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Renato Paro - One of the best experts on this subject based on the ideXlab platform.
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Polycomb purification by in vivo biotinylation tagging reveals cohesin and Trithorax group Proteins as interaction partners
Proceedings of the National Academy of Sciences of the United States of America, 2011Co-Authors: Gero Strübbe, Christian Beisel, Leonie Ringrose, Christian Popp, Alexander Schmidt, Andrea Pauli, Renato ParoAbstract:The maintenance of specific gene expression patterns during cellular proliferation is crucial for the identity of every cell type and the development of tissues in multicellular organisms. Such a cellular memory function is conveyed by the complex interplay of the Polycomb and Trithorax groups of Proteins (PcG/TrxG). These Proteins exert their function at the level of chromatin by establishing and maintaining repressed (PcG) and active (TrxG) chromatin domains. Past studies indicated that a core PcG protein complex is potentially associated with cell type or even cell stage-specific sets of accessory Proteins. In order to better understand the dynamic aspects underlying PcG composition and function we have established an inducible version of the biotinylation tagging approach to purify Polycomb and associated factors from Drosophila embryos. This system enabled fast and efficient isolation of Polycomb containing complexes under near physiological conditions, thereby preserving substoichiometric interactions. Novel interacting Proteins were identified by highly sensitive mass spectrometric analysis. We found many TrxG related Proteins, suggesting a previously unrecognized extent of molecular interaction of the two counteracting chromatin regulatory protein groups. Furthermore, our analysis revealed an association of PcG protein complexes with the cohesin complex and showed that Polycomb-dependent silencing of a transgenic reporter depends on cohesin function.
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Silencing chromatin: comparing modes and mechanisms
Nature Reviews Genetics, 2011Co-Authors: Christian Beisel, Renato ParoAbstract:The transcriptional activity of a gene is dependent on the local composition and organization of its chromatin environment. Chromatin-based silencing of sequence information is based on three sequential steps: a decision-making process that targets specific silencing complexes to DNA sequences to be inactivated; a chromatin-structuring process that results in efficient inhibition of RNA polymerases or other nuclear enzymes that interfere with genetic information; and the epigenetic part, the propagation of the silent chromatin through DNA replication and mitosis to the daughter cells. Heterochromatin formation and Polycomb-mediated gene repression are two major gene-silencing mechanisms responsible for the stable transmission of repressed transcription states through cell generations. Heterochromatin and the Polycomb system apply similar molecular mechanisms to gene targeting. These mechanisms include: trans -acting DNA-binding Proteins, cis -acting DNA elements, non-coding RNAs and Proteins that set and recognize specific histone marks. Different targeting pathways acting in parallel could ensure proper silencing of important genomic regions and developmental regulators. Alternatively, some pathways could act separately on specific sets of target genes, whereas others could act in a combinatorial way. The initiation of PcG silencing, as well as heterochromatin formation, seems to rely on DNA-binding Proteins, implying that the specificity is generated by underlying DNA sequences rather than by certain protein features of the chromatin environment. Histone methylation marks and cis -acting non-coding RNAs provide multiple binding sites that may increase the local concentration of heterochromatin and PcG complexes in cis . Although both types of interaction are of relatively low affinity, the multitude of binding sites may generate a local high-affinity environment that acts as a molecular cage to dynamically maintain chromatin-regulating protein complexes in place at the target genes. HOTAIR , a trans -acting long intergenic non-coding RNA that is involved in the repression of Polycomb target genes at the mammalian HOXD locus, seems to act as a scaffold, organizing the concerted action of Polycomb repressive complex 2 (PRC2) and the histone H3 lysine 4 (H3K4)-specific demethylase LSD1. Similarly, nascent chromatin-associated transcripts serve as assembly platforms for heterochromatin complexes in fission yeast. The maintenance of epigenetic signals through the process of replication may be explained