Genetic Conflicts in Human Pregnancy

@article{Haig1993GeneticCI,
  title={Genetic Conflicts in Human Pregnancy},
  author={David Haig},
  journal={The Quarterly Review of Biology},
  year={1993},
  volume={68},
  pages={495 - 532}
}
  • D. Haig
  • Published 1 December 1993
  • Medicine, Biology
  • The Quarterly Review of Biology
Pragnancy has commonly been viewed as a cooperative interaction between a mother and her fetus. The effects of natural selection on genes expressed in fetuses, however, may be opposed by the effects of natural selection on genes expressed in mothers. In this sense, a genetic conflict can be said to exist between maternal and fetal genes. Fetal genes will be selected to increase the transfer of nutrients to their fetus, and maternal genes will be selected to limit transfers in excess of some… 

Altercation of Generations: Genetic Conflicts of Pregnancy

  • D. Haig
  • Biology
    American journal of reproductive immunology
  • 1996
Pregnancy is traditionally viewed as a harmonious collaboration between mother and fetus, but this view fails to recognize aspects of genetic conflict that lie at the heart of gestation.

Evolutionary conflicts in pregnancy and calcium metabolism--a review.

  • D. Haig
  • Biology, Medicine
    Placenta
  • 2004

Maternal–fetal conflict, genomic imprinting and mammalian vulnerabilities to cancer

  • D. Haig
  • Biology
    Philosophical Transactions of the Royal Society B: Biological Sciences
  • 2015
Gene networks that are battlegrounds of intragenomic conflict are expected to be less robust than networks that evolve in the absence of conflict.

Fetal microchimerism and maternal health: A review and evolutionary analysis of cooperation and conflict beyond the womb

An evolutionary framework is used to make testable predictions about the role of fetal microchimerism in lactation, thyroid function, autoimmune disease, cancer and maternal emotional, and psychological health.

Maternal-fetal conflict: rapidly evolving proteins in the rodent placenta.

The genomic consequences of placental expression in rodents are investigated and a substantial proportion of genes specifically expressed in the mature placenta are rapidly evolving, suggesting that placental proteins, which mediate interactions between mother and offspring, often may be the targets of evolutionary conflict.

The influence of the maternal uterine immune response on placentation in human subjects

Since aberrant implantation can cause a variety of clinical problems, including miscarriage, intrauterine growth retardation and pre-eclampsia, an understanding of the immunological mechanism by which this process is controlled could lead to the development of regimens to improve fetal growth and development.

Placental hormones, genomic imprinting, and maternal—fetal communication

An evolutionary model is presented for a hypothetical hormone that increases the nutrient content of maternal blood and predicts that, at an evolutionary equilibrium, the hormone will be produced solely by the mother or exclusively by the placenta, but not by both.

The etiology of preeclampsia: the role of the father.

...

References

SHOWING 1-10 OF 325 REFERENCES

HLA and maternal‐fetal recognition

  • J. S. HuntH. Orr
  • Biology
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 1992
Multiple regulatory mechanisms prevent the cells that sequester the embryo from the mother from expressing the potentially deleterious paternal HLA antigens, immunological rejection is avoided and successful pregnancy ensues.

Evolution of placenta-specific gene expression: comparison of the equine and human gonadotropin alpha-subunit genes.

Though the equine gene is expressed and induced by cAMP, it does not contain the elements known to confer tissue-specific expression to the human gene, the cAMP response element (CRE) and the trophoblast-specific element (TSE), nor does it bind to the trans-acting factors CREB and TSEB.

IGF2 is parentally imprinted during human embryogenesis and in the Beckwith–Wiedemann syndrome

By exploiting sequence polymorphisms in exon nine of the human insulin–like growth factor 2 (IGF2) gene, it is shown that only the paternally–inherited allele is active in embryonic and extra–embryonic cells from first trimester pregnancies.

Relaxation of imprinted genes in human cancer

In contrast, 69% of Wilms' tumours not undergoing loss of heterozygosity at lip showed biallelic expression of one or both genes, suggesting that relaxation or loss of imprinting could represent a new epigenetic mutational mechanism in carcinogenesis.

Genomic imprinting in mammalian development: a parental tug-of-war.

Parental genomic imprinting of the human IGF2 gene

It is concluded that, as in the mouse, human IGF2, the human homologue, is parentally imprinted.

Trophoblast Invasion and Placentation in the Human: Morphological Aspects

The evolution of viviparity in mammals has been possible because of the development of placentation, which means the apposition of two vascular systems, maternal and fetal to allow physiological

Relaxation of insulin-like growth factor II gene imprinting implicated in Wilms' tumour

The IGF2 gene is expressed from the paternal allele in human fetal tissue, but that in Wilms' tumour expression can occur biallelically, providing the first evidence that relaxation of imprinting may play a role in the onset of disease.

Two different phenotypes of fetuses with chromosomal triploidy: correlation with parental origin of the extra haploid set.

Although these findings suggest that in human triploids the parental origin of the extra haploid set is important in determination of both fetal and placental phenotype it is not clear to what degree placental development and function affect the resultant fetal phenotype.
...