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  • Review Article
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What good is genomic imprinting: the function of parent-specific gene expression

Nature Reviews Genetics volume 4, pages 359–368 (2003)Cite this article

Key Points

  • Genomic imprinting describes a form of non-Mendelian gene expression, in which the expression of an allele depends on its parent of origin. In most cases, one allele (either the one inherited from mother or the one inherited from father) is expressed and the other is transcriptionally inactive, although more complex patterns are also observed.

  • So far, more than 60 imprinted genes have been identified in mice. In most cases, these genes are also imprinted in humans.

  • Among the vertebrates, imprinting seems to be restricted to the marsupials and the placental mammals.

  • Many imprinted genes influence fetal growth, although some affect behavioural phenotypes that persist into adulthood.

  • The most commonly accepted explanation for the prevalence of diploidy is that it shields the individual from the effects of recessive deleterious mutations. Monoallelic expression exposes these mutations to selection, resulting in a 'cost of imprinting'. Therefore, there must be selective forces that overcome these costs at imprinted loci.

  • This review discusses three theories that attempt to explain the selective advantage of genomic imprinting: 'evolvability' models propose that imprinting enhances the adaptive evolution of a species in the face of a changing environment; the ovarian timebomb hypothesis proposes that imprinting protects female mammals from the ravages of trophoblastic disease; and the kinship theory proposes that imprinting arises as a result of an evolutionary conflict in organisms between genes of maternal and paternal origin.

  • Although the kinship theory has been the most successful theory in explaining the observed patterns of imprinting, it is still unclear whether it can account for all instances of imprinting. This determination will have to await a more detailed understanding of the phenotypic effects of imprinted genes.

Abstract

Parent-specific gene expression (genomic imprinting) is an evolutionary puzzle because it forgoes an important advantage of diploidy — protection against the effects of deleterious recessive mutations. Three hypotheses claim to have found a countervailing selective advantage of parent-specific expression. Imprinting is proposed to have evolved because it enhances evolvability in a changing environment, protects females against the ravages of invasive trophoblast, or because natural selection acts differently on genes of maternal and paternal origin in interactions among kin. The last hypothesis has received the most extensive theoretical development and seems the best supported by the properties of known imprinted genes. However, the hypothesis is yet to provide a compelling explanation for many examples of imprinting.

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References

  1. Stern, C. The nucleus and somatic cell variation. J. Cell. Comp. Physiol. 52 (Suppl.), 1–34 (1958).

    CAS  Google Scholar 

  2. Crouse, H. V. The controlling element in sex chromosome behavior in Sciara. Genetics 45, 1429–1443 (1960).

    CAS  PubMed  PubMed Central  Google Scholar 

  3. Hayward, B. E., Moran, V., Strain, L. & Bonthron, D. T. Bidirectional imprinting of a single gene: GNAS1 encodes maternally, paternally, and biallelically derived proteins. Proc. Natl Acad. Sci. USA 95, 15475–15480 (1998).

    CAS  PubMed  PubMed Central  Google Scholar 

  4. Otto, S. P. & Goldstein, D. B. Recombination and the evolution of diploidy. Genetics 131, 745–751 (1992).

    CAS  PubMed  PubMed Central  Google Scholar 

  5. McGowan, R. & Martin, C. C. DNA methylation and genome imprinting in the zebrafish, Danio rerio: some evolutionary ramifications. Biochem. Cell Biol. 75, 499–506 (1997).

    CAS  PubMed  Google Scholar 

  6. Beaudet, A. L. & Jiang, Y. A rheostat model for a rapid and reversible form of imprinting-dependent evolution. Am. J. Hum. Genet. 70, 1389–1397 (2002). The proposal that genomic imprinting enhances the evolvability of a population.

    CAS  PubMed  PubMed Central  Google Scholar 

  7. Varmuza, S. & Mann, M. Genomic imprinting — defusing the ovarian time bomb. Trends Genet. 10, 118–123 (1994). The proposal that genomic imprinting evolved to protect female mammals from the ravages of trophoblastic disease.

