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Schematic illustration of the mouse embryo transfer model used in this study to determine maternal genotype and fetal genotype effect on fetal weight. F/F, FVB/NJ (F) embryo transferred into F foster mother; C/F, C57BL/6J (C) embryo transferred into F foster mother; C/C, C embryo transferred into C foster mother; F/C, F embryo transferred into C foster mother. Transferred embryos were gestated in foster mothers for 18.5 days (E18.5) and then collected to record fetal and placental weights.
Source publication
The mechanisms for provisioning maternal resources to offspring in placental mammals involve complex interactions between maternally regulated and fetally regulated gene networks in the placenta, a tissue that is derived from the zygote and therefore of fetal origin. Here we describe a novel use of an embryo transfer system in mice to identify gene...
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... growth in utero. To determine fetal and maternal genotype control over fetal weights, embryo-transferred surrogate mothers (F and C) were dissected at E18.5 (18.5 dpc) ( Fig. 1) and fetal weights were recorded. A MANCOVA was performed to analyze the maternal and fetal genotypic effects on fetal weight while controlling for sex and litter size (Table 2). Fetal weight was significantly determined by the maternal genotype ( P Ͻ 0.0001). Fetal genotype was not a determining factor on fetal weight itself ( P ϭ 0.6242). Both C (C/C) and F (F/C) embryos were smaller in C mothers compared with C (C/F) and F (F/F) embryos from F mothers (Fig. 2). Fetal and maternal genotype interactions were not statistically significant in determining fetal weights ( P ϭ 0.3107). These results show that the maternal genotype significantly overrides the fetal genotype to control fetal weight. On average, fetuses from F mothers weighed 115.64 mg more than fetuses from C mothers. The sex variable of being female versus male decreased the fetal weight by 107.24 mg ( P Ͻ 0.0001) and a decrease in fetal weight by 21.28 mg per pup was attributed to the litter size variable ( P Ͻ 0.0001). The average maternal weight of the FVB/NJ mothers (23.50 g) was not significantly different from that of the C57BL/6J mothers (22.15 g), showing that the difference in the fetal weight of F/F and C/F embryos was not due to heavier F mothers. naturally conceived embryos in both mouse strains. The fetal weights of the naturally conceived and embryo-transferred E18.5 embryos of the C57BL/6J and FVB/NJ strains were analyzed by using MANCOVA to see whether the embryo transfer technique introduced any artifacts into the fetal weight analysis. Results of the analysis show that the fetal weights of the naturally conceiving and embryo-transferred mothers of both strains did not show a significant difference (source ϫ strain interaction P ϭ 0.72). The fetal weights at E18.5 (18.5 dpc) of the naturally conceived and embryo-transferred embryos of the FVB/NJ strain were 1.25 Ϯ 0.04 g and 1.23 Ϯ 0.04 g, respectively; for the C57BL/6J strain, the fetal weights of the naturally conceived and embryo-transferred pups were 1.11 Ϯ 0.04 g and 1.07 Ϯ 0.04 g, respectively. None of the other interactions with source was significant for fetal weight (Supplemental Fig. S1 and Supplemental Table ...
Citations
... Maternal × offspring (M×O) interaction at different loci is ubiquitous in mammals [Wolf, 2000]. In a mouse model, it was shown that maternal thyroid hormones bind the embryonic thyroid receptors [Nucera et al., 2010] and a list of 81 foetal genes have been identified that are maternally regulated [SenthamaraiKannan et al., 2011]. M×O interactions may partially determine birth-weight, a trait associated with many adulthood diseases [Wolf, 2000]. ...
The analyses of genetic interaction between maternal and offspring genotypes are usually conducted considering a single locus. Here, we propose testing maternal × offspring (M×O) and maternal × maternal (M×M) genotype interactions involving two unlinked loci. We reformulate the log-linear approach of analyzing cases and their parents (family trios) to accommodate two loci, fit fuller models to avoid confounding in a first analysis step and propose that the model be reduced to the most prominent effects in a second step. We conduct extensive simulations to assess the validity and power of this approach under various model assumptions. We show that the approach is valid and has good power to detect M×O and M×M interactions. For example, the power to detect a dominant interaction relative risk of 1.5 (both M×O and M×M) is 70% with 300 trios and approaches 100% with 1,000 trios. Unlike the main effects, M×O and M×M interactions are conditionally independent of mating types, and consequently, their power is not affected by missing paternal genotypes. When applied to single-locus M×O interaction, our method is as powerful as other existing methods. Applying the method to testicular cancer, we found a nominally significant M×M interaction between single nucleotide polymorphisms from C-Kit Ligand (KITLG) and Sex Hormone Binding Globulin (SHBG) using 210 families (relative risk 2.2, P = 0.03). This finding supports a role of maternal hormones in offspring testicular cancer and warrants confirmation in a larger dataset.
The aim of this work was to evaluate the influence of maternal and embryonic genotype on prenatal survival and foetal growth during pregnancy. Embryos were recovered at 48 h of gestation from two different donor lines (R = 46 and A = 40) and transferred to nulliparous recipient does (26 R and 24 A). Each recipient doe received six embryos into one oviduct from line R, and six embryos form line A into the other. Laparoscopy was performed at Day 14 to determine implantation rate. Recipient females were slaughter at Days 14, 24 and 30 (12, 24, and 14, respectively) to determine the number of live foetuses and the weight of live foetuses, foetal placenta and maternal placenta. A transcriptome analysis was performed to search for differences between foetal placentas at Days 14 and 24 of development. Prenatal survival at Days 14, and 24 was affected by embryonic genotype and determined by maternal genotype at Day 30. Foetal weight at Day 14 was influenced by both genotypes, being the weight higher for group A/A (0.29 ± 0.01 g vs 0.19 ± 0.01 g, for group R/R). However, both genotypes were determinant for foetal placenta weight at Day 24, while those genotypes affected maternal placenta weight at Day 30. Nevertheless, no differences in foetal placenta at transcriptome level and progesterone and IGF-I plasma levels in recipient does were found. In conclusion, results indicate that the influence of embryo and maternal genotype on the prenatal survival and growth seems to be changing over gestation.
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