Loss of maternal <i>Trim28</i> causes male-predominant early embryonic lethality

Kumar, Abhishek Sampath; Seah, Michelle K. Y.; Ling, Ka Yi; Wang, Yaju; Tan, Joel Heng Loong; Nitsch, Sandra; Lim, Seng Han; Lorthongpanich, Chanchao; Wollmann, Heike; Low, Diana; Guccione, Ernesto; Messerschmidt, Daniel M.

doi:10.1101/gad.291195.116

Cited by 24 publications

(11 citation statements)

References 29 publications

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“…TRIM28, previously known as Krüppel-associated box-associated protein 1, is a nuclear corepressor for kruppel-associated box domain-containing zinc finger proteins 18. TRIM28 participates in many aspects of cellular biology, either promoting proliferation or leading to anti-proliferation.…”

Section: Discussionmentioning

confidence: 99%

TRIM28 activates autophagy and promotes cell proliferation in glioblastoma

Peng¹,

Zhang²,

Jiang³

et al. 2019

OTT

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BackgroundTripartite motif-containing protein 28 (TRIM28) is a transcriptional corepressor involved in the regulation of several cancers, including glioma. It has been reported that TRIM28 takes part in the process of autophagy. However, its effect on the autophagy and cell proliferation in gliomas has not been elucidated. Here, we report a novel tumor cell proliferation mechanism in which TRIM28-regulated autophagy promotes glioma tumor cell proliferation.Materials and methodsWe analyzed the expressions of TRIM28 and LC3 in different WHO grades of gliomas by IHC assays. We then knocked down and overexpressed TRIM28 or knocked down ATG5 in U251 cells and confirmed its roles in autophagy and cell proliferation via cell counting, immunofluorescence, and Western blot.ResultsThe results showed that TRIM28 and autophagy levels were significantly increased with the progression of tumor grade in glioma. TRIM28 promoted glioblastoma cell proliferation. Knockdown of TRIM28 inhibited autophagy in glioblastoma cells. Meanwhile, TRIM28 promoted glioblastoma cell proliferation by modulating TRIM28.ConclusionThese data demonstrated that TRIM28 activates autophagy and increases cell proliferation in glioma.

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Section: Discussionmentioning

confidence: 99%

TRIM28 activates autophagy and promotes cell proliferation in glioblastoma

Peng¹,

Zhang²,

Jiang³

et al. 2019

OTT

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“…As well as paternally imprinted loci and endogenous retroviruses, individual genes in the paternal genome resist demethylation; for example, the Y chromosome gene Rbmy1a1 in the mouse. The zygotic expression of this gene is repressed by sperm-inherited DNA methylation of its promoter, which has been demonstrated by the loss of methylation, ectopic expression, and periimplantation lethality of male embryos in the absence of maternal TRIM28 (Sampath Kumar et al 2017). In the near future, the catalogue of regions resistant to reprogramming will probably expand with development of the miniaturisation of sequencing technologies and growth in the number of studies on the DNA methylation landscape of embryos.…”

Section: Postfertilisation Reprogramming Of the Sperm Dna Methylomementioning

confidence: 99%

DNA methylation in bull spermatozoa: evolutionary impacts, interindividual variability, and contribution to the embryo

Kiefer

Perrier

2020

Can. J. Anim. Sci.

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The DNA methylome of spermatozoa results from a unique epigenetic reprogramming crucial for chromatin compaction and the protection of the paternal genetic heritage. Although bull semen is widely used for artificial insemination (AI), little is known about the sperm epigenome in cattle. The purpose of this review is to synthetize recent work on the bull sperm methylome in light of the knowledge accumulated in humans and model species. We will address sperm-specific DNA methylation features and their potential evolutionary impacts, with particular emphasis on hypomethylated regions and repetitive elements. We will review recent examples of interindividual variability and intra-individual plasticity of the bull sperm methylome as related to fertility and age, respectively. Finally, we will address paternal methylome reprogramming after fertilization, as well as the mechanisms potentially involved in epigenetic inheritance, and provide some examples of disturbances that alter the dynamics of reprogramming in cattle. Because the selection of AI bulls is closely based on their genotypes, we will also discuss the complex interplay between sequence polymorphism and DNA methylation, which represents both a difficulty in addressing the role of DNA methylation in shaping phenotypes and an opportunity to better understand genome plasticity.

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“…Tripartite motif-containing 28 (TRIM28), also known as KAP1 and TIF1β, is required for the maintenance of genomic imprinting [ 6 , 58 , 59 ]. TRIM28 is a maternal-effect protein, as indicated by the highly early embryonic lethality resulting from the dysregulation of genomic imprinting in mice lacking maternal TRIM28 [ 59 , 60 ]. It has also been reported that maternal TRIM28 not only maintains DNA methylation at germline imprints during early genome-wide reprogramming, but also regulates DNA methylation at imprinted gene promoters after genome-wide reprogramming [ 61 ].…”

Section: Resultsmentioning

confidence: 99%

Potential Roles of Intrinsic Disorder in Maternal-Effect Proteins Involved in the Maintenance of DNA Methylation

Liu

Wei

Huang

et al. 2017

IJMS

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DNA methylation is an important epigenetic modification that needs to be carefully controlled as a prerequisite for normal early embryogenesis. Compelling evidence now suggests that four maternal-effect proteins, primordial germ cell 7 (PGC7), zinc finger protein 57 (ZFP57), tripartite motif-containing 28 (TRIM28) and DNA methyltransferase (cytosine-5) 1 (DNMT1) are involved in the maintenance of DNA methylation. However, it is still not fully understood how these maternal-effect proteins maintain the DNA methylation imprint. We noticed that a feature common to these proteins is the presence of significant levels of intrinsic disorder so in this study we started from an intrinsic disorder perspective to try to understand these maternal-effect proteins. To do this, we firstly analysed the intrinsic disorder predispositions of PGC7, ZFP57, TRIM28 and DNMT1 by using a set of currently available computational tools and secondly conducted an intensive literature search to collect information on their interacting partners and structural characterization. Finally, we discuss the potential effect of intrinsic disorder on the function of these proteins in maintaining DNA methylation.

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Loss of maternal Trim28 causes male-predominant early embryonic lethality

Cited by 24 publications

References 29 publications

TRIM28 activates autophagy and promotes cell proliferation in glioblastoma

TRIM28 activates autophagy and promotes cell proliferation in glioblastoma

DNA methylation in bull spermatozoa: evolutionary impacts, interindividual variability, and contribution to the embryo

Potential Roles of Intrinsic Disorder in Maternal-Effect Proteins Involved in the Maintenance of DNA Methylation

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