    CAS  PubMed  Google Scholar 

  8. Haig, D. Genomic Imprinting and Kinship (Rutgers Univ. Press, New Brunswick, 2002). A collection of papers that trace the development of the kinship theory, with retrospective commentaries.

    Google Scholar 

  9. Haig, D. & Trivers, R. in Genomic Imprinting: Causes and Consequences (eds Ohlsson, R., Hall, K. & Ritzen, M.) 17–28 (Cambridge Univ. Press, Cambridge, UK, 1995).

    Google Scholar 

  10. Hurst, L. D. in Genomic Imprinting (eds Reik, W. & Surani, A.) 211–237 (Oxford Univ. Press, Oxford, UK, 1997).

    Google Scholar 

  11. Iwasa, Y. & Pomiankowski, A. Sex specific X chromosome expression caused by genomic imprinting. J. Theor. Biol. 197, 487–495 (1999).

    CAS  PubMed  Google Scholar 

  12. Pardo-Manuel de Villena, F., de la Casa-Esperón, E. & Sapienza, C. Natural selection and the function of genome imprinting: beyond the silenced minority. Trends Genet. 16, 573–579 (2000).

    CAS  PubMed  Google Scholar 

  13. Ohlsson, R., Paldi, A. & Graves, J. A. M. Did genomic imprinting and X chromosome inactivation arise from stochastic expression? Trends Genet. 17, 136–141 (2001).

    CAS  PubMed  Google Scholar 

  14. Sleutels, F. & Barlow, D. P. The origins of genomic imprinting in mammals. Adv. Genet. 46, 119–163 (2002).

    CAS  PubMed  Google Scholar 

  15. Reik, W. & Walter, J. Genomic imprinting: parental influence on the genome. Nature Rev. Genet. 2, 21–32 (2001).

    CAS  PubMed  Google Scholar 

  16. Tycko, B. & Morison, I. M. Physiological functions of imprinted genes. J. Cell. Physiol. 192, 245–258 (2002).

    CAS  PubMed  Google Scholar 

  17. Spencer, H. G. Mutation-selection balance under genomic imprinting at an autosomal locus. Genetics 147, 281–287 (1997).

    CAS  PubMed  PubMed Central  Google Scholar 

  18. Iwasa, Y., Mochizuki, A. & Takeda, Y. The evolution of genomic imprinting: abortion and overshoot explain aberrations. Evol. Ecol. Res. 1, 129–150 (1999).

    Google Scholar 

  19. Greenwood-Lee, J. M., Taylor, P. D. & Haig, D. The inclusive fitness dynamics of genomic imprinting. Selection 2, 101–116 (2001).

    Google Scholar 

  20. Weisstein, A. E., Feldman, M. W. & Spencer, H. G. Evolutionary genetic models of the ovarian time bomb hypothesis for the evolution of genomic imprinting. Genetics 162, 425–439 (2002).

    CAS  PubMed  PubMed Central  Google Scholar 

  21. O'Neill, M. J., Ingram, R. S., Vrana, P. B. & Tilghman, S. M. Allelic expression of IGF2 in marsupials and birds. Dev. Genes Evol. 210, 18–20 (2000). This paper shows that IGF2 is imprinted in an opossum but not in chickens.

    CAS  PubMed  Google Scholar 

  22. Killian, J. K. et al. Divergent evolution in M6P/IGF2R imprinting from the Jurassic to the Quaternary. Hum. Mol. Genet. 10, 1721–1728 (2001).

    CAS  PubMed  Google Scholar 

  23. Mossman, H. W. Vertebrate Fetal Membranes (Rutgers Univ. Press, New Brunswick, New Jersey, 1987).

    Google Scholar 

  24. Feil, R., Khosla, S., Cappai, P. & Loi, P. Genomic imprinting in ruminants: allele-specific gene expression in parthenogenetic sheep. Mamm. Genome 9, 831–834 (1998).

