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Journal articles on the topic 'Genomic imprinting'

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Published: 4 June 2021

Last updated: 31 July 2024

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1

Bajrami, Emirjeta, and Mirko Spiroski. "Genomic Imprinting." Open Access Macedonian Journal of Medical Sciences 4, no. 1 (February 4, 2016): 181–84. http://dx.doi.org/10.3889/oamjms.2016.028.

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BACKGROUND: Genomic imprinting is the inheritance out of Mendelian borders. Many of inherited diseases and human development violates Mendelian law of inheritance, this way of inheriting is studied by epigenetics.AIM: The aim of this review is to analyze current opinions and options regarding to this way of inheriting.RESULTS: Epigenetics shows that gene expression undergoes changes more complex than modifications in the DNA sequence; it includes the environmental influence on the gametes before conception. Humans inherit two alleles from mother and father, both are functional for the majority of the genes, but sometimes one is turned off or “stamped” and doesn’t show in offspring, that gene is imprinted. Imprinting means that that gene is silenced, and gene from other parent is expressed. The mechanisms for imprinting are still incompletely defined, but they involve epigenetic modifications that are erased and then reset during the creation of eggs and sperm. Genomic imprinting is a process of silencing genes through DNA methylation. The repressed allele is methylated, while the active allele is unmethylated. The most well-known conditions include Prader-Willi syndrome, and Angelman syndrome. Both of these syndromes can be caused by imprinting or other errors involving genes on the long arm of chromosome 15.CONCLUSIONS: Genomic imprinting and other epigenetic mechanisms such as environment is shown that plays role in offspring neurodevelopment and autism spectrum disorder.

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2

Monk, M. "Genomic imprinting." Genes & Development 2, no. 8 (August 1, 1988): 921–25. http://dx.doi.org/10.1101/gad.2.8.921.

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3

Maher, E. R. "Genomic Imprinting." Journal of Medical Genetics 28, no. 9 (September 1, 1991): 647. http://dx.doi.org/10.1136/jmg.28.9.647.

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4

Hall, J. G. "Genomic imprinting." Archives of Disease in Childhood 65, no. 10 Spec No (October 1, 1990): 1013–15. http://dx.doi.org/10.1136/adc.65.10_spec_no.1013.

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5

Jones, Peter A. "Genomic Imprinting." American Journal of Human Genetics 63, no. 3 (September 1998): 927. http://dx.doi.org/10.1086/302003.

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6

Pedersen, C. "Genomic imprinting." Reproductive Toxicology 11, no. 2-3 (June 1997): 309–16. http://dx.doi.org/10.1016/s0890-6238(96)00213-4.

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7

da Rocha, Simao Teixeira, and Anne C. Ferguson-Smith. "Genomic imprinting." Current Biology 14, no. 16 (August 2004): R646—R649. http://dx.doi.org/10.1016/j.cub.2004.08.007.

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8

Hultén, M., A. Kerr, and WilliamH James. "Genomic imprinting." Lancet 338, no. 8760 (July 1991): 188–89. http://dx.doi.org/10.1016/0140-6736(91)90180-w.

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9

Lambertini, Luca. "Genomic imprinting." Current Opinion in Pediatrics 26, no. 2 (April 2014): 237–42. http://dx.doi.org/10.1097/mop.0000000000000072.

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10

Hodgson, Shirley. "Genomic Imprinting." Developmental Medicine & Child Neurology 33, no. 6 (November 12, 2008): 552–56. http://dx.doi.org/10.1111/j.1469-8749.1991.tb14920.x.

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11

Hall, Judith G. "Genomic imprinting." Current Opinion in Genetics & Development 1, no. 1 (June 1991): 34–39. http://dx.doi.org/10.1016/0959-437x(91)80038-n.

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12

Haig, David. "Genomic imprinting." American Journal of Human Biology 10, no. 5 (1998): 679–80. http://dx.doi.org/10.1002/(sici)1520-6300(1998)10:5<679::aid-ajhb14>3.0.co;2-5.

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13

Gadagkar, Raghavendra. "Genomic imprinting." Resonance 5, no. 9 (September 2000): 58–68. http://dx.doi.org/10.1007/bf02836218.

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14

Bartolomei, M. S., and A. C. Ferguson-Smith. "Mammalian Genomic Imprinting." Cold Spring Harbor Perspectives in Biology 3, no. 7 (May 16, 2011): a002592. http://dx.doi.org/10.1101/cshperspect.a002592.

