Overcoming Intrinsic H3K27me3 Imprinting Barriers Improves Post-implantation Development after Somatic Cell Nuclear Transfer

Wang, Le-Yun; Li, Zhikun; Wang, Libin; Liu, Chao; Sun, Xuehan; Feng, Guihai; Wang, Jiaqiang; Li, Yufei; Qiao, Lianyong; Nie, Hu; Jiang, Liyuan; Sun, Hao; Xie, Yali; Ma, Sinan; Wang, Haifeng; Lu, Falong; Li, Wei; Zhou, Qi

doi:10.1016/j.stem.2020.05.014

Cited by 49 publications

(54 citation statements)

References 57 publications

(70 reference statements)

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“…Shortly after this report, Wang et al achieved corrections of multiple noncanonical genes in SCNT placentas by using genetically manipulated haploid ES cells. The best result was obtained when the maternal alleles of four genes (Gab1, Sfmbt2, Jade1/Phf17, and Smoc1) were deleted; the resulting placental morphologies were nearly normal, and the birth rate of clones was increased to about 14% (Wang et al 2020). Although Sfmbt2 miRNAs were not depleted in their Sfmbt2 knockout mice, this result was another clear demonstration of the involvement of noncanonical imprinted genes in SCNT-specific placental anomalies and poor embryo development rates to term.…”

Section: Noncanonical (H3k27me3-dependent) Imprintingmentioning

confidence: 92%

“…However, the unique broad domains of H3K27me3 were completely lost in SCNT embryos as well as in donor somatic cells; as a result, the H3K27me3dependently imprinted genes were abnormally expressed from both maternal and paternal alleles after NT . Recently, two groups, including ours, have reported independently that the loss of imprinting (LOI) of a set of H3K27me3-imprinted genes, such as Sfmbt2 or its associated microRNA cluster, was responsible for the poor development rate and large placentas in mouse SCNT models (Inoue et al 2020, Wang et al 2020) (see below).…”

Section: A Ogura and Othersmentioning

confidence: 98%

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Epigenetic abnormalities associated with somatic cell nuclear transfer

Ogura

Matoba²,

Inoue

2021

Reproduction

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Twenty-five years have passed since the birth of Dolly the sheep, the first mammalian clone produced by adult somatic cell nuclear transfer (SCNT). During that time, the main thrust of SCNT-related research has been the elucidation of SCNT-associated epigenetic abnormalities and their correction, with the aim of improving the efficiency of cloned animal production. Through these studies, it has become clear that some epigenomic information can be reprogrammed by the oocyte, while some cannot. Now we know that the imprinting memories in the donor genome, whether canonical (DNA-methylation-dependent) or noncanonical (H3K27me3-dependent), are not reprogrammed by SCNT. Thus, SCNT-derived embryos have the normal canonical imprinting and the erased noncanonical imprinting, both being inherited from the donor cells. The latter can cause abnormal phenotypes in SCNT-derived placentas arising from biallelic expressions of noncanonically imprinted genes. By contrast, repressive epigenomic information, such as DNA methylation and histone modifications, might be more variably reprogrammed, leaving room for technical improvements. Low-input analytical technologies now enable us to analyze the genome of gametes and embryos in a high-throughput, genome-wide manner. These technologies are being applied rapidly to the SCNT field, providing evidence for incomplete reprogramming of the donor genome in cloned embryos or offspring. Insights from the study of epigenetic phenomena in SCNT are highly relevant for our understanding of the mechanisms of genomic reprogramming that can induce totipotency in the mammalian genome.