    CAS  PubMed  Google Scholar 

  25. Haig, D. Placental hormones, genomic imprinting, and maternal-fetal communication. J. Evol. Biol. 9, 357–380 (1996).

    CAS  Google Scholar 

  26. Hamilton, W. D. The genetical evolution of social behaviour. J. Theor. Biol. 7, 1–52 (1964).

    CAS  PubMed  Google Scholar 

  27. Haig, D. Parental antagonism, relatedness asymmetries, and genomic imprinting. Proc. R. Soc. Lond. B 264, 1657–1662 (1997). A paper that generalizes the kinship theory to all interactions among kin.

    CAS  Google Scholar 

  28. Trivers, R. & Burt, A. in Genomic Imprinting: An Interdisciplinary Approach (ed. Ohlsson, R.) 1–21 (Springer, Berlin, 1999).

    Google Scholar 

  29. Haig, D. The kinship theory of genomic imprinting. Ann. Rev. Ecol. Syst. 31, 9–32 (2000).

    Google Scholar 

  30. Burt, A. & Trivers, R. Genetic conflicts in genomic imprinting. Proc. R. Soc. Lond. B 265, 2393–2397 (1998). A paper that discusses the possible conflicts between imprinted genes and the genes that are responsible for the establishment of imprints in parental germlines.

    CAS  Google Scholar 

  31. Lessells, C. M. & Parker, G. A. Parent-offspring conflict: the full-sib-half-sib fallacy. Proc. R. Soc. Lond. B 266, 1637–1643 (1999).

    Google Scholar 

  32. Haig, D. Genomic imprinting, sex-biased dispersal, and social behaviour. Ann. NY Acad. Sci. 907, 149–163 (2000).

    CAS  PubMed  Google Scholar 

  33. Haig, D. Asymmetric relations: internal conflicts and the horror of incest. Evol. Hum. Behav. 20, 83–98 (1999).

    Google Scholar 

  34. Wilkins, J. F. & Haig, D. Inbreeding, maternal care and genomic imprinting. J. Theor. Biol. 221, 559–564 (2003).

    PubMed  Google Scholar 

  35. Haig, D. & Wilkins, J. F. Genomic imprinting, sibling solidarity and the logic of collective action. Phil. Trans. R. Soc. Lond. B 355, 1593–1597 (2000).

    CAS  Google Scholar 

  36. Mochizuki, A., Takeda, Y. & Iwasa, Y. The evolution of genomic imprinting. Genetics 144, 1283–1295 (1996).

    CAS  PubMed  PubMed Central  Google Scholar 

  37. Iwasa, Y., Mochizuki, A. & Takeda, Y. The evolution of genomic imprinting: abortion and overshoot explain aberrations. Evol. Ecol. Res. 1, 129–150 (1999).

    Google Scholar 

  38. Kondoh, M. & Higashi, M. Reproductive isolation mechanism resulting from resolution of intragenomic conflict. Am. Nat. 156, 511–518 (2000).

    PubMed  Google Scholar 

  39. Wilkins, J. F. & Haig, D. Genomic imprinting at two antagonistic loci. Proc. R. Soc. Lond. B 268, 1861–1867 (2001).

    CAS  Google Scholar 

  40. Killian, J. K. et al. M6P/IGF2R imprinting evolution in mammals. Mol. Cell 5, 707–716 (2000). This paper shows that M6P/IGF2R is not imprinted in monotremes and lacks an IGF2 binding site. The binding site is present in marsupials and the gene is imprinted.

    CAS  PubMed  Google Scholar 

  41. Killian, J. K. et al. Monotreme IGF2 expression and ancestral origin of genomic imprinting. J. Exp. Zool. 291, 205–212 (2001).

    CAS  PubMed  Google Scholar 

  42. Spencer, H. G. & Williams, M. J. M. The evolution of imprinting: two modifier-locus models. Theor. Pop. Biol. 51, 23–35 (1997).

    CAS  Google Scholar 

  43. Wilkins, J. F. & Haig, D. Parental modifiers, antisense transcripts and loss of imprinting. Proc. R. Soc. Lond. B 269, 1841–1846 (2002). A theoretical paper, which predicts that imprints that are established in paternal germlines will be evolutionarily less stable than imprints that are established in maternal germlines.

