Stella controls chromocenter formation through regulation of Daxx expression in 2-cell embryos

Arakawa, Tatsuhiko; Nakatani, Tsunetoshi; Oda, Masaaki; Kimura, Yasuyoshi; Sekita, Yoichi; Kimura, Tohru; Nakamura, Toshinobu; Nakano, Toru

doi:10.1016/j.bbrc.2015.08.106

Cited by 20 publications

(16 citation statements)

References 25 publications

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“…The reverse takes place in the maternal pronucleus where maternally-imprinted genes (blue closed circles), which have assembled a ZFP57-directed heterochromatin-like complex, preferentially translocate to the ring of HP1β the paternally-imprinted genes (open red circles) in the maternal pro-nucleus remain in the nucleoplasm. At the end of the 1 cell stage the CF pathway is triggered and STELLA increases the levels of DAXX, which, as part of the ATRX/DAXX complex, in turn increases the incorporation of histone H3.3 into constitutive heterochromatin (Arakawa et al 2015). Concomitant with CF is ZGA, where there is a transient burst of transcription from the zygotic genome.…”

Section: Specification Of Imprints: a Mouse Modelmentioning

confidence: 99%

“…97% of embryos lacking maternal STELLA do not develop to the blastocyst stage and by the 2-4 cell stage already exhibit abnormal cleavage and chromosome segregation defects that cannot be rescued by the paternal genome (Nakamura et al 2007). STELLA-deficient embryos fail because there is disruption of a pathway required for CF (Arakawa et al 2015) (Figure 6). The proximate lesion is a reduction in the levels of H3.3-specific chaperone DAXX in the pro-nuclei, which has the effect of reducing the incorporation of H3.3 into constitutive heterochromatin surrounding the PNBs and this in turn reduces the burst of reverse major satellite RNA expression in the 2-cell embryos; injection of DAXX mRNA into one cell embryos can rescue CF along with H3.3 incorporation and the expression of reverse major satellite RNAs (Arakawa et al 2015).…”

Section: Specification Of Imprints In the Mouse Occurs Around The Timmentioning

confidence: 99%

“…STELLA-deficient embryos fail because there is disruption of a pathway required for CF (Arakawa et al 2015) (Figure 6). The proximate lesion is a reduction in the levels of H3.3-specific chaperone DAXX in the pro-nuclei, which has the effect of reducing the incorporation of H3.3 into constitutive heterochromatin surrounding the PNBs and this in turn reduces the burst of reverse major satellite RNA expression in the 2-cell embryos; injection of DAXX mRNA into one cell embryos can rescue CF along with H3.3 incorporation and the expression of reverse major satellite RNAs (Arakawa et al 2015). It is known that either incorporation of mutant H3.3 or interference with expression of reverse major satellite RNAs affects CF and blocks development at the 2-cell stage (Santenard et al 2010;Casanova et al, 2013).…”

Section: Specification Of Imprints In the Mouse Occurs Around The Timmentioning

confidence: 99%

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Heterochromatin and the molecular mechanisms of ‘parent-of-origin’ effects in animals

Singh

2016

J Biosci

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Twenty five years ago it was proposed that conserved components of constitutive heterochromatin assemble heterochromatinlike complexes in euchromatin and this could provide a general mechanism for regulating heritable (cell-to-cell) changes in gene expressibility. As a special case, differences in the assembly of heterochromatin-like complexes on homologous chromosomes might also regulate the parent-of-origin-dependent gene expression observed in placental mammals. Here, the progress made in the intervening period with emphasis on the role of heterochromatin and heterochromatin-like complexes in parent-of-origin effects in animals is reviewed.[Singh PB 2016 Heterochromatin and the molecular mechanisms of 'parent-of-origin' effects in animals. J. Biosci.] http://www.ias.ac.in/jbiosci J. Biosci. * Indian Academy of Sciences DOI: 10.1007/s12038-016-9650-9Keywords. Epigenetics; genomic imprinting; heterochromatin; HP1; KRAB-ZFP Abbreviations used: 5hmC, 5-hydroxymethylcytosine; 5mC, 5-methylcytosine; ADD, ATRX-DNMT3-DNMT3L domain; ATRX, Alpha Thalassemia/Mental Retardation Syndrome X-Linked; CAF-1, chromatin assembly factor 1; CD, chromodomain; CE, controlling element; CF, chromocenter formation; CGIs, CpG islands; CSD, chromo shadow domain; DamID, DNA adenine methyltransferase identification; DAXX, Death Domain associated protein; DNMT1, maintenance DNA methyltransferase 1; DNMT3A, de novo DNA methyltransferase 3A; DNMT3B, de novo DNA methyltransferase 3B; DNMT3L, DNA methyltransferase 3L; ES, embryonic stem; G9a, K9H3 HMTase; GLP, G9a-like protein K9H3 HMTase; gDMRs, germline differentially methylated regions; H3K9me2, di-methylated lysine 9 on histone H3; H3K9me3, tri-methylated lysine 9 on histone H3; H3S10P, phosphorylation of serine 10 on histone H3; H4K20me3, tri-methylated lysine 20 on histone