by self-reinforcing loops that propagate histone-methylation patterns to the two daughter strands. On the other hand, the reactivation of the RNAi machinery at centromeric repeats in early S phase resembles the re-establishment of heterochromatin and its propagation through the replication process in fission yeast, offering an attractive alternative model. PcG-mediated repression may be the default state, whereas Trithorax group Proteins such as mammalian mixed lineage leukaemia 1 (MLL1) may act as anti-silencing factors that bookmark genes during mitosis in order to render them rapidly activatable on mitotic exit. Recent transcriptome analyses show that substantial proportions of eukaryotic genomes can be copied into RNAs, many of which do not encode protein sequences. However, cells have developed mechanisms to control and counteract the high transcriptional activity of RNA polymerases in order to achieve cell-specific gene activity or to prevent the expression of deleterious sequences. Here we compare how two silencing modes — the Polycomb system and heterochromatin — are targeted, established and maintained at different chromosomal locations and how DNA-binding Proteins and non-coding RNAs connect these epigenetically stable and heritable structures to the sequence information of the DNA. How are specific genomic regions targeted for transcriptional silencing and how is stable silencing maintained? The Polycomb and heterochromatin silencing systems have distinct roles and yet share some interesting features, such as the involvement of non-coding RNAs, histone modifications and dynamic protein complexes.
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About Combs, Notches, and Tumors: Epigenetics Meets Signaling
Developmental cell, 2009Co-Authors: Gunter Merdes, Renato ParoAbstract:The identities of cells, determined by differential gene expression, are heritably maintained by the antagonistic functions of Polycomb group (PcG) and Trithorax group Proteins. Two recent papers shed new light on tumor suppressive functions of PcG by reporting direct silencing of the Notch and JAK/STAT signaling pathways in Drosophila melanogaster.
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Comparing active and repressed expression states of genes controlled by the Polycomb/Trithorax group Proteins
Proceedings of the National Academy of Sciences of the United States of America, 2007Co-Authors: Christian Beisel, Andreas Buness, Ian M. Roustan-espinosa, B. Koch, Sabine Schmitt, Stefan A. Haas, Marc Hild, Tomonori Katsuyama, Renato ParoAbstract:Drosophila Polycomb group (PcG) and Trithorax group (TrxG) Proteins are responsible for the maintenance of stable transcription patterns of many developmental regulators, such as the homeotic genes. We have used ChIP-on-chip to compare the distribution of several PcG/TrxG Proteins, as well as histone modifications in active and repressed genes across the two homeotic complexes ANT-C and BX-C. Our data indicate the colocalization of the Polycomb repressive complex 1 (PRC1) with Trx and the DNA binding protein Pleiohomeotic (Pho) at discrete sequence elements as well as significant chromatin assembly differences in active and inactive regions. Trx binds to the promoters of active genes and noncoding transcripts. Most strikingly, in the active state, Pho covers extended chromatin domains over many kilobases. This feature of Pho, observed on many polytene chromosome puffs, reflects a previously undescribed function. At the hsp70 gene, we demonstrate in mutants that Pho is required for transcriptional recovery after heat shock. Besides its presumptive function in recruiting PcG complexes to their site of action, our results now uncover that Pho plays an additional role in the repression of already induced genes.
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Epigenetic inheritance of active chromatin after removal of the main transactivator.
Science (New York N.Y.), 1999Co-Authors: Giacomo Cavalli, Renato ParoAbstract:The Drosophila Polycomb and trithorax group Proteins act through chromosomal elements such as Fab-7 to maintain repressed or active gene expression, respectively. A Fab-7 element is switched from a silenced to a mitotically heritable active state by an embryonic pulse of transcription. Here, histone H4 hyperacetylation was found to be associated with Fab-7 after activation, suggesting that H4 hyperacetylation may be a heritable epigenetic tag of the activated element. Activated Fab-7 enables transcription of a gene even after withdrawal of the primary transcription factor. This feature may allow epigenetic maintenance of active states of developmental genes after decay of their early embryonic regulators.