    CAS  Google Scholar 

  44. Reik, W. & Walter, J. Evolution of imprinting mechanisms: the battle of the sexes begins in the zygote. Nature Genet. 27, 255–256 (2001). Most methylation imprints are established in maternal germlines. Many padumnally silent genes are inactivated indirectly by the methylation of maternal antisense promoters.

    CAS  PubMed  Google Scholar 

  45. Spencer, H. G., Feldman, M. W. & Clark A. G. Genetic conflicts, multiple paternity and the evolution of genomic imprinting. Genetics 148, 893–904 (1998).

    CAS  PubMed  PubMed Central  Google Scholar 

  46. Spencer, H. G. Population genetics and the evolution of genomic imprinting. Ann. Rev. Genet. 34, 457–477 (2000). A review of the formal population genetic models of genomic imprinting.

    CAS  PubMed  Google Scholar 

  47. Eshel, I. On the changing concept of evolutionary population stability as a reflection of a changing point of view in the quantitative theory of evolution. J. Math. Biol. 34, 485–510 (1996).

    CAS  PubMed  Google Scholar 

  48. Haig, D. Multiple paternity and genomic imprinting. Genetics 151, 1229–1231 (1999).

    CAS  PubMed  PubMed Central  Google Scholar 

  49. Hurst, L. D. & McVean, G. T. Growth effects of uniparental disomies and the conflict theory of genomic imprinting. Trends Genet. 13, 436–443 (1997).

    CAS  PubMed  Google Scholar 

  50. Dawson, W. D. Fertility and size inheritance in a Peromyscus species cross. Evolution 19, 44–55 (1965).

    Google Scholar 

  51. Vrana, P. B., Guan, X. -J., Ingram, R. S. & Tilghman, S. M. Genomic imprinting is disrupted in interspecific Peromyscus hybrids. Nature Genet. 20, 362–365 (1998). A paper showing that imprinting can contribute to reproductive isolation between species.

    CAS  PubMed  Google Scholar 

  52. Vrana, P. B. et al. Genetic and epigenetic incompatibilities underlie hybrid dysgenesis in Peromyscus. Nature Genet. 25, 120–124 (2000).

    CAS  PubMed  Google Scholar 

  53. Hurst, L. D. Peromysci, promiscuity and imprinting. Nature Genet. 20, 315–316 (1998).

    CAS  PubMed  Google Scholar 

  54. Hurst, L. D. & McVean, G. T. Do we understand the evolution of genomic imprinting? Curr. Opin. Genet. Dev. 8, 701–708 (1998).

    CAS  PubMed  Google Scholar 

  55. Haig, D. Genetic conflicts and the private life of Peromyscus polionotus. Nature Genet. 22, 131 (1999).

    CAS  PubMed  Google Scholar 

  56. Foltz, D. W. Genetic evidence for long-term monogamy in a small rodent, Peromyscus polionotus. Am. Nat. 117, 665–675 (1981).

    Google Scholar 

  57. Moore, T. & Mills, W. Imprinting and monogamy. Nature Genet. 22, 130–131 (1999).

    CAS  PubMed  Google Scholar 

  58. Lefebvre, L. et al. Abnormal maternal behaviour and growth retardation associated with loss of the imprinted gene Mest. Nature Genet. 20, 163–169 (1998).

    CAS  PubMed  Google Scholar 

  59. Li, L. -L. et al. Regulation of maternal behavior and offspring growth by paternally expressed Peg3. Science 284, 330–333 (1999).

    CAS  PubMed  Google Scholar 

  60. Smits, G., Parma, J. & Vassart, G. Peg3 and the conflict hypothesis. Science 287, 1167 (2000).

    Google Scholar 

  61. Hurst, L. D., Pomiankowski, A. & McVean, G. Peg3 and the conflict hypothesis. Science 287, 1167 (2000).

    Google Scholar 

  62. Haig, D. & Westoby, M. Parent-specific gene expression and the triploid endosperm. Am. Nat. 134, 147–155 (1989). The first published version of the kinship theory.

    Google Scholar 

  63. Haig, D. & Westoby, M. Genomic imprinting in endosperm: its effects on seed development in crosses between species and between different ploidies of the same species, and its implications for the evolution of apomixis. Phil. Trans R. Soc. Lond. B 333, 1–13 (1991).

