Submitted to: Journal of Animal Science Supplement
Publication Type: Abstract only
Publication Acceptance Date: 12/6/2002
Publication Date: 12/20/2003
Citation: Vallet, J.L., Freking, B.A., Leymaster, K.A., Christenson, R.K. 2003. A polymorphism in the pig erythropoietin receptor (EPOR) gene is associated with uterine capacity [abstract]. Journal of Animal Science 81(Supplement 2):61. Interpretive Summary:
Technical Abstract: Selection for uterine capacity increased fetal hematocrits measured on d 105 of gestation. We hypothesized that this increase might be partially due to polymorphism(s) in the EPOR gene. The likely positions of the introns were predicted within the porcine EPOR gene by comparing the porcine EPOR cDNA to the human EPOR gene. Oligonucleotide primers based on the porcine cDNA were designed to amplify by PCR a region of the porcine EPOR gene that was likely to contain two moderately sized introns. The genomic DNA from 96 gilts from populations available at the Meat Animal Research Center (including 24 half Meishan, half white crossbred gilts, 24 gilts from lines selected either at random (CO), for ovulation rate (OR) or for uterine capacity (UC); and 48 pigs from other populations) were amplified by PCR using these primers, and the products were sequenced. The sequences were aligned and polymorphisms were identified. A genotyping assay for a C/T polymorphism in one of the introns was developed based on primer extension and mass spectrometry using Sequenom technology. This assay was used to genotype 212 gilts from the CO, OR and UC lines. The gilts had been unilaterally hysterectomized-ovariectomized, mated, and then slaughtered at 105 d of gestation. At slaughter, number of corpora lutea (CL) and litter size (a measure of uterine capacity) were recorded. Fetal and placental weights were also recorded, and a blood sample was collected from each fetus. Blood samples were measured for hematocrit and fetal plasma iron. Gilts were either homozygous CC or heterozygous CT, no TT gilts were observed. Litter size was greater (P<0.01) in CT gilts (8.3+/-0.5, n=21) compared to CC gilts (6.9+/-0.2, n=191). CL number (15.1+/-0.6,15.2+/-0.2), fetal weight (778+/-33, 800+/-11), placental weight (174+/-11, 189+/-4), fetal hematocrit (36.9+/-0.6, 36.8+/-0.2) and fetal plasma iron (1.17+/-0.05, 1.20+/-0.02) did not differ between CT and CC genotypes, respectively. These results suggest that variation within the EPOR gene or another nearby gene is associated with differences in uterine capacity, but this effect is not mediated by changes in hematocrit, placental or fetal weights, CL number or fetal plasma iron.