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15

Deal, Cheri L. "Parental genomic imprinting." Current Opinion in Pediatrics 7, no. 4 (August 1995): 445–58. http://dx.doi.org/10.1097/00008480-199508000-00018.

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16

Murrell, A. "Beyond genomic imprinting." Briefings in Functional Genomics 9, no. 4 (July 1, 2010): 279–80. http://dx.doi.org/10.1093/bfgp/elq019.

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17

Swales, A. K. E., and N. Spears. "Genomic imprinting and reproduction." Reproduction 130, no. 4 (October 2005): 389–99. http://dx.doi.org/10.1530/rep.1.00395.

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Genomic imprinting is the parent-of-origin specific gene expression which is a vital mechanism through both development and adult life. One of the key elements of the imprinting mechanism is DNA methylation, controlled by DNA methyltransferase enzymes. Germ cells undergo reprogramming to ensure that sex-specific genomic imprinting is initiated, thus allowing normal embryo development to progress after fertilisation. In some cases, errors in genomic imprinting are embryo lethal while in others they lead to developmental disorders and disease. Recent studies have suggested a link between the use of assisted reproductive techniques and an increase in normally rare imprinting disorders. A greater understanding of the mechanisms of genomic imprinting and the factors that influence them are important in assessing the safety of these techniques.

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18

Chandra, H. Sharat, and Vidyanand Nanjundiah. "The evolution of genomic imprinting." Development 108, Supplement (April 1, 1990): 47–53. http://dx.doi.org/10.1242/dev.108.supplement.47.

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We explore three possible pathways for the evolution of genomic imprinting. (1) Imprinting may be advantageous in itself when imprinted and unimprinted alleles of a locus confer different phenotypes. If a segment of DNA is imprinted in the gametes of one sex but not in those of the other, it might lead to effects correlated with sexual dimorphism. More fundamentally, in certain organisms, sex determination might have evolved because of imprinting. When imprinting leads to chromosome elimination or inactivation and occurs in some embryos but not in others, two classes of embryos, differing in the number of functional gene copies, would result. A model for sex determination based on inequality in the actual or effective copy-number of particular noncoding, regulatory sequences of DNA has been proposed (Chandra, Proc. natn. Acad. Sci. U.S.A. 82. 1165–1169 and 6947–6949, 1985). Maternal control of offspring sex is another possible consequence of imprinting; this would indicate a potential role for imprinting in sex ratio evolution. (2) Genes responsible for imprinting may have pleiotropic effects and they may have been selected for reasons other than their imprinting ability. Lack of evidence precludes further consideration of this possibility. (3) Imprinting could have co-evolved with other traits. For instance, gamete-specific imprinting could lead to a lowered fitness of androgenetic or gynogenetic diploids relative to the fitness of ‘normal’ diploids. This in turn would reinforce the evolution of anisogamy. The reversibility of imprinting raises the possibility of occasional incomplete or improper erasure. If the site of imprinting is the egg – as appears to be the case with the human X (Chandra and Brown, Nature 253. 165–168, 1975) – either improper imprinting or improper erasure could lead to unusual patterns of inheritance (as in the fragile-X syndrome) or fitness effects skipping generations.

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19

Pearce, G. P., and H. G. Spencer. "Population genetic models of genomic imprinting." Genetics 130, no. 4 (April 1, 1992): 899–907. http://dx.doi.org/10.1093/genetics/130.4.899.

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Abstract The phenomenon of genomic imprinting has recently excited much interest among experimental biologists. The population genetic consequences of imprinting, however, have remained largely unexplored. Several population genetic models are presented and the following conclusions drawn: (i) systems with genomic imprinting need not behave similarly to otherwise identical systems without imprinting; (ii) nevertheless, many of the models investigated can be shown to be formally equivalent to models without imprinting; (iii) consequently, imprinting often cannot be discovered by following allele frequency changes or examining equilibrium values; (iv) the formal equivalences fail to preserve some well known properties. For example, for populations incorporating genomic imprinting, parameter values exist that cause these populations to behave like populations without imprinting, but with heterozygote advantage, even though no such advantage is present in these imprinting populations. We call this last phenomenon "pseudoheterosis." The imprinting systems that fail to be formally equivalent to nonimprinting systems are those in which males and females are not equivalent, i.e., two-sex viability systems and sex-chromosome inactivation.

