Abstract

Heterozygotes for a deficiency of uridine-5’-monophosphate synthase, a metabolic disease that interferes with pyrimidine biosynthesis, were related to a common ancestor, Skokie Sensation Ned. Predicted Differences of milk, fat, dollars, and protein from the July 1986 sire evaluation on 290 Holstein bulls born between 1975 and 1981 were analyzed for differences in the following groups: 5 heterozygous sons, 7 heterozygous grandsons, 5 normal sons, 20 normal grandsons of Ned, and a random sample of 253 normal bulls unrelated to Ned. From generalized least squares analysis, heterozygotes had higher estimates of genetic merit by 158kg PD milk, 37 PD dollars, and 4.9kg PD protein. Although an advantage was observed for heterozygotes within a family, descendants of Ned had lower estimates of genetic merit than their normal contemporaries. Sons of Ned had higher PD protein than grandsons of Ned, regardless of their uridine-5’-monophosphate synthase level. Propagation of the reproductively undesirable allele for deficiency of uridine-5’-monophosphate synthase should be controlled.

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