Embryonic stem cell self-renewal and differentiation balance maintenance mechanism
Scientists at Harvard Medical School, Boston Children ’s Hospital Dana-Farber Cancer Institute, Howard Hughes Medical Institute, Massachusetts General Hospital and the University of Wisconsin School of Medicine and Public Health have made the latest progress in stem cell research Polycomb Activity and Self-Renewal versus Differentiation of Stem Cells was published in the latest issue of Cell Magazine.
The corresponding author of the article is Professor Stuart H. Orkin of Harvard Medical School, Howard Hughes Medical College, and academician of the American Academy of Sciences. He is mainly engaged in the research of stem cells, especially stem cells in the hematopoietic system, and the relationship between cancer and stem cells.
Histone H3 lysine 27 (histone H3 lysine 27, H3K27me3) methylation must be completed under the action of PRC2 inhibitory complex. H3K27me3 plays an important role in regulating the self-renewal and differentiation of embryonic stem cells.
Polycomb group (PcG) protein is a group of transcriptional repressors that regulate target genes through chromatin modification, and it can be divided into two major core protein complexes, PRC1 (Polycomb repressive complex 1) and PRC2 (Polycomb repressive complex), from the perspective of biochemistry and function 2). Studies have found that PcG protein not only controls the correct developmental pattern of individuals, but also is related to cell proliferation, differentiation and tumorigenesis.
However, the mechanism of action of PRC2 is not clear. In this article, the Stuart H. Orkin research team found that the members of the Jumonji family, JMJ (JUMONJI or JARID2), are related to the function of PRC2, co-localize with PRC2 and H3K27me3 on chromatin, and have the function of adjusting PRC2.
In an in vitro experiment, the Stuart H. Orkin research team found that JMJ inhibited the activity of PRC2 methylase, while enhancing the labeling of embryonic stem cells H3K27me3 at the target site of PRC2. JMJ plays an important role in regulating the function of PRC2.
These research results show that JMJ dynamically regulates the function of PRC2 to maintain the balance between self-renewal and differentiation of embryonic stem cells. Once JMJ is abnormal, the balance between embryonic stem cells' self-renewal and differentiation may be broken, affecting the embryonic stem cell's Maintenance of normal function. (Bioon.com)
Bio Valley recommends the original source:
Cell, 24 December 2009 doi: 10.1016 / j.cell.2009.12.003
Jumonji Modulates Polycomb Activity and Self-Renewal versus Differentiation of Stem Cells
Xiaohua Shen1, Woojin Kim1, Yuko Fujiwara1, Matthew D. Simon5, Yingchun Liu4, Matthew R. Mysliwiec6, Guo-Cheng Yuan4, Youngsook Lee6 and Stuart H. Orkin1, 2, 3,,
1 Department of Pediatric Oncology, Dana-Farber Cancer Institute, Childrens Hospital, and Harvard Medical School, Boston, MA 02115, USA
2 Howard Hughes Medical Institute, Boston, MA 02115, USA
3 Harvard Stem Cell Institute, Boston, MA 02115, USA
4 Department of Biostatistics & Computational Biology, Dana-Farber Cancer Institute, and Harvard School of Public Health, Boston, MA 02115, USA
5 Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA
6 Department of Anatomy, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53706, USA
Trimethylation on histone H3 lysine 27 (H3K27me3) by Polycomb repressive complex 2 (PRC2) regulates the balance between self-renewal and differentiation of embryonic stem cells (ESCs). The mechanisms controlling the activity and recruitment of PRC2 are largely unknown. Here we demonstrate that the founding member of the Jumonji family, JMJ (JUMONJI or JARID2), is associated with PRC2, colocalizes with PRC2 and H3K27me3 on chromatin, and modulates PRC2 function. In vitro JMJ inhibits PRC2 methyltransferase activity, consistent with increased H3K27me3 marks at PRC2 targets in Jmj-/-ESCs. Paradoxically, JMJ is required for efficient binding of PRC2, indicating that the interplay of PRC2 and JMJ fine-tunes deposition of the H3K27me3 mark. During differentiation, activation of genes marked by H3K27me3 and lineage commitments are delayed in Jmj-/-ESCs. Our results demonstrate that dynamic regulation of Polycomb complex activity orchestrated by JMJ balances self-renewal and differentiation, highlighting the involvement of chromatin dynamics in cell-fate transitions.
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