Leonie Ringrose - One of the best experts on this subject based on the ideXlab platform.
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A theoretical model of Polycomb/Trithorax action unites stable epigenetic memory and dynamic regulation.
Nature communications, 2020Co-Authors: Jeannette Reinig, Frank Ruge, Martin Howard, Leonie RingroseAbstract:Polycomb and Trithorax group Proteins maintain stable epigenetic memory of gene expression states for some genes, but many targets show highly dynamic regulation. Here we combine experiment and theory to examine the mechanistic basis of these different modes of regulation. We present a mathematical model comprising a Polycomb/Trithorax response element (PRE/TRE) coupled to a promoter and including Drosophila developmental timing. The model accurately recapitulates published studies of PRE/TRE mediated epigenetic memory of both silencing and activation. With minimal parameter changes, the same model can also recapitulate experimental data for a different PRE/TRE that allows dynamic regulation of its target gene. The model predicts that both cell cycle length and PRE/TRE identity are critical for determining whether the system gives stable memory or dynamic regulation. Our work provides a simple unifying framework for a rich repertoire of PRE/TRE functions, and thus provides insights into genome-wide Polycomb/Trithorax regulation.
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Theoretical analysis of Polycomb-Trithorax systems predicts that poised chromatin is bistable and not bivalent.
Nature communications, 2019Co-Authors: Kim Sneppen, Leonie RingroseAbstract:Polycomb (PcG) and Trithorax (TrxG) group Proteins give stable epigenetic memory of silent and active gene expression states, but also allow poised states in pluripotent cells. Here we systematically address the relationship between poised, active and silent chromatin, by integrating 73 publications on PcG/TrxG biochemistry into a mathematical model comprising 144 nucleosome modification states and 8 enzymatic reactions. Our model predicts that poised chromatin is bistable and not bivalent. Bivalent chromatin, containing opposing active and silent modifications, is present as an unstable background population in all system states, and different subtypes co-occur with active and silent chromatin. In contrast, bistability, in which the system switches frequently between stable active and silent states, occurs under a wide range of conditions at the transition between monostable active and silent system states. By proposing that bistability and not bivalency is associated with poised chromatin, this work has implications for understanding the molecular nature of pluripotency. Polycomb and Trithorax group Proteins regulate silent and active gene expression states, but also allow poised states in pluripotent cells. Here the authors present a mathematical model that integrates data on Polycomb/ Trithorax biochemistry into a single coherent framework which predicts that poised chromatin is not bivalent as previously proposed, but is bistable, meaning that the system switches frequently between stable active and silent states.
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“In Vivo Biochemistry”: Absolute Quantification and Kinetic Modeling Applied to Polycomb and Trithorax Regulation
Epigenetics and Systems Biology, 2017Co-Authors: Leonie RingroseAbstract:Abstract Absolute quantification of molecule numbers (How many molecules are there? Where are they?) and their kinetic properties (How long do they stay? How fast do they move?) opens the door to quantitative modeling. In this chapter, I will explore methods for measuring these absolute values in vivo and show how we have combined this with quantitative kinetic modeling to gain new mechanistic insights into how the Polycomb and Trithorax group Proteins interact with chromatin during the cell cycle in living Drosophila. This work has implications for our quantitative understanding of epigenetic memory and how it may be modulated in different contexts.
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Quantitative in vivo analysis of chromatin binding of Polycomb and Trithorax group Proteins reveals retention of ASH1 on mitotic chromatin.
