scholarly journals The central role of EED in the orchestration of polycomb group complexes

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Qi Cao ◽  
Xiaoju Wang ◽  
Meng Zhao ◽  
Rendong Yang ◽  
Rohit Malik ◽  
...  
Keyword(s):  
Polycomb Group ◽  
Polycomb Group Complexes

Abstract LB-132: The central role of EED in orchestration of polycomb group complexes

2014 ◽  
Author(s):  
Qi Cao ◽  
Xiaoju Wang ◽  
Meng Zhao ◽  
Rendong Yang ◽  
Rohit Malik ◽  
...  
Keyword(s):  
Polycomb Group ◽  
Polycomb Group Complexes

scholarly journals The role of Polycomb-group response elements in regulation of engrailed transcription in Drosophila

Development ◽  
2008 ◽  
Vol 135 (4) ◽  
pp. 669-676 ◽  
Author(s):  
S. K. DeVido ◽  
D. Kwon ◽  
J. L. Brown ◽  
J. A. Kassis
Keyword(s):  
Polycomb Group ◽  
Response Elements ◽  
Group Response

scholarly journals The Polycomb group protein MEDEA controls cell proliferation and embryonic patterning in Arabidopsis

2020 ◽  
Author(s):  
Sara Simonini ◽  
Marian Bemer ◽  
Stefano Bencivenga ◽  
Valeria Gagliardini ◽  
Nuno D. Pires ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lineage ◽  
Embryonic Cell ◽  
The Body ◽  
Polycomb Group ◽  
Normal Embryo ◽  
Embryonic Patterning ◽  
Polycomb Group Protein ◽  
Group Protein

Establishing the body plan of a multicellular organism relies on precisely orchestrated cell divisions coupled with pattern formation. In animals, cell proliferation and embryonic patterning are regulated by Polycomb group (PcG) proteins that form various multisubunit complexes (Grossniklaus and Paro, 2014). The evolutionary conserved Polycomb Repressive Complex 2 (PRC2) trimethylates histone H3 at lysine 27 (H3K27me3) and comes in different flavors in the model plant Arabidopsis thaliana (Förderer et al., 2016; Grossniklaus and Paro, 2014). The histone methyltransferase MEDEA (MEA) is part of the FERTILIZATION INDEPENDENT SEED (FIS)-PRC2 required for seed development4. Although embryos derived from mea mutant egg cells show morphological abnormalities (Grossniklaus et al., 1998), defects in the development of the placenta-like endosperm are considered the main cause of seed abortion (Kinoshita et al., 1999; Scott et al., 1998), and a role of FIS-PRC2 in embryonic patterning was dismissed (Bouyer et al., 2011; Leroy et al., 2007). Here, we demonstrate that endosperm lacking MEA activity sustains normal embryo development and that embryos derived from mea mutant eggs abort even in presence of a wild-type endosperm because MEA is required for embryonic patterning and cell lineage determination. We show that, similar to PcG proteins in mammals, MEA regulates embryonic growth by repressing the transcription of core cell cycle components. Our work demonstrates that Arabidopsis embryogenesis is under epigenetic control of maternally expressed PcG proteins, revealing that PRC2 was independently recruited to control embryonic cell proliferation and patterning in animals and plants.

scholarly journals Structure and function of an ectopic Polycomb chromatin domain

2019 ◽  
Vol 5 (1) ◽  
pp. eaau9739 ◽  
Author(s):  
Sandip De ◽  
Yuzhong Cheng ◽  
Ming-an Sun ◽  
Natalie D. Gehred ◽  
Judith A. Kassis
Keyword(s):  
Domain Structure ◽  
Regulatory Elements ◽  
Structure And Function ◽  
Polycomb Group ◽  
Chromatin Domain ◽  
Repressive Mark ◽  
Group Response ◽  
Dna Elements ◽  
And Function

Polycomb group proteins (PcGs) drive target gene repression and form large chromatin domains. InDrosophila, DNA elements known as Polycomb group response elements (PREs) recruit PcGs to the DNA. We have shown that, within theinvected-engrailed(inv-en) Polycomb domain, strong, constitutive PREs are dispensable for Polycomb domain structure and function. We suggest that the endogenous chromosomal location imparts stability to this Polycomb domain. To test this possibility, a 79-kbentransgene was inserted into other chromosomal locations. This transgene is functional and forms a Polycomb domain. The spreading of the H3K27me3 repressive mark, characteristic of PcG domains, varies depending on the chromatin context of the transgene. Unlike at the endogenous locus, deletion of the strong, constitutive PREs from the transgene leads to both loss- and gain-of function phenotypes, demonstrating the important role of these regulatory elements. Our data show that chromatin context plays an important role in Polycomb domain structure and function.

