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Title:   Author  item
                                            Vanraden, Paulitem
                                            MILLER, ROBERT - RETIRED, ARS
  Submitted to: Journal of Dairy Science
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 3/23/2004
                                    Publication  Date: 7/25/2004
                                    Citation: VanRaden, P.M., Miller, R.H. 2004. Contribution of inbreeding and recessive defects to early embryo losses [abstract]. Journal of Dairy Science. 87(Suppl. 1):3.Interpretive Summary:
                                Technical Abstract: Lethal recessive genes that cause early embryo losses are difficult to detect because they may simply appear to result in more failed inseminations or missed heats. The 70-d non-return rate percentage (NR70) as a trait of the embryo was evaluated from 1,739,055 first services using a non-additive genetic model. Effects modeled included herd-year-season, parity of cow, sire of cow, service bull, interaction of service bull with sire of cow, and regression on inbreeding of embryo. Simultaneous solutions for all effects were not possible; thus, main effect variances were estimated using restricted maximum likelihood (REML) and these effects were removed from the data. Interaction variance was estimated from the residuals using the tilde-hat approximation to REML. Service bull effects were assumed constant across time and unrelated. An additive relationship matrix was used for sire of cow and a dominance relationship matrix for the interaction term. Data included observations from January 1995 through January 2001 and represented 1251 Holstein service bulls and sires of cows. NR70 declined by an estimated 0.096 for each 1% increase in inbreeding. A regression of this size could be explained by >20% of animals carrying defects causing early embryo loss. Of the total variance, service bull contributed 0.36%, sire of cow 0.24% (heritability of 1.0%), and interaction 0.18% (dominance variance of 2.8%). Number of observations per interaction averaged only 6 but with a maximum of 2077, and 50 bull pairs had >500 observations, resulting in reliabilities >50% for their interactions. Predicted interactions including effects of inbreeding ranged from -3.6 to +2.9 as compared to the mean NR70 of 56%. The poorest interactions were not caused by known recessive defects. Complex vertebral malformation (CVM) generally causes loss of pregnancies later in gestation, and few current bulls carry the gene for deficiency of uridine monophosphate synthase (DUMPS). Further study of the families with poorest interactions could uncover new recessive defects.


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