Nucleic acids research, 2013Co-Authors: Philipp A. Steffen, Christian Beisel, João Pedro Fonseca, Cornelia Gänger, Eva Dworschak, Tobias Kockmann, Leonie RingroseAbstract:The Polycomb (PcG) and Trithorax (TrxG) group Proteins work antagonistically on several hundred developmentally important target genes, giving stable mitotic memory, but also allowing flexibility of gene expression states. How this is achieved in quantitative terms is poorly understood. Here, we present a quantitative kinetic analysis in living Drosophila of the PcG Proteins Enhancer of Zeste, (E(Z)), Pleiohomeotic (PHO) and Polycomb (PC) and the TrxG protein absent, small or homeotic discs 1 (ASH1). Fluorescence recovery after photobleaching and fluorescence correlation spectroscopy reveal highly dynamic chromatin binding behaviour for all Proteins, with exchange occurring within seconds. We show that although the PcG Proteins substantially dissociate from mitotic chromatin, ASH1 remains robustly associated with chromatin throughout mitosis. Finally, we show that chromatin binding by ASH1 and PC switches from an antagonistic relationship in interphase, to a cooperative one during mitosis. These results provide quantitative insights into PcG and TrxG chromatin-binding dynamics and have implications for our understanding of the molecular nature of epigenetic memory.
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Polycomb purification by in vivo biotinylation tagging reveals cohesin and Trithorax group Proteins as interaction partners
Proceedings of the National Academy of Sciences of the United States of America, 2011Co-Authors: Gero Strübbe, Christian Beisel, Leonie Ringrose, Christian Popp, Alexander Schmidt, Andrea Pauli, Renato ParoAbstract:The maintenance of specific gene expression patterns during cellular proliferation is crucial for the identity of every cell type and the development of tissues in multicellular organisms. Such a cellular memory function is conveyed by the complex interplay of the Polycomb and Trithorax groups of Proteins (PcG/TrxG). These Proteins exert their function at the level of chromatin by establishing and maintaining repressed (PcG) and active (TrxG) chromatin domains. Past studies indicated that a core PcG protein complex is potentially associated with cell type or even cell stage-specific sets of accessory Proteins. In order to better understand the dynamic aspects underlying PcG composition and function we have established an inducible version of the biotinylation tagging approach to purify Polycomb and associated factors from Drosophila embryos. This system enabled fast and efficient isolation of Polycomb containing complexes under near physiological conditions, thereby preserving substoichiometric interactions. Novel interacting Proteins were identified by highly sensitive mass spectrometric analysis. We found many TrxG related Proteins, suggesting a previously unrecognized extent of molecular interaction of the two counteracting chromatin regulatory protein groups. Furthermore, our analysis revealed an association of PcG protein complexes with the cohesin complex and showed that Polycomb-dependent silencing of a transgenic reporter depends on cohesin function.
Giacomo Cavalli - One of the best experts on this subject based on the ideXlab platform.
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Trithorax group Proteins: switching genes on and keeping them active
Nature reviews. Molecular cell biology, 2011Co-Authors: Bernd Schuettengruber, Anne-marie Martinez, Nicola Iovino, Giacomo CavalliAbstract:Cellular memory is provided by two counteracting groups of chromatin Proteins termed Trithorax group (TrxG) and Polycomb group (PcG) Proteins. TrxG Proteins activate transcription and are perhaps best known because of the involvement of the TrxG protein MLL in leukaemia. However, in terms of molecular analysis, they have lived in the shadow of their more famous counterparts, the PcG Proteins. Recent advances have improved our understanding of TrxG protein function and demonstrated that the heterogeneous group of TrxG Proteins is of critical importance in the epigenetic regulation of the cell cycle, senescence, DNA damage and stem cell biology.
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From linear genes to epigenetic inheritance of three-dimensional epigenomes.
Journal of molecular biology, 2011Co-Authors: Giacomo CavalliAbstract:Fifty years ago Jacob and Monod reported their findings on the regulation of gene activity. Working on lambda bacteriophage lysogeny and the regulation of the production of an enzyme that cleaves lactose, they observed that its production was induced by the presence of lactose in the medium and came to general conclusions about gene expression that still hold true today. Thanks to decades of intense multidisciplinary research, these conclusions have been extended by several fundamental discoveries. In particular, gene regulatory circuits include the ability to propagate the memory of a specific gene regulatory state long after being established and even when the original inducer is no longer present. Furthermore, in addition to being regulated by binding of regulators such as RNAs or Proteins in the vicinity of the site of transcription initiation, genes can be regulated by factor binding at incredible distances from their transcriptional start sites. Prominent among the regulatory components involved in these processes are Polycomb and Trithorax group Proteins, pleiotropic gene regulators of critical importance in development, physiology and disease.
