Chromatin "prepattern" and histone modifiers in a fate choice for liver and pancreas

Cheng Ran Xu; Philip A. Cole; David J. Meyers; Jay Kormish; Sharon Dent; Kenneth S. Zaret

doi:10.1126/science.1202845

Chromatin "prepattern" and histone modifiers in a fate choice for liver and pancreas

Cheng Ran Xu, Philip A. Cole, David J. Meyers, Jay Kormish, Sharon Dent, Kenneth S. Zaret

Epigenetics & Molecular Carcinogenesis

Research output: Contribution to journal › Article › peer-review

165 Scopus citations

Abstract

Transcriptionally silent genes can be marked by histone modifications and regulatory proteins that indicate the genes' potential to be activated. Such marks have been identified in pluripotent cells, but it is unknown how such marks occur in descendant, multipotent embryonic cells that have restricted cell fate choices. We isolated mouse embryonic endoderm cells and assessed histone modifications at regulatory elements of silent genes that are activated upon liver or pancreas fate choices. We found that the liver and pancreas elements have distinct chromatin patterns. Furthermore, the histone acetyltransferase P300, recruited via bone morphogenetic protein signaling, and the histone methyltransferase Ezh2 have modulatory roles in the fate choice. These studies reveal a functional "prepattern" of chromatin states within multipotent progenitors and potential targets to modulate cell fate induction.

Original language	English (US)
Pages (from-to)	963-966
Number of pages	4
Journal	Science
Volume	332
Issue number	6032
DOIs	https://doi.org/10.1126/science.1202845
State	Published - May 20 2011

ASJC Scopus subject areas

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MD Anderson CCSG core facilities

Genetically Engineered Mouse Facility

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10.1126/science.1202845

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abstract = "Transcriptionally silent genes can be marked by histone modifications and regulatory proteins that indicate the genes' potential to be activated. Such marks have been identified in pluripotent cells, but it is unknown how such marks occur in descendant, multipotent embryonic cells that have restricted cell fate choices. We isolated mouse embryonic endoderm cells and assessed histone modifications at regulatory elements of silent genes that are activated upon liver or pancreas fate choices. We found that the liver and pancreas elements have distinct chromatin patterns. Furthermore, the histone acetyltransferase P300, recruited via bone morphogenetic protein signaling, and the histone methyltransferase Ezh2 have modulatory roles in the fate choice. These studies reveal a functional {"}prepattern{"} of chromatin states within multipotent progenitors and potential targets to modulate cell fate induction.",

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AU - Xu, Cheng Ran

AU - Cole, Philip A.

AU - Meyers, David J.

AU - Kormish, Jay

AU - Dent, Sharon

AU - Zaret, Kenneth S.

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AB - Transcriptionally silent genes can be marked by histone modifications and regulatory proteins that indicate the genes' potential to be activated. Such marks have been identified in pluripotent cells, but it is unknown how such marks occur in descendant, multipotent embryonic cells that have restricted cell fate choices. We isolated mouse embryonic endoderm cells and assessed histone modifications at regulatory elements of silent genes that are activated upon liver or pancreas fate choices. We found that the liver and pancreas elements have distinct chromatin patterns. Furthermore, the histone acetyltransferase P300, recruited via bone morphogenetic protein signaling, and the histone methyltransferase Ezh2 have modulatory roles in the fate choice. These studies reveal a functional "prepattern" of chromatin states within multipotent progenitors and potential targets to modulate cell fate induction.

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Chromatin "prepattern" and histone modifiers in a fate choice for liver and pancreas

Abstract

ASJC Scopus subject areas

MD Anderson CCSG core facilities

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