444. Embryonic survival in prolific ewes

Abstract

Introduction: A significant proportion of potential lambs are lost (commonly 15–20%) between ovulation and birth. Little is currently known about factors associated with multiple birth capacity of the uterus which are essential to convert gains in ovulation rate to live lambs. The relationship between maternal uterine and hormonal environment as well as the heritability of embryonic survival (ES) in prolific ewes is investigated. Methods: Litter size (LS) from known ovulation rate (OR) records (n = 6393) collected over 16 years were assessed for heritability with ASREML analysis and to identify the pedigree of outliers. From this flock, closely related high ovulation rate ewes with significantly different litter sizes (High ES; OR2.6/LS2.4 v. Low ES; OR2.9/LS1.6) were selected. Uterine anatomy collected from Day 14 cyclic (n = 5 High and n = 5 Low ES) and Day 16 pregnant ewes (n = 14 high and n = 10 Low) as well as systemic concentrations of hormones indicative of uterine (activin-A, follistatin) and ovarian (inhibin-{α}, progesterone) function were compared. Results and Discussion: ASREML analysis reported ES to be a trait of low repeatability (r = 0.10) and even lower heritability (h2 = 0.04). However, pedigrees of outlier animals indicated a segregation pattern consistent with a single autosomal gene with a major effect on enhanced ES. No anatomical differences between high and low ES ewes were discerned. However, significant differences for circulating levels of activin-A (depressed), time of activin-A peak (earlier), follistatin (elevated), progesterone (early rise) and inhibin-{α} (depressed) concentrations were found around the time of oestrus in High v. Low ES ewes. Given the involvement of activin-A in injury-induced inflammation, these results suggest a role for the activin-follistatin system, possibly through increased residency of immune cells and cytokine activation, for increasing ES in prolific ewes. Acknowledgements; Norma Hudson and Stan Lun for progesterone and inhibin-{α} assays.