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Epigenetic inheritance of chromatin states mediated by Polycomb and trithorax group Proteins in Drosophila.
Progress in molecular and subcellular biology, 2005Co-Authors: Jérôme Déjardin, Giacomo CavalliAbstract:Proteins of the Polycomb group (PcG) and of the trithorax group (trxG) are involved in the regulation of key developmental genes, such as homeotic genes. PcG Proteins maintain silent states of gene expression, while the trxG of genes counteracts silencing with a chromatin opening function. These factors form multimeric complexes that act on their target chromatin by regulating post-translational modifications of histones as well as ATPdependent remodelling of nucleosome positions. In Drosophila, PcG and trxG complexes are recruited to specific DNA elements named as PcG and trxG response elements (PREs and TREs, respectively). Once recruited, these complexes seem to be able to establish silent or open chromatin states that can be inherited through multiple cell divisions even after decay of the primary silencing or activating signal. In recent years, many components of both groups of factors have been characterized, and the molecular mechanisms underlying their recruitment as well as their mechanism of action on their target genes have been partly elucidated. This chapter summarizes our current knowledge on these aspects and outlines crucial open questions in the field.
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Chromatin inheritance upon Zeste-mediated Brahma recruitment at a minimal cellular memory module
The EMBO journal, 2004Co-Authors: Jérôme Déjardin, Giacomo CavalliAbstract:Polycomb group and trithorax group Proteins maintain the memory of repressed and active chromatin states by regulating chromatin of their target genes via DNA sequences termed Polycomb- and trithorax response elements. Since these elements often overlap and are able to convey the memory of both silent and active chromatin through cell division, they were also defined as cellular memory modules (CMMs). We identify here a minimal CMM of 219 bp from the Drosophila Fab-7 region that regulates the homeotic gene Abdominal-B. This CMM conveys the inheritance of active chromatin states induced by an embryonic pulse of transcriptional activation via recruitment of the trithorax group Proteins Trithorax (TRX) and Brahma (BRM), the Drosophila homologue of the SWI2/SNF2 ATPase involved in chromatin remodelling. Within this CMM, DNA-binding sites for the Zeste protein are necessary for the inheritance of active chromatin through Zeste-dependent recruitment of BRM, while TRX can bind the CMM even in their absence. Thus, epigenetic inheritance of active chromatin states involves the recruitment of multiple cooperative chromatin-modifying complexes at closely spaced but distinct sites within a CMM.
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Chromatin as a eukaryotic template of genetic information.
Current opinion in cell biology, 2002Co-Authors: Giacomo CavalliAbstract:In eukaryotes, chromatin is essential for heredity. Chromatin architecture is sometimes "epistatic" over the DNA and imparts a different heritable state to the same DNA sequence or the same functional state to unrelated DNA sequences. This has been documented recently in a wide variety of studies focused on regulation of the yeast mating type, the function of Polycomb and trithorax group Proteins, the specification of eukaryotic centromeres and neocentromeres, and genomic imprinting.
John W. Tamkun - One of the best experts on this subject based on the ideXlab platform.
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Transcriptional Regulation by Trithorax-Group Proteins
Cold Spring Harbor perspectives in biology, 2014Co-Authors: Robert E. Kingston, John W. TamkunAbstract:The trithorax group of genes (trxG) was identified in mutational screens that examined developmental phenotypes and suppression of Polycomb mutant phenotypes. The protein products of these genes are primarily involved in gene activation, although some can also have repressive effects. There is no central function for these Proteins. Some move nucleosomes about on the genome in an ATP-dependent manner, some covalently modify histones such as methylating lysine 4 of histone H3, and some directly interact with the transcription machinery or are a part of that machinery. It is interesting to consider why these specific members of large families of functionally related Proteins have strong developmental phenotypes.
