EZ Switch From EZH2 to EZH1

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EZ Switch From EZH2 to EZH1

An important area of research is the functional significance of posttranslational modifications of histone proteins. The modification of histones is maintained by a balance of enzymes which place specific modifications (writers), factors which read modifications (readers), and enzymes which remove modifications (erasers). Histone methylation is regulated by histone methyltransferases (writers) ...

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Developmental control of polycomb subunit composition by GATA factors mediates a switch to non-canonical functions.

Polycomb repressive complex 2 (PRC2) plays crucial roles in transcriptional regulation and stem cell development. However, the context-specific functions associated with alternative subunits remain largely unexplored. Here we show that the related enzymatic subunits EZH1 and EZH2 undergo an expression switch during blood cell development. An erythroid-specific enhancer mediates transcriptional ...

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Polycomb subunits Ezh1 and Ezh2 regulate the Merkel cell differentiation program in skin stem cells.

While the Polycomb complex is known to regulate cell identity in ES cells, its role in controlling tissue-specific stem cells is not well understood. Here we show that removal of Ezh1 and Ezh2, key Polycomb subunits, from mouse skin results in a marked change in fate determination in epidermal progenitor cells, leading to an increase in the number of lineage-committed Merkel cells, a specialize...

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EZH1 and EZH2 promote skeletal growth by repressing inhibitors of chondrocyte proliferation and hypertrophy

Histone methyltransferases EZH1 and EZH2 catalyse the trimethylation of histone H3 at lysine 27 (H3K27), which serves as an epigenetic signal for chromatin condensation and transcriptional repression. Genome-wide associated studies have implicated EZH2 in the control of height and mutations in EZH2 cause Weaver syndrome, which includes skeletal overgrowth. Here we show that the combined loss of...

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ژورنال

عنوان ژورنال: Circulation Research

سال: 2017

ISSN: 0009-7330,1524-4571

DOI: 10.1161/circresaha.117.311351