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20

Reik, Wolf, and Nicholas D. Allen. "Genomic Imprinting: Imprinting with and without methylation." Current Biology 4, no. 2 (February 1994): 145–47. http://dx.doi.org/10.1016/s0960-9822(94)00034-5.

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21

Horsthemke, Bernhard. "In Brief: Genomic imprinting and imprinting diseases." Journal of Pathology 232, no. 5 (January 29, 2014): 485–87. http://dx.doi.org/10.1002/path.4326.

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22

Mochizuki, Atsushi, Yasuhiko Takeda, and Yoh Iwasa. "The Evolution of Genomic Imprinting." Genetics 144, no. 3 (November 1, 1996): 1283–95. http://dx.doi.org/10.1093/genetics/144.3.1283.

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Abstract In some mammalian genes, the paternally and maternally derived alleles are expressed differently: this phenomenon is called genomic imprinting. Here we study the evolution of imprinting using multivariate quantitative genetic models to examine the feasibility of the genetic conflict hypothesis. This hypothesis explains the observed imprinting patterns as an evolutionary outcome of the conflict between the paternal and maternal alleles. We consider the expression of a zygotic gene, which codes for an embryonic growth factor affecting the amount of maternal resources obtained through the placenta. We assume that the gene produces the growth factor in two different amounts depending on its parental origin. We show that genomic imprinting evolves easily if females have some probability of multiple partners. This is in conflict with the observation that not all genes controlling placental development are imprinted and that imprinting in some genes is not conserved between mice and humans. We show however that deleterious mutations in the coding region of the gene create selection against imprinting.

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23

Prawitt, Dirk, and Thomas Haaf. "Basics and disturbances of genomic imprinting." Medizinische Genetik 32, no. 4 (November 18, 2020): 297–304. http://dx.doi.org/10.1515/medgen-2020-2042.

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Abstract Genomic imprinting ensures the parent-specific expression of either the maternal or the paternal allele, by different epigenetic processes (DNA methylation and histone modifications) that confer parent-specific marks (imprints) in the paternal and maternal germline, respectively. Most protein-coding imprinted genes are involved in embryonic growth, development, and behavior. They are usually organized in genomic domains that are regulated by differentially methylated regions (DMRs). Genomic imprints are erased in the primordial germ cells and then reset in a gene-specific manner according to the sex of the germline. The imprinted genes regulate and interact with other genes, consistent with the existence of an imprinted gene network. Defects of genomic imprinting result in syndromal imprinting disorders. To date a dozen congenital imprinting disorders are known. Usually, a given imprinting disorder can be caused by different types of defects, including point mutations, deletions/duplications, uniparental disomy, and epimutations. Causative trans-acting factors in imprinting disorders, including ZFP57 and the subcortical maternal complex (SCMC), have the potential to affect multiple DMRs across the genome, resulting in a multi-locus imprinting disturbance. There is evidence that mutations in components of the SCMC can confer an increased risk for imprinting disorders.

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24

Garnier, Olivier, Sylvia Laoueillé-Duprat, and Charles Spillane. "Genomic imprinting in plants." Epigenetics 3, no. 1 (January 17, 2008): 14–20. http://dx.doi.org/10.4161/epi.3.1.5554.

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25

Barlow, D. P., and M. S. Bartolomei. "Genomic Imprinting in Mammals." Cold Spring Harbor Perspectives in Biology 6, no. 2 (February 1, 2014): a018382. http://dx.doi.org/10.1101/cshperspect.a018382.

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26

Sapienza, C. "Genetic Complexities: Genomic Imprinting." Science 273, no. 5273 (July 19, 1996): 316b—317b. http://dx.doi.org/10.1126/science.273.5273.316b.

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27

Mitchell, Braxton D., and Toni I. Pollin. "Genomic imprinting in diabetes." Genome Medicine 2, no. 8 (2010): 55. http://dx.doi.org/10.1186/gm176.

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28

Hoffman, Andrew R., Thanh H. Vu, and Jifan Hu. "Mechanisms of genomic imprinting." Growth Hormone & IGF Research 10 (January 2000): S18—S19. http://dx.doi.org/10.1016/s1096-6374(00)90008-x.

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29

Pfeifer, Karl. "Mechanisms of Genomic Imprinting." American Journal of Human Genetics 67, no. 4 (October 2000): 777–87. http://dx.doi.org/10.1086/303101.

