H2AK119ub1 guides maternal inheritance and zygotic deposition of H3K27me3 in mouse embryos

Mei, Hailiang; Kozuka, Chisayo; Hayashi, Ryoya; Kumon, Mami; Koseki, Haruhiko; Inoue, Atsuyuki

doi:10.1038/s41588-021-00820-3

Cited by 99 publications

(123 citation statements)

References 91 publications

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“…Recent evidence further suggests that PRC2 activity is, at least in part, dependent on PRC1 ubiquitination of H2AK119, which is colocalized with the broad domains of H3K27me3 (Fig. 1; Mei et al 2021). PRC2 enzymatic activity is tightly regulated throughout oogenesis through the action of the germline-specific PRC2 cofactor EZHIP, which represses deposition of H3K27me3 in the late stages of oogenesis (Ragazzini et al 2019).…”

Section: Establishment Mechanism: Targeting Of H3k27me3 In the Oocytementioning

confidence: 97%

Features and mechanisms of canonical and noncanonical genomic imprinting

Hanna

Kelsey

2021

Genes Dev.

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Genomic imprinting is the monoallelic expression of a gene based on parent of origin and is a consequence of differential epigenetic marking between the male and female germlines. Canonically, genomic imprinting is mediated by allelic DNA methylation. However, recently it has been shown that maternal H3K27me3 can result in DNA methylation-independent imprinting, termed "noncanonical imprinting." In this review, we compare and contrast what is currently known about the underlying mechanisms, the role of endogenous retroviral elements, and the conservation of canonical and noncanonical genomic imprinting.Supplemental material is available for this article.

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Section: Establishment Mechanism: Targeting Of H3k27me3 In the Oocytementioning

confidence: 97%

Features and mechanisms of canonical and noncanonical genomic imprinting

Hanna

Kelsey

2021

Genes Dev.

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“…The key gametic imprinting mark of the "non-canonical" (DNA methylation-independent) imprinting is the repressive histone mark H3K27me3 (trimethylation of H3 at lysine 27) in the oocyte, which was found to transiently imprint several loci within pre-implantation (Inoue et al, 2017a). Furthermore, H2AK119ub1 (mono-ubiquitinated histone H2A at lysine 119) was highly colocalized with H3K27me3 in oocytes, which is equalized mainly at the two-cell stage but guides maternal H3K27me3 inheritance after fertilization (Chen et al, 2021;Mei et al, 2021). Thus, H2AK119ub1 and H3K27me3, which are catalyzed by the polycomb repressive complexes (PRC1 and PRC2), mediate maternal allele-specific silencing of at least seven imprinted genes, namely Sfmbt2, Phf17, Gab1, Sall1, Platr20 (5133400J02Rik), Smoc1, and Slc38a4, in mice (Figure 1C), several of which have been previously shown to play important roles in placental function and development (Itoh et al, 2000;Miri et al, 2013;Matoba et al, 2019).…”

Section: Non-canonical Imprinting Is Mediated By Maternal Histone Modificationmentioning

confidence: 99%

“…Thus, H2AK119ub1 and H3K27me3, which are catalyzed by the polycomb repressive complexes (PRC1 and PRC2), mediate maternal allele-specific silencing of at least seven imprinted genes, namely Sfmbt2, Phf17, Gab1, Sall1, Platr20 (5133400J02Rik), Smoc1, and Slc38a4, in mice (Figure 1C), several of which have been previously shown to play important roles in placental function and development (Itoh et al, 2000;Miri et al, 2013;Matoba et al, 2019). Maternal H3K27me3 and H2AK119ub1 are not maintained beyond pre-implantation development (Hanna et al, 2019;Chen et al, 2021;Mei et al, 2021), and transition to a more permanent epigenetic state is required to preserve paternal expression during post-implantation development (Inoue et al, 2017a;Chen et al, 2019;Hanna et al, 2019). The long terminal repeats (LTRs) of endogenous retroviral elements can act as alternative promoters for non-canonical imprinted genes and paternal allele-specific accumulation of the active histone mark H3K4me3 (trimethylation of H3 at lysine 4) occurs at these LTR promoters (Hanna et al, 2019).…”

Section: Non-canonical Imprinting Is Mediated By Maternal Histone Modificationmentioning

confidence: 99%

Canonical and Non-canonical Genomic Imprinting in Rodents

Kobayashi

2021

Front. Cell Dev. Biol.

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Genomic imprinting is an epigenetic phenomenon that results in unequal expression of homologous maternal and paternal alleles. This process is initiated in the germline, and the parental epigenetic memories can be maintained following fertilization and induce further allele-specific transcription and chromatin modifications of single or multiple neighboring genes, known as imprinted genes. To date, more than 260 imprinted genes have been identified in the mouse genome, most of which are controlled by imprinted germline differentially methylated regions (gDMRs) that exhibit parent-of-origin specific DNA methylation, which is considered primary imprint. Recent studies provide evidence that a subset of gDMR-less, placenta-specific imprinted genes is controlled by maternal-derived histone modifications. To further understand DNA methylation-dependent (canonical) and -independent (non-canonical) imprints, this review summarizes the loci under the control of each type of imprinting in the mouse and compares them with the respective homologs in other rodents. Understanding epigenetic systems that differ among loci or species may provide new models for exploring genetic regulation and evolutionary divergence.

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“…The distribution of many epigenetic marks is dynamic during development 9,42 . To determine the temporal dynamics of H2Bub1 occupancy during cardiomyocyte differentiation, differential binding analysis on the H2Bub1 ChIP-seq data was performed during the progression from iPSCs to CMs.…”

Section: H2bub1 Is Selectively Maintained On Sarcomeric Calcium Genesmentioning

confidence: 99%

Tissue-specific H2Bub1 is required for cardiomyocyte development

Barish¹,

Drozd

Berg

et al. 2021

Preprint

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De-novo mutations affecting Histone2B-K120 monoubiquitination (H2Bub1) are enriched in congenital heart disease; however, how H2Bub1 affects heart development beyond its function in establishing left-right asymmetry remains unknown. Here we show that the RNF20-core complex (RNF20-RNF40-UBE2B), which catalyzes H2Bub1, is required for cardiac development in-vivo in mice and in-vitro in iPSC-derived cardiomyocytes. Mice with cardiac-specific deletion of Rnf20 have abnormal myocardium and ventricular septal defects; iPSCs with mutations affecting H2Bub1 cannot efficiently differentiate into cardiomyocytes. Sarcomeric gene expression is dependent on normal H2Bub1 both in mice and in iPSC-derived cardiomyocytes. Finally, we identify an accumulation of H2Bub1 near the center of tissue-specific genes in cardiomyocytes and MEFs associated with transcriptional efficiency that is reduced in UBE2B-/- cardiomyocytes. In summary, normal H2Bub1 distribution is required in cardiac development, and H2Bub1 accumulation acts as a general mechanism for tissue-specific regulation of transcriptional elongation efficiency.

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H2AK119ub1 guides maternal inheritance and zygotic deposition of H3K27me3 in mouse embryos

Cited by 99 publications

References 91 publications

Features and mechanisms of canonical and noncanonical genomic imprinting

Features and mechanisms of canonical and noncanonical genomic imprinting

Canonical and Non-canonical Genomic Imprinting in Rodents

Tissue-specific H2Bub1 is required for cardiomyocyte development

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