There is another: H3K27me3-mediated genomic imprinting

Raas, Maximilian W.D.; Zijlmans, Dick W.; Vermeulen, Michiel; Marks, Hendrik

doi:10.1016/j.tig.2021.06.017

Cited by 24 publications

(14 citation statements)

References 113 publications

(173 reference statements)

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“…The potential role of SMCHD1 in solidifying initial silencing by Polycomb may then allow some of its targets to transition to other modes of repression, in particular H3K9 methylation and DNA methylation. Preimplantation Polycomb imprints acquire secondary DNA methylation and H3K9me2 in the placenta Hanna et al (2019) ; Chen et al (2019) ; Zeng et al (2021) ; Andergassen et al (2021) ; Raas et al (2021) , similar to the Xi CpG islands becoming methylated by DNMT3B and H3K9me3 accumulating on the Xi ( Gendrel et al, 2012 ; Keniry et al, 2016 ; Ichihara et al, 2021 ). In the absence of SMCHD1, these transitions fail: DNA methylation at non-canonical imprinted gene Jade1 does not accumulate Wanigasuriya et al (2020) , nor does Xi CpG island methylation ( Gendrel et al, 2012 )(this study).…”

Section: Discussionmentioning

confidence: 99%

Maternal SMCHD1 controls both imprinted Xist expression and imprinted X chromosome inactivation

Wanigasuriya

Kinkel

Beck

et al. 2021

Preprint

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Embryonic development is dependent on the maternal supply of proteins through the oocyte, including factors setting up the adequate epigenetic patterning of the zygotic genome. We previously reported that one such factor is the epigenetic repressor SMCHD1, whose maternal supply controls autosomal imprinted expression in mouse preimplantation embryos and mid-gestation placenta. In mouse preimplantation embryos, X chromosome inactivation is also an imprinted process. Combining genomics and imaging, we show that maternal SMCHD1 is required not only for the imprinted expression of Xist in preimplantation embryos, but also for the efficient silencing of the inactive X in both the preimplantation embryo and mid-gestation placenta. These results expand the role of SMCHD1 in enforcing the silencing of Polycomb targets. The inability of zygotic SMCHD1 to fully restore imprinted X inactivation further points to maternal SMCHD1's role in setting up the appropriate chromatin environment during preimplantation development, a critical window of epigenetic remodelling.

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Section: Discussionmentioning

confidence: 99%

Maternal SMCHD1 controls both imprinted Xist expression and imprinted X chromosome inactivation

Wanigasuriya

Kinkel

Beck

et al. 2021

Preprint

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“…The consequence of histone methylation can be repression or activation of transcription, depending on the methylated residues ( Black et al, 2012 ). In general, trimethylation of lysine 4 on H3 (H3K4me3) ( Hughes et al, 2020 ) signifies activation of gene transcription, whereas the trimethylation of lysine 9 (H3K9me3) ( Feng et al, 2020 ) and 27 (H3K27me3) ( Raas et al, 2022 ) on H3 represents inhibition of gene transcription. EZH2 belongs to the polycomb repressive complex 2 (PRC2), which is responsible for the catalysis of methylation of lysine 27 of histone H3 ( Pan et al, 2016 ; Jiang et al, 2021 ).…”

Section: Epigenetic Phenomenon and Cancermentioning

confidence: 99%

Recent advances in epigenetic anticancer therapeutics and future perspectives

Ren

Yang

et al. 2023

Front. Genet.

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Tumor development is frequently accompanied by abnormal expression of multiple genomic genes, which can be broadly viewed as decreased expression of tumor suppressor genes and upregulated expression of oncogenes. In this process, epigenetic regulation plays an essential role in the regulation of gene expression without alteration of DNA or RNA sequence, including DNA methylation, RNA methylation, histone modifications and non-coding RNAs. Therefore, drugs developed for the above epigenetic modulation have entered clinical use or preclinical and clinical research stages, contributing to the development of antitumor drugs greatly. Despite the efficacy of epigenetic drugs in hematologic caners, their therapeutic effects in solid tumors have been less favorable. A growing body of research suggests that epigenetic drugs can be applied in combination with other therapies to increase efficacy and overcome tumor resistance. In this review, the progress of epigenetics in tumor progression and oncology drug development is systematically summarized, as well as its synergy with other oncology therapies. The future directions of epigenetic drug development are described in detail.

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“…Genomic imprinting refers to an allele's expression being dependent on its parent of origin (Haig, 2002). The proximate cause of this phenomenon is the placement of epigenetic marks, or imprints, on genomes during gametogenesis (Reik & Walter, 2001; Raas et al ., 2022). These imprints are then erased in the germline of the new diploid individual, and the appropriate imprints applied during the next round of gametogenesis.…”

Section: The Kin Selection Theory Of Genomic Imprintingmentioning

confidence: 99%

“…The evolution of genomic imprinting, the monoallelic expression of genes based on an allele's parent of origin, may be explained by kin selection acting through asymmetries in the probabilities of alleles being shared by common descent between individuals depending on the alleles' parental origin (Wilkins & Haig, 2003). This phenomenon is well established in flowering plants and mammals, and is mechanistically best understood in mammals, including humans (Peters, 2014; Reik & Walter, 2001; Raas et al ., 2022). Although not confirmed in the eusocial Hymenoptera (ants, bees and wasps with a worker caste) (Oldroyd & Yagound, 2021), these insects are predicted to be prime candidates for the evolution of genomic imprinting because their haplodiploid sex determination creates extreme relatedness asymmetries between parental alleles, and because of the rich set of behavioural interactions affecting the development and reproduction of colony members (Haig, 1992; Dobata & Tsuji, 2012; Wild & West, 2009; Queller, 2003).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The kin selection theory of genomic imprinting and modes of reproduction in the eusocial Hymenoptera

Silva

2022

Biological Reviews

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Genomic imprinting is known from flowering plants and mammals but has not been confirmed for the Hymenoptera even though the eusocial Hymenoptera are prime candidates for this peculiar form of gene expression. Here, the kin selection theory of genomic imprinting is reviewed and applied to the eusocial Hymenoptera. The evidence for imprinting in eusocial Hymenoptera with the typical mode of reproduction, involving the sexual production of diploid female offspring, which develop into workers or gynes, and the arrhenotokous parthenogenesis of haploid males, is also reviewed briefly. However, the focus of this review is how atypical modes of reproduction, involving thelytokous parthenogenesis, hybridisation and androgenesis, may also select for imprinting. In particular, naturally occurring hybridisation in several genera of ants may provide useful tests of the role of kin selection in the evolution of imprinting. Hybridisation is expected to disrupt the coadaptation of antagonistically imprinted loci, and thus affect the phenotypes of hybrids. Some of the limited data available on hybrid worker reproduction and on colony sex ratios support predictions about patterns of imprinting derived from kin selection theory.

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There is another: H3K27me3-mediated genomic imprinting

Cited by 24 publications

References 113 publications

Maternal SMCHD1 controls both imprinted Xist expression and imprinted X chromosome inactivation

Maternal SMCHD1 controls both imprinted Xist expression and imprinted X chromosome inactivation

Recent advances in epigenetic anticancer therapeutics and future perspectives

The kin selection theory of genomic imprinting and modes of reproduction in the eusocial Hymenoptera

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