Role of Polycomb in the control of transposable elements

Deleris, Angélique; Berger, Frédéric; Duharcourt, Sandra

doi:10.1016/j.tig.2021.06.003

Cited by 52 publications

(56 citation statements)

References 65 publications

(86 reference statements)

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“…In mammals and flowering plants in wild-type conditions, H3K27me3 marks chromatin domains of facultative heterochromatin that are distinct from those of constitutive heterochromatin marked by H3K9 methylation (H3K9me) and/or DNA methylation ([ 154 , 155 , 280 ], reviewed in the works of [ 9 , 281 ]). Increasing evidence nevertheless points to the interplay between mechanisms establishing H3K27me3- and H3K9me/DNAme-marked chromatin in eukaryotes ( Table S2 ) (reviewed in the work of [ 9 , 49 ]). First, H3K27me3 is found to be targeted to TEs in wild-type situations in several unicellular species, including the diatom Phaeodactylum tricornutum [ 165 ], the red alga C. merolae [ 63 ], or the ciliate Paramecium tetraurelia [ 106 ], but also in multicellular species, such as the bryophyte M. polymorpha [ 166 ] or even A. thaliana [ 282 ].…”

Section: Prc2 Targeting To Repeats and Regions Of Constitutive Heterochromatinmentioning

confidence: 99%

“…Fourth, disruption of PRC2 can lead to transcriptional activation of TEs in mouse ES cells [ 294 ], in ciliates [ 106 , 230 ], or in the green alga Chlamydomonas reinhardtii [ 31 ]. These pieces of evidence led to the proposal of an ancestral role of PRC2 in repressing transposable elements (reviewed in the work of [ 49 ]). However, the contribution of PRC2 to TE silencing may be limited to some TE families [ 282 ], as its absence does not aggravate TE de-repression in A. thaliana hypomethylated tissues [ 289 , 290 ].…”

Section: Prc2 Targeting To Repeats and Regions Of Constitutive Heterochromatinmentioning

confidence: 99%

“…Increasing evidence suggests the ancestral function of PRC2 in facultative heterochromatin organization [ 49 ]. A pattern seems to be emerging of H3K27me3 targeting repetitive genomic elements in simple eukaryotes, while gene-specific targeting seems to prevail in complex eukaryotic species.…”

Section: Emerging Patterns and Questions In Prc2 Evolutionmentioning

confidence: 99%

“…In model species of both animals and plants, H3K27me3 is largely associated with transcriptional silencing of developmental genes ([ 37 , 38 ], reviewed in the work of [ 39 , 40 ]). PRC2 composition, its biochemical and developmental functions are well studied in animal and in flowering plant model species, and we refer to recent reviews for detailed information [ 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 ]. Here, we bring a comparative overview of PRC2 core composition and biochemical function in different eukaryotic groups, with focus on the green lineage, to highlight emerging concepts of PRC2 evolution.…”

Section: Introductionmentioning

confidence: 99%

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Polycomb Repressive Complex 2 in Eukaryotes—An Evolutionary Perspective

2022

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Polycomb repressive complex 2 (PRC2) represents a group of evolutionarily conserved multi-subunit complexes that repress gene transcription by introducing trimethylation of lysine 27 on histone 3 (H3K27me3). PRC2 activity is of key importance for cell identity specification and developmental phase transitions in animals and plants. The composition, biochemistry, and developmental function of PRC2 in animal and flowering plant model species are relatively well described. Recent evidence demonstrates the presence of PRC2 complexes in various eukaryotic supergroups, suggesting conservation of the complex and its function. Here, we provide an overview of the current understanding of PRC2-mediated repression in different representatives of eukaryotic supergroups with a focus on the green lineage. By comparison of PRC2 in different eukaryotes, we highlight the possible common and diverged features suggesting evolutionary implications and outline emerging questions and directions for future research of polycomb repression and its evolution.