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30

Wilkins, R. J. "Genomic Imprinting and Carcinogenesis." Journal of Urology 140, no. 1 (July 1988): 208–9. http://dx.doi.org/10.1016/s0022-5347(17)41534-5.

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31

Wilkins, RichardJ. "GENOMIC IMPRINTING AND CARCINOGENESIS." Lancet 331, no. 8581 (February 1988): 329–31. http://dx.doi.org/10.1016/s0140-6736(88)91121-x.

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32

Cowley, M., and R. J. Oakey. "Retrotransposition and genomic imprinting." Briefings in Functional Genomics 9, no. 4 (June 29, 2010): 340–46. http://dx.doi.org/10.1093/bfgp/elq015.

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33

Loppin, Benjamin, and Rebecca Oakey. "Genomic imprinting in Singapore." EMBO reports 10, no. 3 (February 13, 2009): 222–27. http://dx.doi.org/10.1038/embor.2009.20.

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34

Brannan, Camilynn I., and Marisa S. Bartolomei. "Mechanisms of genomic imprinting." Current Opinion in Genetics & Development 9, no. 2 (April 1999): 164–70. http://dx.doi.org/10.1016/s0959-437x(99)80025-2.

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35

Bartolomei, Marisa S., and Shirley M. Tilghman. "GENOMIC IMPRINTING IN MAMMALS." Annual Review of Genetics 31, no. 1 (December 1997): 493–525. http://dx.doi.org/10.1146/annurev.genet.31.1.493.

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36

Joyce, J. A., and P. N. Schofield. "Genomic imprinting and cancer." Molecular Pathology 51, no. 4 (August 1, 1998): 185–90. http://dx.doi.org/10.1136/mp.51.4.185.

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37

Nolan, CM, FM O’Sullivan, DC Brabazon, and JJ Callanan. "Genomic Imprinting inCanis familiaris." Reproduction in Domestic Animals 44 (July 2009): 16–21. http://dx.doi.org/10.1111/j.1439-0531.2009.01387.x.

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38

Kobayashi, Hisato, and Takahiro Arima. "Genomic Imprinting in Mammals." Journal of Mammalian Ova Research 23, no. 4 (October 2006): 143–49. http://dx.doi.org/10.1274/jmor.23.143.

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39

Hiura, Hitoshi. "Genomic Imprinting in Oogenesis." Journal of Mammalian Ova Research 26, no. 4 (October 2009): 183–88. http://dx.doi.org/10.1274/jmor.26.183.

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40

Jirtle, Randy L. "Genomic Imprinting and Cancer." Experimental Cell Research 248, no. 1 (April 1999): 18–24. http://dx.doi.org/10.1006/excr.1999.4453.

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41

Squire, J. "Genomic imprinting in tumours." Seminars in Cancer Biology 7, no. 1 (February 1996): 41–47. http://dx.doi.org/10.1006/scbi.1996.0006.

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42

Berry, Colin L. "Genomic imprinting for pathologists." Virchows Archiv A Pathological Anatomy and Histopathology 419, no. 5 (September 1991): 363–64. http://dx.doi.org/10.1007/bf01605068.

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43

Eggermann, Thomas. "Human Reproduction and Disturbed Genomic Imprinting." Genes 15, no. 2 (January 26, 2024): 163. http://dx.doi.org/10.3390/genes15020163.

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Genomic imprinting is a specific mode of gene regulation which particularly accounts for the factors involved in development. Its disturbance affects the fetus, the course of pregnancy and even the health of the mother. In children, aberrant imprinting signatures are associated with imprinting disorders (ImpDis). These alterations also affect the function of the placenta, which has consequences for the course of the pregnancy. The molecular causes of ImpDis comprise changes at the DNA level and methylation disturbances (imprinting defects/ImpDefs), and there is an increasing number of reports of both pathogenic fetal and maternal DNA variants causing ImpDefs. These ImpDefs can be inherited, but prediction of the pregnancy complications caused is difficult, as they can cause miscarriages, aneuploidies, health issues for the mother and ImpDis in the child. Due to the complexity of imprinting regulation, each pregnancy or patient with suspected altered genomic imprinting requires a specific workup to identify the precise molecular cause and also careful clinical documentation. This review will cover the current knowledge on the molecular causes of aberrant imprinting signatures and illustrate the need to identify this basis as the prerequisite for personalized genetic and reproductive counselling of families.