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The trithorax group Proteins Kismet and ASH1 promote H3K36 dimethylation to counteract Polycomb group repression in Drosophila
Development (Cambridge England), 2013Co-Authors: Kristel M. Dorighi, John W. TamkunAbstract:Members of the Polycomb group of repressors and trithorax group of activators maintain heritable states of transcription by modifying nucleosomal histones or remodeling chromatin. Although tremendous progress has been made toward defining the biochemical activities of Polycomb and trithorax group Proteins, much remains to be learned about how they interact with each other and the general transcription machinery to maintain on or off states of gene expression. The trithorax group protein Kismet (KIS) is related to the SWI/SNF and CHD families of chromatin remodeling factors. KIS promotes transcription elongation, facilitates the binding of the trithorax group histone methyltransferases ASH1 and TRX to active genes, and counteracts repressive methylation of histone H3 on lysine 27 (H3K27) by Polycomb group Proteins. Here, we sought to clarify the mechanism of action of KIS and how it interacts with ASH1 to antagonize H3K27 methylation in Drosophila. We present evidence that KIS promotes transcription elongation and counteracts Polycomb group repression via distinct mechanisms. A chemical inhibitor of transcription elongation, DRB, had no effect on ASH1 recruitment or H3K27 methylation. Conversely, loss of ASH1 function had no effect on transcription elongation. Mutations in kis cause a global reduction in the di- and tri-methylation of histone H3 on lysine 36 (H3K36) - modifications that antagonize H3K27 methylation in vitro. Furthermore, loss of ASH1 significantly decreases H3K36 dimethylation, providing further evidence that ASH1 is an H3K36 dimethylase in vivo. These and other findings suggest that KIS antagonizes Polycomb group repression by facilitating ASH1-dependent H3K36 dimethylation.
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Drosophila Kismet Regulates Histone H3 Lysine 27 Methylation and Early Elongation by RNA Polymerase II
PLoS genetics, 2008Co-Authors: Shrividhya Srinivasan, Kristel M. Dorighi, John W. TamkunAbstract:Polycomb and trithorax group Proteins regulate cellular pluripotency and differentiation by maintaining hereditable states of transcription. Many Polycomb and trithorax group Proteins have been implicated in the covalent modification or remodeling of chromatin, but how they interact with each other and the general transcription machinery to regulate transcription is not well understood. The trithorax group protein Kismet-L (KIS-L) is a member of the CHD subfamily of chromatin-remodeling factors that plays a global role in transcription by RNA polymerase II (Pol II). Mutations in CHD7, the human counterpart of kis, are associated with CHARGE syndrome, a developmental disorder affecting multiple tissues and organs. To clarify how KIS-L activates gene expression and counteracts Polycomb group silencing, we characterized defects resulting from the loss of KIS-L function in Drosophila. These studies revealed that KIS-L acts downstream of P-TEFb recruitment to stimulate elongation by Pol II. The presence of two chromodomains in KIS-L suggested that its recruitment or function might be regulated by the methylation of histone H3 lysine 4 by the trithorax group Proteins ASH1 and TRX. Although we observed significant overlap between the distributions of KIS-L, ASH1, and TRX on polytene chromosomes, KIS-L did not bind methylated histone tails in vitro, and loss of TRX or ASH1 function did not alter the association of KIS-L with chromatin. By contrast, loss of kis function led to a dramatic reduction in the levels of TRX and ASH1 associated with chromatin and was accompanied by increased histone H3 lysine 27 methylation—a modification required for Polycomb group repression. A similar increase in H3 lysine 27 methylation was observed in ash1 and trx mutant larvae. Our findings suggest that KIS-L promotes early elongation and counteracts Polycomb group repression by recruiting the ASH1 and TRX histone methyltransferases to chromatin.