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Section: Prc2 Targeting To Repeats and Regions Of Constitutive Heterochromatinmentioning

confidence: 99%

Section: Prc2 Targeting To Repeats and Regions Of Constitutive Heterochromatinmentioning

confidence: 99%

Section: Emerging Patterns and Questions In Prc2 Evolutionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Polycomb Repressive Complex 2 in Eukaryotes—An Evolutionary Perspective

2022

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“…The authors propose that TE targeting by H3K27me3 could be explained by an inefficient self-reinforcing loop between 5mC and H3K9 methylation in M. polymorpha . Targeting of TEs by H3K27me3 would be an ancient silencing mechanism that would have evolved towards dedicated 5mC- and H3K9-methylation-mediated TE silencing pathways throughout the evolution of other embryophyte lineages (discussed in [ 90 ]). In P. tetraurelia or T. thermophila , loss of function of the PRC2 core subunit Enhancer of Zeste E(z)-like1 (EZL1) induces TE silencing defects [ 86 , 87 ].…”

Section: A Plethora Of Sophisticated Epigenetic Pathways Dampen Tesmentioning

confidence: 99%

The Evolutionary Volte-Face of Transposable Elements: From Harmful Jumping Genes to Major Drivers of Genetic Innovation

Nicolau

Picault

Moissiard

2021

Cells

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Transposable elements (TEs) are self-replicating DNA elements that constitute major fractions of eukaryote genomes. Their ability to transpose can modify the genome structure with potentially deleterious effects. To repress TE activity, host cells have developed numerous strategies, including epigenetic pathways, such as DNA methylation or histone modifications. Although TE neo-insertions are mostly deleterious or neutral, they can become advantageous for the host under specific circumstances. The phenomenon leading to the appropriation of TE-derived sequences by the host is known as TE exaptation or co-option. TE exaptation can be of different natures, through the production of coding or non-coding DNA sequences with ultimately an adaptive benefit for the host. In this review, we first give new insights into the silencing pathways controlling TE activity. We then discuss a model to explain how, under specific environmental conditions, TEs are unleashed, leading to a TE burst and neo-insertions, with potential benefits for the host. Finally, we review our current knowledge of coding and non-coding TE exaptation by providing several examples in various organisms and describing a method to identify TE co-option events.

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Transposable elements as new players in neurodegenerative diseases

et al. 2021

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Neurodegenerative diseases (NDs), including the most prevalent Alzheimer’s disease and Parkinson disease, share common pathological features. Despite decades of gene‐centric approaches, the molecular mechanisms underlying these diseases remain widely elusive. In recent years, transposable elements (TEs), long considered ‘junk’ DNA, have gained growing interest as pathogenic players in NDs. Age is the major risk factor for most NDs, and several repressive mechanisms of TEs, such as heterochromatinization, fail with age. Indeed, heterochromatin relaxation leading to TE derepression has been reported in various models of neurodegeneration and NDs. There is also evidence that certain pathogenic proteins involved in NDs (e.g., tau, TDP‐43) may control the expression of TEs. The deleterious consequences of TE activation are not well known but they could include DNA damage and genomic instability, altered host gene expression, and/or neuroinflammation, which are common hallmarks of neurodegeneration and aging. TEs might thus represent an overlooked pathogenic culprit for both brain aging and neurodegeneration. Certain pathological effects of TEs might be prevented by inhibiting their activity, pointing to TEs as novel targets for neuroprotection.

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Role of Polycomb in the control of transposable elements

Cited by 52 publications

References 65 publications

Polycomb Repressive Complex 2 in Eukaryotes—An Evolutionary Perspective

Polycomb Repressive Complex 2 in Eukaryotes—An Evolutionary Perspective

The Evolutionary Volte-Face of Transposable Elements: From Harmful Jumping Genes to Major Drivers of Genetic Innovation

Transposable elements as new players in neurodegenerative diseases

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