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Section: Specification Of Imprints: a Mouse Modelmentioning

confidence: 99%

Section: Specification Of Imprints In the Mouse Occurs Around The Timmentioning

confidence: 99%

Section: Specification Of Imprints In the Mouse Occurs Around The Timmentioning

confidence: 99%

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Heterochromatin and the molecular mechanisms of ‘parent-of-origin’ effects in animals

Singh

2016

J Biosci

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“…42 In mammalian, the structure of the pericentromeric region changed from a ring shape to a dot-like shape during the 2-cell embryo stage. 42 In mammalian, the structure of the pericentromeric region changed from a ring shape to a dot-like shape during the 2-cell embryo stage.…”

Section: Dppa3 In Early Embryogenesismentioning

confidence: 99%

Dppa3 in pluripotency maintenance of ES cells and early embryogenesis

Zhao

Liu

et al. 2018

J of Cellular Biochemistry

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Embryonic development is precisely regulated by a network of signal pathways and specific genes. Dppa3 (also known as Pgc7 or Stella) plays an important role in early embryonic development during the cleavage stage as a maternal effect gene. Dppa3 expresses in many species, and its homologous gene in human and rat genomes is located at the same chromosomal regions and have the same exon‐intron structure. However, unlike mouse embryonic stem (ES) cells, in which the Dppa3 promoter maintains hypomethylation that allows a high transcription level, the DPPA3 promoter region in human ES cells is methylated, much like that of mouse epiblast stem cell. Dppa3 is essential for early embryogenesis and pluripotency maintenance; however, the precise mechanism and downstream passage remains unknown. In this review, we will summarize some important functions of Dppa3 in early embryogenesis and pluripotency maintenance of mouse ES cells.

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“…TET2 and TET3 activity is inhibited by human DPPA3, which localizes to specific loci and is controlled by H3K9me2 marks and DNA sequence, and could specifically protect the female PN from DNA demethylation as well as specific regions such as imprinted genes [61]. In mice, DPPA3-null embryos show impaired DNA replication, ectopic micronuclei, abnormal chromosome segregation of maternal chromosomes, and aberrant H2AX phosphorylation, which inhibits DNA replication [62]. These results demonstrate that DPPA3 protects maternal DNA from aberrant epigenetic modifications to ensure early embryogenesis.…”

Section: Dna Methylation In Early Embryo Developmentmentioning

confidence: 99%

Epigenetics in preimplantation mammalian development

Cánovas

Ross

2016

Theriogenology

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Fertilization is a very dynamic period of comprehensive chromatin remodelling, from which two specialized cells result in a totipotent zygote. The formation of a totipotent cell requires extensive epigenetic remodeling that, while independent of modifications in the DNA sequence, still entails a profound cell fate change, supported by transcriptional profile modifications. As a result of finely-tuned interactions between numerous mechanisms, the goal of fertilization is to form a full healthy new individual. To avoid the persistence of alterations in epigenetic marks, the epigenetic information contained in each gamete is reset during early embryogenesis. Covalent modification of DNA by methylation, as well as post-translational modifications of histone proteins and non-coding RNAs, appear to be the main epigenetic mechanisms that control gene expression. These allow different cells in an organism to express different transcription profiles, despite each cell containing the same DNA sequence. In the context of replacement of spermatic protamine with histones from the oocyte, active cell division, and specification of different lineages, active and passive mechanisms of epigenetic remodeling have been revealed as critical for editing the epigenetic profile of the early embryo. Importantly, redundant factors and mechanisms are likely in place, and only a few have been reported as critical for fertilization or embryo survival by the use of knockout models. The aim of this review is to highlight the main mechanisms of epigenetic remodeling that ensue after fertilization in mammals.

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Stella controls chromocenter formation through regulation of Daxx expression in 2-cell embryos

Cited by 20 publications

References 25 publications

Heterochromatin and the molecular mechanisms of ‘parent-of-origin’ effects in animals

Heterochromatin and the molecular mechanisms of ‘parent-of-origin’ effects in animals

Dppa3 in pluripotency maintenance of ES cells and early embryogenesis

Epigenetics in preimplantation mammalian development

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