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We began analyzing https://www.nature.com/articles/366362a0, but it redirected us to https://www.nature.com/articles/366362a0. The analysis below is for the second page.

Title[redir]:
Role for DNA methylation in genomic imprinting | Nature
Description:
THE paternal and maternal genomes are not equivalent and both are required for mammalian development1,2. The difference between the parental genomes is believed to be due to gamete-specific differential modification, a process known as genomic imprinting. The study of transgene methylation has shown that methylation patterns can be inherited in a parent-of-origin-specific manner3–7, suggesting that DNA methylation may play a role in genomic imprinting. The functional significance of DNA methylation in genomic imprinting was strengthened by the recent finding that CpG islands (or sites) in three imprinted genes, H19, insulin-like growth factor 2 (Igf-2), and lgf-2 receptor (Igf-2r), are differentially methylated depending on their parental origin8–12. We have examined the expression of these three imprinted genes in mutant mice that are deficient in DNA methyltransferase activity13. We report here that expression of all three genes was affected in mutant embryos: the normally silent paternal allele of the HI9 gene was activated, whereas the normally active paternal allele of the Igf-2 gene and the active maternal allele of theIgf-2r gene were repressed. Our results demonstrate that a normal level of DNA methylation is required for controlling differential expression of the paternal and maternal alleles of imprinted genes.

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article, nature, google, scholar, cas, dna, methylation, access, ads, cell, content, imprinting, cookies, genomic, genes, privacy, role, research, data, jaenisch, paternal, development, massachusetts, advertising, information, subscribe, beard, maternal, imprinted, expression, allele, gene, institution, buy, open, surani, sasaki, author, permissions, function, optional, media, personal, parties, policy, journals, log, journal, december, caroline,

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nature portfolio permissions reprints massachusetts general hospital-east privacy policy cardiovascular research center biomedical research advertising social media gamete-specific differential modification subscribe nature nature 308 nature 328 nature 329 nature 362 nature 351 nature 349 nature 321 nature 366 nature placental development personal data dna methylation-mediated na+/ springerlink instant access data protection permissions development 111 origin-specific manner3–7 article li active maternal allele privacy silent paternal allele active paternal allele explore content subscription content european economic area differentially methylated depending institutional subscriptions read nucleic acids res diverse human tissues targeted systematic evolution accepting optional cookies dna methyltransferase activity13 controlling differential expression journals search log issue learn dna methylation signatures manage preferences theigf-2r gene article purchase content

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         description:THE paternal and maternal genomes are not equivalent and both are required for mammalian development1,2. The difference between the parental genomes is believed to be due to gamete-specific differential modification, a process known as genomic imprinting. The study of transgene methylation has shown that methylation patterns can be inherited in a parent-of-origin-specific manner3â7, suggesting that DNA methylation may play a role in genomic imprinting. The functional significance of DNA methylation in genomic imprinting was strengthened by the recent finding that CpG islands (or sites) in three imprinted genes, H19, insulin-like growth factor 2 (Igf-2), and lgf-2 receptor (Igf-2r), are differentially methylated depending on their parental origin8â12. We have examined the expression of these three imprinted genes in mutant mice that are deficient in DNA methyltransferase activity13. We report here that expression of all three genes was affected in mutant embryos: the normally silent paternal allele of the HI9 gene was activated, whereas the normally active paternal allele of the Igf-2 gene and the active maternal allele of theIgf-2r gene were repressed. Our results demonstrate that a normal level of DNA methylation is required for controlling differential expression of the paternal and maternal alleles of imprinted genes.
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