mares and at low levels in pregnant donkeys. When the two species were crossed to produce hinnies (male donkey/female horse) and mules (male horse/female donkey), that very same hormone registered at high levels in the female donkeys that were pregnant by horses and at low levels in the mares that were pregnant to donkeys. This was most puzzling - it seemed that somehow the sires influenced the level of hormone in the pregnant females regardless of the species. No one had an explanation for this unusual turn of events until Professor Surani manipulated fertilized mouse eggs to be either gynogenetic (containing paired chromosomes solely from the mother) or androgenetic (containing paired chromosomes solely from the father). Amazingly, the "all male" androgenetic pregnancies developed large placentas and little embryonic tissue while the "all female" gynogenetic pregnancies developed large embryos but little placental tissue. It was evident that not all copies of the maternal genes behaved in exactly the same manner as the paternal copies. Now the indication was that the male exerted most of the influence over placental development and that the female exerted the most influence over embryonic development. The hypothesis that Surani and his colleagues put forth to explain this was contrary to the century-old Mendel's theory (Genes are either dominant or recessive, where dominant genes are expressed and recessive genes are not, unless 2 recessive genes are paired in the absence of a dominant gene. The exception being genes that are co-dominant or where both are expressed as a blend.) The new theory was that in addition to Mendelian laws, some genes are programmed to be expressed or repressed, depending on the gender of the parent responsible for contributing the gene. This occurrence, which is also found in humans, is known generally as "genomic imprinting" and specifically as being "maternally imprinted" in the case of a gene that is mute when transmitted by the mother or "paternally imprinted" in the case of a gene that is mute when transmitted by the father. Imprinted genes are not missing; they are just inactive or switched off when transmitted by one gender or the other. Further, these imprinted/silent genes can be re-expressed in the next generation if contributed by a parent of the opposite gender and thus the commonly held views on inheritance changed. A female can pass on information on an imprinted gene, but only her son's offspring are able to demonstrate the effect. A male can pass on information on an imprinted gene but only his daughter's offspring are able to demonstrate the effect. This leads to some very interesting zig-zags across a pedigree page. Dr. Antczak summized that the Maternal-Grandsire Effect in horses could very well be the result of imprinted genes whereby performance related genes from a stallion are passed on in an inactive form and are not activated again until passed on by a mare, in this case his daughter. If Dr. Antczak's theory proves true, about 50% of the daughters of such a stallion could be superb broodmares, which seems to be pretty much the case in real life. Imprinting is gender related and therefore different than sex-linked inheritance such as when a sire gets daughters who outperform the sons or vice-versa. Sex-linked inheritance is where a particular trait is passed on in connection with the X and Y chromosomes that determine sex. (Males are XY and females are XX and each parent passes only one of these chromosomes to an offspring.) As a matter of interest, if we examine the pedigrees of the stallions that were used as examples in Dr. Antczak's presentation, we find that they are all out of daughters of prominent broodmare sires. If we delve further, we find that their second dams were also by prominent broodmare sires, as were their third and fourth dams. Secretariat and Key To The Mint are both out of daughters of Princequillo. Buckpasser's broodmare sire, War Admiral, is the sire of Key To The Mint's second dam. Blue Larkspur is the sire of the second dam of Buckpasser and the sire of Key To The Mint's third dam. Secretariat and Buckpasser both descend in tail-female line from daughters of Teddy. Secretariat's second dam was by a horse that only had 76 foals and is now only found in pedigrees through his daughters. Graustark is not an exception; he follows the same pattern. Looking at the progression of broodmare sires back through his tail-female line, you see Alibhai, Beau Pere and Mahmoud, all top broodmare sires. It is not too difficult to see a pattern for the building of a broodmare sire, which is seldom the aim of breeders despite the fact that it is the broodmare sires that seem to have an enduring effect within the breed. Anything beyond the basics of genetics and inheritance may be difficult to fathom for anyone but scientists; there are genes that are dominant or recessive, genes that are co-dominant, genetic influences that are sex-linked and genetic influences that are imprinted. Undoubtedly a myriad of these genetic factors are required to produce an exceptional athlete but imagine what the identification of the crucial imprinted genes, even though they are in the minority, will mean to the breeding industry as we seek to narrow the search for the optimal lineage. A few markers for imprinted genes have already been identified, many of which relate to growth (fetal, placental and neonatal). If the imprinted genes that have been identified in humans equate with genes in the horse, then an imprinted gene connected to the growth of heart muscle (already studied in humans) may also explain Secretariat's large heart (22 pounds compared to the average of 8.5 pounds). This then would shed a slightly different light on the X-Factor theory of sex-linked heart size as reported in Ms. Haun's book. Genetic research may indeed affect breeding decisions even more in the not too distant future, but selecting for performance is just one aspect. Being able to avoid inherent defects will also be a plus - after all, what good are superior performance qualities if they are negated by defects? Due to the complex nature of heredity, it is likely that the intricacies of performance and disease inheritance will continue to be researched for decades to come. Surely some of the toughest questions regarding genetic research and the breeding of racehorses are yet to be faced. If the future brings genetic tests that can identify specific genes for superior performance and these genes are also connected to a major affliction or defect, how will that affect your breeding decisions? November 18, 2001. Copyright by
JW Equine 2001. |