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Section: Noncanonical (H3k27me3-dependent) Imprintingmentioning

confidence: 92%

Section: A Ogura and Othersmentioning

confidence: 98%

Epigenetic abnormalities associated with somatic cell nuclear transfer

Ogura

Matoba²,

Inoue

2021

Reproduction

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“…Such imprinting is lost in embryonic lineages after implantation but is maintained in extraembryonic tissues by DNA methylation instead, which is considered as a more stable epigenetic mark ( Chen et al., 2019b ). The oocyte H3K27me3-mediated imprinting is apparently missing in SCNT embryos, and artificially restoring the monoallelic expression states of four H3K27me3 imprinted genes can significantly improve mouse SCNT efficiency ( Wang et al., 2020 ). Of note, H3K27me3 undergoes a global depletion in human early embryos before ZGA (with the paternal allele likely showing a faster kinetics) ( van de Werken et al., 2014 ; Xia et al., 2019 ; Zhang et al., 2012 ), indicating that H3K27me3-mediated imprinting may be absent in humans.…”

Section: Main Textmentioning

confidence: 99%

Rebooting the Epigenomes during Mammalian Early Embryogenesis

Xia

Xie

2020

Stem Cell Reports

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Summary Upon fertilization, terminally differentiated gametes are transformed to a totipotent zygote, which gives rise to an embryo. How parental epigenetic memories are inherited and reprogrammed to accommodate parental-to-zygotic transition remains a fundamental question in developmental biology, epigenetics, and stem cell biology. With the rapid advancement of ultra-sensitive or single-cell epigenome analysis methods, unusual principles of epigenetic reprogramming begin to be unveiled. Emerging data reveal that in many species, the parental epigenome undergoes dramatic reprogramming followed by subsequent re-establishment of the embryo epigenome, leading to epigenetic “rebooting.” Here, we discuss recent progress in understanding epigenetic reprogramming and their functions during mammalian early development. We also highlight the conserved and species-specific principles underlying diverse regulation of the epigenome in early embryos during evolution.

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“…With this system, 72 candidate genes related to bone development were addressed out, 4 key genes of which were validated essential in the regulation of bone development during embryogenesis [58] .Furthermore, ahaESCs could produce heterozygous mutant mice without long-term mating [57] . Four single allele deletion ( Sfmbt2 , Jade1 , Gab1 and Smoc1 ) mice were successfully constructed and applied to study the function of imprinted genes [71] . Single deletion of these genes can effectively improve the pup rates of SCNT [71] .…”

Section: Characteristics and Application Of Haploid Cellsmentioning

confidence: 99%

“…Four single allele deletion ( Sfmbt2 , Jade1 , Gab1 and Smoc1 ) mice were successfully constructed and applied to study the function of imprinted genes [71] . Single deletion of these genes can effectively improve the pup rates of SCNT [71] .…”

Section: Characteristics and Application Of Haploid Cellsmentioning

confidence: 99%

The milestone of genetic screening: Mammalian haploid cells

Sun

Zhao

Shuai

2020

Computational and Structural Biotechnology Journal

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Mammalian haploid cells provide insights into multiple genetics approaches as have been proved by advances in homozygous phenotypes and function as gametes. Recent achievements make ploidy of mammalian haploid cells stable and improve the developmental efficiency of embryos derived from mammalian haploid cells intracytoplasmic microinjection, which promise great potentials for using mammalian haploid cells in forward and reverse genetic screening. In this review, we introduce breakthroughs of mammalian haploid cells involving in mechanisms of self-diploidization, forward genetics for various targeting genes and imprinted genes related development.

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Overcoming Intrinsic H3K27me3 Imprinting Barriers Improves Post-implantation Development after Somatic Cell Nuclear Transfer

Abstract: Highlights d Increased SCNT cloning by monoallelic deletion of four H3K27me3-imprinted genes d H3K27me3-imprinted gene deletion normalized body and placental weights in cloned pups d Sfmbt2 deletion is the most effective monoallelic deletion for improving SCNT

Cited by 49 publications

References 57 publications

Epigenetic abnormalities associated with somatic cell nuclear transfer

Epigenetic abnormalities associated with somatic cell nuclear transfer

Rebooting the Epigenomes during Mammalian Early Embryogenesis

The milestone of genetic screening: Mammalian haploid cells

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