期刊
DEVELOPMENTAL CELL
卷 8, 期 1, 页码 31-42出版社
CELL PRESS
DOI: 10.1016/j.devcel.2004.10.018
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资金
- NCI NIH HHS [CA68360] Funding Source: Medline
- NIA NIH HHS [AG00057] Funding Source: Medline
- NICHD NIH HHS [HD01177] Funding Source: Medline
- NIGMS NIH HHS [GM46883, GM61948] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA068360] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM046883, R01GM061948] Funding Source: NIH RePORTER
Escape from X inactivation results in expression of genes embedded within inactive chromatin, suggesting the existence of boundary elements between domains. We report that the 5'end of Jarid1c, a mouse escape gene adjacent to an inactivated gene, binds CTCF, displays high levels of histone H3 acetylation, and functions as a CTCF-dependent chromatin insulator. CpG island methylation at Jarid1c was very low during development and virtually absent at the CTCF sites, signifying that CTCF may influence DNA methylation and chromatin modifications. CTCF binding sites were also present at the 5' end of two other escape genes, mouse Eif2s3x and human EIF2S3, each adjacent to an inactivated gene, but not at genes embedded within large escape domains. Thus, CTCF was specifically bound to transition regions, suggesting a role in maintaining both X inactivation and escape domains. Furthermore, the evolution of X chromosome domains appears to be associated with repositioning of chromatin boundary elements.
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