IGF2 is parentally imprinted during human embryogenesis and in the Beckwith-Wiedemann syndrome
The phenomenon of parental imprinting involves the preferential expression of one parental allele of a subset of chromosomal genes and has so far only been documented in the mouse. We show here, by exploiting sequence polymorphisms in exon nine of the human insulin–like growth factor 2 ( IGF2 ) gene...
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| Veröffentlicht in: | Nature genetics 1993-05, Vol.4 (1), p.94-97 |
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| container_title | Nature genetics |
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| creator | Ohlsson, Rolf Nyström, Anders Pfeifer-Ohlsson, Susan Töhönen, Virpi Hedborg, Fredrik Schofield, Paul Flam, Folke Ekström, Tomas J |
| description | The phenomenon of parental imprinting involves the preferential expression of one parental allele of a subset of chromosomal genes and has so far only been documented in the mouse. We show here, by exploiting sequence polymorphisms in exon nine of the human insulin–like growth factor 2 (
IGF2
) gene, that only the paternally–inherited allele is active in embryonic and extra–embryonic cells from first trimester pregnancies. In addition, only the paternal allele is expressed in tissues from a patient who suffered from Beckwith–Wiedemann syndrome. Thus the parental imprinting of
IGF2
appears to be evolutionarily conserved from mouse to man and has implications for the generation of the Beckwith–Wiedemann syndrome. |
| doi_str_mv | 10.1038/ng0593-94 |
| format | Article |
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IGF2
) gene, that only the paternally–inherited allele is active in embryonic and extra–embryonic cells from first trimester pregnancies. In addition, only the paternal allele is expressed in tissues from a patient who suffered from Beckwith–Wiedemann syndrome. Thus the parental imprinting of
IGF2
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IGF2
) gene, that only the paternally–inherited allele is active in embryonic and extra–embryonic cells from first trimester pregnancies. In addition, only the paternal allele is expressed in tissues from a patient who suffered from Beckwith–Wiedemann syndrome. Thus the parental imprinting of
IGF2
appears to be evolutionarily conserved from mouse to man and has implications for the generation of the Beckwith–Wiedemann syndrome.</description><subject>Agriculture</subject><subject>Alleles</subject><subject>Animal Genetics and Genomics</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Beckwith-Wiedemann Syndrome - genetics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Embryonic and Fetal Development - genetics</subject><subject>Gene Expression Regulation</subject><subject>Gene Function</subject><subject>Human Genetics</subject><subject>Insulin-Like Growth Factor II - genetics</subject><subject>Mice - genetics</subject><subject>Molecular Sequence Data</subject><subject>Parents</subject><subject>Polymerase Chain Reaction</subject><subject>Sequence Alignment</subject><subject>Sequence Homology, Nucleic Acid</subject><issn>1061-4036</issn><issn>1546-1718</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkcFLwzAUxoMoU6cH_wAxJ0GhmjRpkx11uDkYeFG8WdLktets05m0yP57Mzp28l3ee7wfH3zfQ-iKkgdKmHy0JUkmLJrwI3RGE55GVFB5HGaS0ogTlp6ic-_XhFDOiRyhkUwoC3WGvhbzWYwrjzfKge1UXW9x1WxcZTsw2PRhKPGqb5TF0ORu25ZgwQdeWYMri7sV4GfQ379Vt4o-KzAQUIv91hrXNnCBTgpVe7jc9zH6mL28T1-j5dt8MX1aRpqxSRdJCVJrmdIcSCxSKAQVItbGcMUTlcdFWuQGWKIY40zmCS3CrtOkyLnJC03YGN0OuhvX_vTgu6ypvIa6Vhba3mciETIVggbwbgC1a713UGTBa6PcNqMk22WZDVlmEx7Y671onzdgDuQ-vHC_H-5-l1cJLlu3vbPB579iNwNsVdc7OIgdXsf-AHtciT0</recordid><startdate>19930501</startdate><enddate>19930501</enddate><creator>Ohlsson, Rolf</creator><creator>Nyström, Anders</creator><creator>Pfeifer-Ohlsson, Susan</creator><creator>Töhönen, Virpi</creator><creator>Hedborg, Fredrik</creator><creator>Schofield, Paul</creator><creator>Flam, Folke</creator><creator>Ekström, Tomas