THE MORTALITY AND CYTOGENETICS OF MOUSE EMBRYOS DERIVED FROM OOCYTES EXPOSED TO MATERNAL HYPERTHERMIA DURING MEIOTIC MATURATION
Abstract
Embryonic mortality, one of the leading causes of decreased reproduction, is greatly increased by hyperthermia in reproducing animals. These investigations are concerned with the underlying causes of early embryonic mortality due to acute maternal heat stress. The viability, morphology, and chromosomal constitution of embryos derived from hyperthermic dams was investigated at several stages of the reproductive cycle. Oocyte maturation and synchronized ovulation were induced by intraperitoneal injection of Pregnant Mare Serum Gonadotropin (PMSG) and human Chorionic Gonadotropin (hCG). Females to be stressed were exposed to 35 (+OR-) 1 C and 65 (+OR-) 3% RH for 12.5 h immediately after injection of hCG. At all other times, animals were housed at control conditions (21 (+OR-) 2 C and 65 (+OR-) 5% RH). Females were either killed for oocyte collection or paired with fertile males for 5.5 h. The presence of a copulatory plug confirmed mating. Analyses were done on oocytes and embryos collected at days 3.5, 9, and 19 of gestation. Anomalous oocyte morphology was highly correlated to aberrant cytology (r = 0.96). Heat stress stopped maturation, disrupted the meiotic spindle, and caused significant numbers of oocytes to degenerate. Embryos derived from surviving oocytes were developmentally retarded and had significantly increased pre- and post-implantation death rates. Severely retarded embryos were frequently cytogenetically abnormal, and several heteroploid embryos with discordant chromosome counts also had fragmenting interphase nuclei. Genetically aberrant embryos did not survive to day 19 of gestation. High pre-implantation death rates were attributed to increased numbers of degenerate ova and delayed or inhibited early cleavage, resulting in embryo/uterine dis-synchrony. Increased post-implantation losses were due to dominant lethal mutations, induced heteroploidy (especially triploidy), and embryo/uterine dis-synchrony. Analysis of F(,2) data revealed a decrease in the proportion of male offspring without an accompanying decrease in litter size. Several explanations were proposed to account for this change. Heat exposure may have induced heritable changes in autosomal genes involved in sex determination. Male offspring of hyperthermic dams may produce a preponderance of X bearing sperm, or female offspring of hyperthermic dams may have a uterine environment where X bearing sperm are prepotent. Further studies are necessary to determine the causes of these effects.
Degree
Ph.D.
Subject Area
Genetics
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