4.8 Article

Genetic conflict reflected in tissue-specific maps of genomic imprinting in human and mouse

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NATURE GENETICS
卷 47, 期 5, 页码 544-U158

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NATURE PUBLISHING GROUP
DOI: 10.1038/ng.3274

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资金

  1. US National Institutes of Health (NIH) grant [1R01GM097171-01A1]
  2. US NIH grant [U01HG007593]
  3. Hewlett-Packard Stanford Graduate Fellowship
  4. US National Science Foundation grant [OCI-1053575]
  5. Common Fund of the Office of the Director of the US NIH
  6. National Cancer Institute
  7. National Human Genome Research Institute
  8. National Heart, Lung, and Blood Institute
  9. National Institute of Mental Health
  10. National Cancer Institute/SAIC-Frederick, Inc. [10XS170]
  11. Roswell Park Cancer Institute [10XS171]
  12. Science Care, Inc. [X10S172]
  13. Laboratory, Data Analysis and Coordinating Center (LDACC) [HHSN268201000029C]
  14. SAIC-Frederick [10ST1035, HHSN261200800001E]
  15. University of Miami grant [DA006227]
  16. University of Chicago [MH090951, MH090937]
  17. University of North Carolina, Chapel Hill [MH090936]
  18. Harvard University [MH090948]
  19. National Institute on Drug Abuse
  20. National Institute Neurological Disorders and Stroke
  21. [MH090941]

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Genomic imprinting is an epigenetic process that restricts gene expression to either the maternally or paternally inherited allele(1,2). Many theories have been proposed to explain its evolutionary origin(3,4), but understanding has been limited by a paucity of data mapping the breadth and dynamics of imprinting within any organism. We generated an atlas of imprinting spanning 33 mouse and 45 human developmental stages and tissues. Nearly all imprinted genes were imprinted in early development and either retained their parent-of-origin expression in adults or lost it completely. Consistent with an evolutionary signature of parental conflict, imprinted genes were enriched for coexpressed pairs of maternally and paternally expressed genes, showed accelerated expression divergence between human and mouse, and were more highly expressed than their non-imprinted orthologs in other species. Our approach demonstrates a general framework for the discovery of imprinting in any species and sheds light on the causes and consequences of genomic imprinting in mammals.

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