J</creator><general>Nature Publishing Group US</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19930501</creationdate><title>IGF2 is parentally imprinted during human embryogenesis and in the Beckwith-Wiedemann syndrome</title><author>Ohlsson, Rolf ; Nyström, Anders ; Pfeifer-Ohlsson, Susan ; Töhönen, Virpi ; Hedborg, Fredrik ; Schofield, Paul ; Flam, Folke ; Ekström, Tomas J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c339t-88e8cc861be0276ef71772cdd4a45ab2f6fbde35a33438b51ffbdc65fb4dbfc03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Agriculture</topic><topic>Alleles</topic><topic>Animal Genetics and Genomics</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Beckwith-Wiedemann Syndrome - genetics</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Embryonic and Fetal Development - genetics</topic><topic>Gene Expression Regulation</topic><topic>Gene Function</topic><topic>Human Genetics</topic><topic>Insulin-Like Growth Factor II - genetics</topic><topic>Mice - genetics</topic><topic>Molecular Sequence Data</topic><topic>Parents</topic><topic>Polymerase Chain Reaction</topic><topic>Sequence Alignment</topic><topic>Sequence Homology, Nucleic Acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ohlsson, Rolf</creatorcontrib><creatorcontrib>Nyström, Anders</creatorcontrib><creatorcontrib>Pfeifer-Ohlsson, Susan</creatorcontrib><creatorcontrib>Töhönen, Virpi</creatorcontrib><creatorcontrib>Hedborg, Fredrik</creatorcontrib><creatorcontrib>Schofield, Paul</creatorcontrib><creatorcontrib>Flam, Folke</creatorcontrib><creatorcontrib>Ekström, Tomas J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Nature genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ohlsson, Rolf</au><au>Nyström, Anders</au><au>Pfeifer-Ohlsson, Susan</au><au>Töhönen, Virpi</au><au>Hedborg, Fredrik</au><au>Schofield, Paul</au><au>Flam, Folke</au><au>Ekström, Tomas J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IGF2 is parentally imprinted during human embryogenesis and in the Beckwith-Wiedemann syndrome</atitle><jtitle>Nature genetics</jtitle><stitle>Nat Genet</stitle><addtitle>Nat Genet</addtitle><date>1993-05-01</date><risdate>1993</risdate><volume>4</volume><issue>1</issue><spage>94</spage><epage>97</epage><pages>94-97</pages><issn>1061-4036</issn><eissn>1546-1718</eissn><abstract>The phenomenon of parental imprinting involves the preferential expression of one parental allele of a subset of chromosomal genes and has so far only been documented in the mouse. We show here, by exploiting sequence polymorphisms in exon nine of the human insulin–like growth factor 2 (
IGF2
) gene, that only the paternally–inherited allele is active in embryonic and extra–embryonic cells from first trimester pregnancies. In addition, only the paternal allele is expressed in tissues from a patient who suffered from Beckwith–Wiedemann syndrome. Thus the parental imprinting of
IGF2
appears to be evolutionarily conserved from mouse to man and has implications for the generation of the Beckwith–Wiedemann syndrome.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>8513333</pmid><doi>10.1038/ng0593-94</doi><tpages>4</tpages></addata></record> |
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| ispartof | Nature genetics, 1993-05, Vol.4 (1), p.94-97 |
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| source | MEDLINE; Nature; SpringerNature Journals |
| subjects | Agriculture Alleles Animal Genetics and Genomics Animals Base Sequence Beckwith-Wiedemann Syndrome - genetics Biomedical and Life Sciences Biomedicine Cancer Research Embryonic and Fetal Development - genetics Gene Expression Regulation Gene Function Human Genetics Insulin-Like Growth Factor II - genetics Mice - genetics Molecular Sequence Data Parents Polymerase Chain Reaction Sequence Alignment Sequence Homology, Nucleic Acid |
| title | IGF2 is parentally imprinted during human embryogenesis and in the Beckwith-Wiedemann syndrome |
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