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Programming off and on states in chromatin: mechanisms of Polycomb and trithorax group complexes.
Current opinion in genetics & development, 2002Co-Authors: Jeffrey A. Simon, John W. TamkunAbstract:Polycomb and trithorax group Proteins are evolutionarily conserved chromatin components that maintain stable states of gene expression. Recent studies have identified and characterized several multiprotein complexes containing these transcriptional regulators. Advances in understanding molecular activities of these complexes in vitro, and functional domains present in their subunits, suggest that they control transcription through multistep mechanisms that involve nucleosome modification, chromatin remodeling, and interaction with general transcription factors.
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The Drosophila trithorax group Proteins BRM, ASH1 and ASH2 are subunits of distinct protein complexes
Development (Cambridge England), 1998Co-Authors: Ophelia Papoulas, Shelley J. Beek, Sarah L. Moseley, Claire M. Mccallum, Melinda Sarte, Allen Shearn, John W. TamkunAbstract:The trithorax group gene brahma (brm) encodes an activator of Drosophila homeotic genes that functions as the ATPase subunit of a large protein complex. To determine if BRM physically interacts with other trithorax group Proteins, we purified the BRM complex from Drosophila embryos and analyzed its subunit composition. The BRM complex contains at least seven major polypeptides. Surprisingly, the majority of the subunits of the BRM complex are not encoded by trithorax group genes. Furthermore, a screen for enhancers of a dominant-negative brm mutation identified only one trithorax group gene, moira (mor), that appears to be essential for brm function in vivo. Four of the subunits of the BRM complex are related to subunits of the yeast chromatin remodeling complexes SWI/SNF and RSC. The BRM complex is even more highly related to the human BRG1 and hBRM complexes, but lacks the subunit heterogeneity characteristic of these complexes. We present biochemical evidence for the existence of two additional complexes containing trithorax group Proteins: a 2 MDa ASH1 complex and a 500 kDa ASH2 complex. These findings suggest that BRM plays a role in chromatin remodeling that is distinct from the function of most other trithorax group Proteins.
Lars Hennig - One of the best experts on this subject based on the ideXlab platform.
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The Polycomb Group Protein Regulatory Network
Annual Review of Plant Biology, 2015Co-Authors: Iva Mozgová, Lars HennigAbstract:Correct expression of specific sets of genes in time and space ensures the establishment and maintenance of cell identity, which is required for proper development of multicellular organisms. Polycomb and Trithorax group Proteins form multisubunit complexes that antagonistically act in epigenetic gene repression and activation, respectively. The traditional view of Poly-comb repressive complexes (PRCs) as executors of long-lasting and stable gene repression is being extended by evidence of flexible repression in re-sponse to developmental and environmental cues, increasing the complexity of mechanisms that ensure selective and properly timed PRC targeting and release of Polycomb repression. Here, we review advances in understanding of the composition, mechanisms of targeting, and function of plant PRCs and discuss the parallels and differences between plant and animal models.
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Regulation of cell identity by plant Polycomb and trithorax group Proteins.
Current opinion in genetics & development, 2010Co-Authors: Claudia Köhler, Lars HennigAbstract:Descendants of stem cells have to make the decision whether to differentiate or whether to maintain a proliferation-competent state. This decision is mediated by the balanced activity of Polycomb group (PcG) and trithorax group (trxG) Proteins. PcG Proteins keep genes in a transcriptional repressed state while trxG Proteins antagonize PcG activity and maintain genes in a transcriptional active state. PcG Proteins act as global regulators of genomic programs that prevent the untimely expression of genes during development and, therefore, ensure that a correct set of genes is active during defined stages of development. Here we will discuss the recent progress in our understanding of the action of PcG Proteins and the factors that antagonize PcG function to control cell fate and differentiation during plant development.
