The effect of embryo and maternal genotypes on prolificacy, intrauterine growth retardation and postnatal development of Nos3-knockout mice.
Mice deficient for endothelial nitric oxide synthase (NOS3(-/-)) may represent a good model for studying embryo loss and intrauterine growth retardation caused by vascular deficiencies. We determined the effects of embryo genotype (homozygous vs. heterozygous descendants with paternal or maternal source of the non-functional NOS3 allele) and maternal environment (NOS3(-/-) vs. wild-type NOS3(+/+) females) on the appearance of estrus, fertility and prolificacy rates and live weight in the first week of life as well as phenotypic characteristics of offspring during the postnatal period. The results indicated that pregnancy outcomes and postnatal development of NOS3(-/-) mice seem to be related to deficiencies in fetal programming mainly determined by maternal genotype.
Animal Reproduction Department, INIA, Av. Puerta de Hierro s/n. 28040-Madrid, Spain. pallares.pilar@inia.es
Pilar
P
Pallares
Antonio
A
Gonzalez-Bulnes
D000818:Animals; D000831:Animals, Newborn; D001835:Body Weight; D020964:Embryo Loss / Q000235:genetics*; D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics*; D006579:Heterozygote; D006720:Homozygote; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D052250:Nitric Oxide Synthase Type III / Q000172:deficiency / Q000235:genetics*; D011247:Pregnancy
D052250:Nitric Oxide Synthase Type III; C496315:Nos3 protein, mouse