    Google Scholar 

  64. Grossniklaus, U., Vielle-Calzada, J. -P., Hoeppner, M. A. & Gagliano, W. B. Maternal control of embryogenesis by MEDEA, a Polycomb group gene in Arabidopsis. Science 280, 446–450 (1998). The first imprinted gene that was identified in Arabidopsis.

    CAS  PubMed  Google Scholar 

  65. DeChiara, T. M., Robertson, E. J. & Efstratiadis, A. Parental imprinting of the mouse insulin-like growth factor II gene. Cell 64, 849–859 (1991).

    CAS  PubMed  Google Scholar 

  66. Barlow, D. P., Stöger, R., Herrmann, B. G., Saito, K. & Schweifer, N. The mouse insulin-like growth factor type-2 receptor is imprinted and closely linked to the Tme locus. Nature 349, 84–87 (1991).

    CAS  PubMed  Google Scholar 

  67. Ludwig, T. et al. Mouse mutants lacking the type 2 IGF receptor (IGF2R) are rescued from perinatal lethality in Igf2 and Igf1r null backgrounds. Dev. Biol. 177, 517–535 (1996).

    CAS  PubMed  Google Scholar 

  68. Haig, D. & Graham, C. Genomic imprinting and the strange case of the insulin-like growth factor-II receptor. Cell 64, 1045–1046 (1991).

    CAS  PubMed  Google Scholar 

  69. Kornfeld, S. Structure and function of the mannose 6-phosphate/insulinlike growth factor II receptors. Annu. Rev. Biochem. 61, 307–330 (1992).

    CAS  PubMed  Google Scholar 

  70. Dahms, N. M. & Hancock, M. K. P-type lectins. Biochim. Biophys. Acta 1572, 317–340 (2002).

    CAS  PubMed  Google Scholar 

  71. Dahms, N. M., Brzycki-Wessell, M. A., Ramanujam, K. S. & Seethram, B. Characterization of mannose 6-phosphate receptors (MPRs) from opossum liver: opossum cation-independent MPR binds insulin-like growth factor-II. Endocrinology 133, 440–446 (1993).

    CAS  PubMed  Google Scholar 

  72. Yandell, C. A., Dunbar, A. J., Wheldrake, J. F. & Upton, Z. The kangaroo cation-independent mannose 6-phosphate receptor binds insulin-like growth factor II with low affinity. J. Biol. Chem. 274, 27076–27082 (1999).

    CAS  PubMed  Google Scholar 

  73. Clairmont, K. B. & Czech, M. P. Chicken and Xenopus mannose 6-phosphate receptors fail to bind insulin-like growth factor II. J. Biol. Chem. 264, 16390–16392 (1989).

    CAS  PubMed  Google Scholar 

  74. Nolan, C. M., Killian, J. K., Pettite, J. N. & Jirtle, R. L. Imprint status of M6P/IGF2R and IGF2 in chickens. Dev. Genes Evol. 211, 179–183 (2001).

    CAS  PubMed  Google Scholar 

  75. Hughes, R. L. & Hall, L. S. Early development and embryology of the platypus. Phil. Trans. R. Soc. Lond. B 353, 1101–1114 (1998).

    CAS  Google Scholar 

  76. Grant, T. R. & Temple-Smith, P. D. Field biology of the platypus (Ornithorhynchus anatinus): historical and current perspectives. Phil. Trans. R. Soc. Lond. B 353, 1081–1091 (1998).

    CAS  Google Scholar 

  77. Constância, M. et al. Placental-specific IGF-II is a major modulator of placental and fetal growth. Nature 417, 945–948 (2002).

    PubMed  Google Scholar 

  78. Sleutels, F., Zwart, R. & Barlow, D. P. The non-coding Air RNA is required for silencing autosomal imprinted genes. Nature 415, 810–813 (2002).

    CAS  PubMed  Google Scholar 

  79. Gimenez-Roqueplo, A. -P. et al. The R22X mutation of the SDHD gene in hereditary paraganglioma abolishes the enzymatic activity of complex II in the mitochondrial respiratory chain and activates the hypoxia pathway. Am. J. Hum. Genet. 69, 1186–1197 (2001).