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44

Edwards, Carol A., Nozomi Takahashi, Jennifer A. Corish, and Anne C. Ferguson-Smith. "The origins of genomic imprinting in mammals." Reproduction, Fertility and Development 31, no. 7 (2019): 1203. http://dx.doi.org/10.1071/rd18176.

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Genomic imprinting is a process that causes genes to be expressed according to their parental origin. Imprinting appears to have evolved gradually in two of the three mammalian subclasses, with no imprinted genes yet identified in prototheria and only six found to be imprinted in marsupials to date. By interrogating the genomes of eutherian suborders, we determine that imprinting evolved at the majority of eutherian specific genes before the eutherian radiation. Theories considering the evolution of imprinting often relate to resource allocation and recently consider maternal–offspring interactions more generally, which, in marsupials, places a greater emphasis on lactation. In eutherians, the imprint memory is retained at least in part by zinc finger protein 57 (ZFP57), a Kruppel associated box (KRAB) zinc finger protein that binds specifically to methylated imprinting control regions. Some imprints are less dependent on ZFP57invivo and it may be no coincidence that these are the imprints that are found in marsupials. Because marsupials lack ZFP57, this suggests another more ancestral protein evolved to regulate imprints in non-eutherian subclasses, and contributes to imprinting control in eutherians. Hence, understanding the mechanisms acting at imprinting control regions across mammals has the potential to provide valuable insights into our understanding of the origins and evolution of genomic imprinting.

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45

Renfree, Marilyn B., Shunsuke Suzuki, and Tomoko Kaneko-Ishino. "The origin and evolution of genomic imprinting and viviparity in mammals." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1609 (January 5, 2013): 20120151. http://dx.doi.org/10.1098/rstb.2012.0151.

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Genomic imprinting is widespread in eutherian mammals. Marsupial mammals also have genomic imprinting, but in fewer loci. It has long been thought that genomic imprinting is somehow related to placentation and/or viviparity in mammals, although neither is restricted to mammals. Most imprinted genes are expressed in the placenta. There is no evidence for genomic imprinting in the egg-laying monotreme mammals, despite their short-lived placenta that transfers nutrients from mother to embryo. Post natal genomic imprinting also occurs, especially in the brain. However, little attention has been paid to the primary source of nutrition in the neonate in all mammals, the mammary gland. Differentially methylated regions (DMRs) play an important role as imprinting control centres in each imprinted region which usually comprises both paternally and maternally expressed genes ( PEG s and MEG s). The DMR is established in the male or female germline (the gDMR). Comprehensive comparative genome studies demonstrated that two imprinted regions, PEG10 and IGF2-H19 , are conserved in both marsupials and eutherians and that PEG10 and H19 DMRs emerged in the therian ancestor at least 160 Ma, indicating the ancestral origin of genomic imprinting during therian mammal evolution. Importantly, these regions are known to be deeply involved in placental and embryonic growth. It appears that most maternal gDMRs are always associated with imprinting in eutherian mammals, but emerged at differing times during mammalian evolution. Thus, genomic imprinting could evolve from a defence mechanism against transposable elements that depended on DNA methylation established in germ cells.

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46

Renfree, Marilyn B., Eleanor I. Ager, Geoff Shaw, and Andrew J. Pask. "Genomic imprinting in marsupial placentation." REPRODUCTION 136, no. 5 (November 2008): 523–31. http://dx.doi.org/10.1530/rep-08-0264.

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Genomic imprinting is a widespread epigenetic phenomenon in eutherian mammals, which regulates many aspects of growth and development. Parental conflict over the degree of maternal nutrient transfer is the favoured hypothesis for the evolution of imprinting. Marsupials, like eutherian mammals, are viviparous but deliver an altricial young after a short gestation supported by a fully functional placenta, so can shed light on the evolution and time of acquisition of genomic imprinting. All orthologues of eutherian imprinted genes examined have a conserved expression in the marsupial placenta regardless of their imprint status. Differentially methylated regions (DMRs) are the most common mechanism controlling genomic imprinting in eutherian mammals, but none were found in the marsupial imprinted orthologues of IGF2 receptor (IGF2R), INS or mesoderm-specific transcript (MEST). Instead, histone modification appears to be the mechanism used to silence these genes. At least three genes in marsupials have DMRs: H19, IGF2 and PEG10. PEG10 is particularly interesting as it is derived from a retrotransposon, providing the first direct evidence that retrotransposon insertion can drive the evolution of an imprinted region and of a DMR in mammals. The insertion occurred after the prototherian–therian mammal divergence, suggesting that there may have been strong selection for the retention of imprinted regions that arose during the evolution of placentation. There is currently no evidence for genomic imprinting in the egg-laying monotreme mammals. However, since these mammals do have a short-lived placenta, imprinting appears to be correlated with viviparity but not placentation.

