Molecular evidence for a relationship between LINE-1 elements and X chromosome inactivation: The Lyon repeat hypothesis

Jeffrey A. Bailey, Laura Carrel, Aravinda Chakravarti, Evan E. Eichler

Research output: Contribution to journalArticle

Abstract

X inactivation is a chromosome-specific form of genetic regulation in which thousands of genes on one homologue become silenced early in female embryogenesis. Although many aspects of X inactivation are now understood, the spread of the X inactivation signal along the entire length of the chromosome remains enigmatic. Extending the Gartler-Riggs model [Gartler, S. M. and Riggs, A.D. (1983) Annu. Rev. Genet. 17, 155-190], Lyon recently proposed [Lyon, M. F. (1998) Cytogenet. Cell Genet. 80, 133-137] that a nonrandom organization of long interspersed element (LINE) repetitive sequences on the X chromosome might be responsible for its facultative heterochromatization. In this paper, we present data indicating that the LINE-1 (L1) composition of the human X chromosome is fundamentally distinct from that of human autosomes. The X chromosome is enriched 2-fold for L1 repetitive elements, with the greatest enrichment observed for a restricted subset of LINE-1 elements that were active

Original languageEnglish (US)
Pages (from-to)6634-6639
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume97
Issue number12
DOIs
StatePublished - Jun 6 2000
Externally publishedYes

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X Chromosome Inactivation
Viverridae
X Chromosome
Long Interspersed Nucleotide Elements
Chromosomes
Chromosomes, Human, X
Interspersed Repetitive Sequences
Embryonic Development
Genes

ASJC Scopus subject areas

  • Genetics
  • General

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Molecular evidence for a relationship between LINE-1 elements and X chromosome inactivation : The Lyon repeat hypothesis. / Bailey, Jeffrey A.; Carrel, Laura; Chakravarti, Aravinda; Eichler, Evan E.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 97, No. 12, 06.06.2000, p. 6634-6639.

Research output: Contribution to journalArticle

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