Evol Ecol Res 1: 129-150 (1999) Full PDF if your library subscribes.
The evolution of genomic imprinting: Abortion and overshoot explain aberrations
Atsushi Mochizuki and Yasuhiko Takeda
Department of Biology, Faculty of Science, Kyushu University, Fukuoka, 812–8581, Japan
Author to whom all correspondence should be addressed.
In a previous paper, we presented a quantitative genetic model of the evolution of genomic imprinting in mammals – differential gene expression of an embryonic growth factor gene depending on the parental origin. We have shown that the verbal argument of the genetic conflict hypothesis can be justified by a formal genetic model. The model predicts the evolution of an expressed paternal allele and a silent maternal allele for a growth-enhancing gene increasing maternal resource acquisition, while the reverse pattern will evolve for an inhibitor gene. This may, however, be prevented if there are recessive deleterious mutations on coding regions in the population. In this paper, we examine potential problems for the genetic conflict hypothesis and discuss how the theory can account for them. First, we show that the reverse pattern of genomic imprinting of a growth factor gene can evolve if the risk of abortion in early gestation is enhanced by the overproduction of the growth enhancer. Such a pattern is observed in Mash2. Second, paternal disomies (double dose of paternal origin and none from maternal origin) with respect to a part of a chromosome sometimes result in a decrease (rather than an increase) in embryo size. Here we show that this can be explained if the imprinted genes regulate the allocation between placenta and embryo proper by modifying the developmental fate of cells. Third, an alternative non-conflict hypothesis is studied in the same modelling framework, which states that genomic imprinting has evolved because it reduces the risk of spontaneous development of parthenogenetic embryos that cause serious risk to the mother's life (ovarian time-bomb hypothesis). Finally, we point out that genes on the X chromosome receive selection different from autosomes, resulting in the evolution of genomic imprinting in the opposite direction.
Keywords: abortion, genetic conflict, genomic imprinting, Mash2, multivariate quantitative genetics, overshoot, parthenogenesis prevention, uniparental disomy.
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