A transgenic mouse model demonstrating the oncogenic role of mutations in the polycomb-group gene EZH2 in lymphomagenesis

Blood ◽  
2014 ◽  
Vol 123 (25) ◽  
pp. 3914-3924 ◽  
Author(s):  
Tobias Berg ◽  
Silvia Thoene ◽  
Damian Yap ◽  
Tracee Wee ◽  
Nathalie Schoeler ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Polycomb Group ◽  
Key Points ◽  
Polycomb Group Gene

Key Points A functional demonstration of the oncogenic role of mutated EZH2 in a mouse model is presented. The global effects of mutated EZH2 on expression and epigenome have been characterized.

scholarly journals Epigenetic regulation by polycomb group complexes: focus on roles of CBX proteins

2014 ◽  
Vol 15 (5) ◽  
pp. 412-428 ◽  
Author(s):  
Rong-gang Ma ◽  
Yang Zhang ◽  
Ting-ting Sun ◽  
Bo Cheng
Keyword(s):  
Epigenetic Regulation ◽  
Polycomb Group ◽  
Polycomb Group Complexes

Polycomb Group Member Rybp Is a Functional Tumor Suppressor Repressed By Mir-9 in MLL-Rearranged AML

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 871-871
Author(s):  
Colles Price ◽  
Ping Chen ◽  
Shenglai Li ◽  
Zejuan Li ◽  
Yuanyuan Li ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cancer Biology ◽  
Chromosomal Rearrangements ◽  
Polycomb Group ◽  
Aberrant Expression ◽  
Molecular Abnormalities ◽  
Group Member

Abstract MicroRNAs (miRNAs), are small non-coding RNA molecules known to be important regulators of cancer biology. Notably, we and others have shown that miRNAs play important roles in Acute Myeloid Leukemia (AML), a heterogeneous malignancies with multiple chromosomal and molecular abnormalities. Patients with chromosomal rearrangements involving mixed lineage leukemia (MLL), the mammalian homology of trithorax gene, are associated with poor survival. Previously, we have found that MLL-rearranged AML drives aberrant expression of several miRNAs, most notably microRNA-9 (miR-9). Expression of miR-9 with MLL-AF9, a common MLL-translocation, was sufficient to promote transformation normal hematopoietic progenitor cells in vitro and leukemogenesis in vivo. We previously found that miR-9 reduces expression of several genes but we did not know which genes were critical tumor suppressors. We found that the polycomb group member RING1- and YY1-Bindin Protein (RYBP) was consistently inhibited upon miR-9 expression. To assess the regulation of RYBP we used publically available data from the Cancer Genome Atlas (TCGA) and looked at genome-wide Illumina 450K methylation data. We did not find a strong correlation with methylation and RYBP expression, suggesting that expression of RYBP is likely not regulated by the DNA methylation machinery in patients. Upon looking at copy number alterations we found that a small population of AML patients contained either homozygous or heterozygous loss of RYBP, suggesting a potential role of RYBP in leukemia pathogenesis. To assess the role of RYBP we did a series of in vitro experiments. We found that expression of RYBP was sufficient to attenuate colony-forming growth driven by MLL- AF9. Furthermore, RYBP expression was able to reduce proliferation, increase apoptosis, and significantly reduce immature cell population. To determine the role of RYBP expression in vivo, we transplanted lethally irradiated mice with progenitors retrovirally transduced with MLL-AF9 compared to MLL-AF9 and RYBP. We found that expression of RYBP was sufficient to reduce leukemia burden in vivo as well as induce differentiation as shown by flow cytometry and histological analysis. Thus, this demonstrates that RYBP is a functional tumor suppressor in MLL-rearranged AML. In conclusion, we have demonstrated that chromosomal rearrangements involving MLL, the mammalian homology of trithorax, downregulates a member of the polycomb complex through upregulation of miR-9. Disclosures No relevant conflicts of interest to declare.

scholarly journals A Drosophila ESC-E(Z) Protein Complex Is Distinct from Other Polycomb Group Complexes and Contains Covalently Modified ESC

2000 ◽  
Vol 20 (9) ◽  
pp. 3069-3078 ◽  
Author(s):  
Joyce Ng ◽  
Craig M. Hart ◽  
Kelly Morgan ◽  
Jeffrey A. Simon
Keyword(s):  
Germ Line ◽  
Gel Filtration ◽  
Developmental Time ◽  
Polycomb Group ◽  
Sex Combs ◽  
Sex Comb ◽  
Z Protein ◽  
Polycomb Group Complexes

ABSTRACT The extra sex combs (ESC) and Enhancer of zeste [E(Z)] proteins, members of the Polycomb group (PcG) of transcriptional repressors, interact directly and are coassociated in fly embryos. We report that these two proteins are components of a 600-kDa complex in embryos. Using gel filtration and affinity chromatography, we show that this complex is biochemically distinct from previously described complexes containing the PcG proteins Polyhomeotic, Polycomb, and Sex comb on midleg. In addition, we present evidence that ESC is phosphorylated in vivo and that this modified ESC is preferentially associated in the complex with E(Z). Modified ESC accumulates between 2 and 6 h of embryogenesis, which is the developmental time whenesc function is first required. We find that mutations inE(z) reduce the ratio of modified to unmodified ESC in vivo. We have also generated germ line transformants that express ESC proteins bearing site-directed mutations that disrupt ESC-E(Z) binding in vitro. These mutant ESC proteins fail to provideesc function, show reduced levels of modification in vivo, and are still assembled into complexes. Taken together, these results suggest that ESC phosphorylation normally occurs after assembly into ESC-E(Z) complexes and that it contributes to the function or regulation of these complexes. We discuss how biochemically separable ESC-E(Z) and PC-PH complexes might work together to provide PcG repression.

Sign in / Sign up

Export Citation Format

Share Document