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47

Hirasawa, Ryutaro, and Robert Feil. "Genomic imprinting and human disease." Essays in Biochemistry 48 (September 20, 2010): 187–200. http://dx.doi.org/10.1042/bse0480187.

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In many epigenetic phenomena, covalent modifications on DNA and chromatin mediate somatically heritable patterns of gene expression. Genomic imprinting is a classical example of epigenetic regulation in mammals. To date, more than 100 imprinted genes have been identified in humans and mice. Many of these are involved in foetal growth and deve lopment, others control behaviour. Mono-allelic expression of imprinted genes depends on whether the gene is inherited from the mother or the father. This remarkable pattern of expression is controlled by specialized sequence elements called ICRs (imprinting control regions). ICRs are marked by DNA methylation on one of the two parental alleles. These allelic marks originate from either the maternal or the paternal germ line. Perturbation of the allelic DNA methylation at ICRs is causally involved in several human diseases, including the Beckwith–Wiedemann and Silver–Russell syndromes, associated with aberrant foetal growth. Perturbed imprinted gene expression is also implicated in the neuro-developmental disorders Prader–Willi syndrome and Angelman syndrome. Embryo culture and human-assisted reproduction procedures can increase the occurrence of imprinting-related disorders. Recent research shows that, besides DNA methylation, covalent histone modifications and non-histone proteins also contribute to imprinting regulation. The involvement of imprinting in specific human pathologies (and in cancer) emphasizes the need to further explore the underlying molecular mechanisms.

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48

Rodrigues, Jessica A., and Daniel Zilberman. "Evolution and function of genomic imprinting in plants." Genes & Development 29, no. 24 (December 15, 2015): 2517–31. http://dx.doi.org/10.1101/gad.269902.115.

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Genomic imprinting, an inherently epigenetic phenomenon defined by parent of origin-dependent gene expression, is observed in mammals and flowering plants. Genome-scale surveys of imprinted expression and the underlying differential epigenetic marks have led to the discovery of hundreds of imprinted plant genes and confirmed DNA and histone methylation as key regulators of plant imprinting. However, the biological roles of the vast majority of imprinted plant genes are unknown, and the evolutionary forces shaping plant imprinting remain rather opaque. Here, we review the mechanisms of plant genomic imprinting and discuss theories of imprinting evolution and biological significance in light of recent findings.

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49

Cattanach, B. M. "Contributions of Mouse Genetic Studies to Genomic Imprinting." Acta geneticae medicae et gemellologiae: twin research 45, no. 1-2 (April 1996): 17. http://dx.doi.org/10.1017/s0001566000001057.

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Maternal and paternal disomies and equivalent duplications for specific chromosome regions can readily be generated in the mouse. Most do not result in abnormality but for 10 regions distributed over 6 chromosomes developmental anomalies ranging from early embryonic lethalities to characteristic phenotypic abnormalities occur. With certain chromosome regions, maternal or paternal duplication leads to different and, in some cases, opposite anomalies so that, in total, 15 different imprinting effects can be distinguished. These observations have provided key evidence on the occurrence of imprinting in mammals.On the basis of the established homologies between mouse and human chromosomes, it is possible to predict which segments of the human genome are subject to equivalent imprinting. In this regard it is significant that candidate imprinting effects for the two classical examples of imprinting in humans, namely the Prader-Willi and Angelman syndromes, have been found in the mouse.Current studies are aimed at reducing the size of the imprinting regions with the objective of facilitating identification of the genes involved. Furthermore, the developmental profiles of genes already identified as being subject to imprinting are being determined.A new approach involves the analysis of a novel mutation that causes growth retardation and cranial abnormalities and which shows the inheritance pattern of an imprinted gene, as originally predicted by Hall (Am J Hum Genet 46: 857, 1990). It is anticipated that the mutation will represent a deletion and will lie within one of the recognised imprinting regions.

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50

Vu, T. H. "Comparative Genomics Sheds Light on Mechanisms of Genomic Imprinting." Genome Research 10, no. 11 (November 1, 2000): 1660–63. http://dx.doi.org/10.1101/gr.166200.

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