    CAS  PubMed  PubMed Central  Google Scholar 

  80. Cavaillé, J. et al. Identification of brain-specific and imprinted small nucleolar RNA genes exhibiting an unusual genomic organization. Proc. Natl Acad. Sci. USA 97, 14311–14316 (2000).

    PubMed  PubMed Central  Google Scholar 

  81. Lau, M. M. H. et al. Loss of the imprinted IGF2/cation-independent mannose 6-phosphate receptor results in fetal overgrowth and perinatal lethality. Genes Dev. 8, 2953–2963 (1994).

    CAS  PubMed  Google Scholar 

  82. Tanaka, M., Gertsenstein, M., Rossant, J. & Nagy, A. Mash2 acts cell autonomously in mouse spongiotrophoblast development. Dev. Biol. 190, 55–65 (1997).

    CAS  PubMed  Google Scholar 

  83. Yu, S. et al. Variable and tissue-specific hormone resistance in heterotrimeric Gs protein α-subunit (Gsα) knockout mice is due to tissue-specific imprinting of the Gsα gene. Proc. Natl Acad. Sci. USA 95, 8715–8720 (1998).

    CAS  PubMed  PubMed Central  Google Scholar 

  84. Sado, T., Wang, Z., Sasaki, H. & Li, E. Regulation of imprinted X-chromosome inactivation in mice by Tsix. Development 128, 1275–1286 (2001).

    CAS  PubMed  Google Scholar 

  85. Fang, P. et al. The spectrum of mutations in UBE3A causing Angelman syndrome. Hum. Mol. Genet. 8, 129–135 (1999).

    CAS  PubMed  Google Scholar 

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Acknowledgements

The authors thank C. Muirhead, R. Trivers and the anonymous reviewers for helpful comments on the manuscript.

Author information

Authors and Affiliations

  1. Society of Fellows, 7 Divinity Avenue, Harvard University, Cambridge, 02138, Massachusetts, USA

    Jon F. Wilkins

  2. Bauer Center for Genomics Research, 7 Divinity Avenue, Harvard University, Cambridge, 02138, Massachusetts, USA

    Jon F. Wilkins

  3. Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, 02138, Massachusetts, USA

    David Haig

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Correspondence to Jon F. Wilkins.

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DATABASES

LocusLink

IGF1R

Igf2

IGF2

IGF-II

Igf2r

IGF2R

Mest

Peg3

OMIM

ovarian teratomas

testicular germ-cell tumours

FURTHER INFORMATION

Harwell imprinting web site

Glossary

EPIGENETIC

Modifications of chromatin or DNA (for example, histone deacetylation and cytosine methylation) that can be stably transmitted through many cell divisions, but can also be reset (unlike the DNA sequence).

EVOLVABILITY

The capacity of a genetic system to generate new adaptations.

FUNCTION

The phenotypic effects of a DNA sequence that are responsible for the selective maintenance of its integrity in the face of mutational processes.

UNIPARENTAL DISOMIES

Both copies of a chromosome derived from one parent.

TERATOMA

A tumour consisting of several cell types.

TROPHOBLAST

The extraembryonic cell population at the maternal–fetal interface. In mice and humans, elements of the trophoblast invade the maternal tissues of the uterus.

CHORIOVITELLINE

A placenta that is derived from the fusion of the extraembryonic yolk sac and the chorion.

KIN

Individuals that share some of their genes by recent common descent.

DEMAND INHIBITOR

A factor that is produced by an offspring reducing the 'demand' on its mother. That is, the production of the factor decreases the individual fitness of the offspring at a benefit to the expected fitness of its mother from other offspring.

DEMAND ENHANCER

A factor that is produced by an offspring increasing the 'demand' on its mother. That is, the production of the factor increases the individual fitness of the offspring at a cost to the expected fitness of its mother from other offspring.

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Wilkins, J., Haig, D. What good is genomic imprinting: the function of parent-specific gene expression. Nat Rev Genet 4, 359–368 (2003). https://doi.org/10.1038/nrg1062

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