Human and mouse ZFP57 proteins are functionally interchangeable in maintaining genomic imprinting at multiple imprinted regions in mouse ES cells

Takikawa, Sachiko; Wang, Xin; Ray, Chelsea; Vakulenko, Max; Bell, Fong T.; Li, Xiajun

doi:10.4161/epi.26544

Cited by 29 publications

(33 citation statements)

References 20 publications

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“…One reason why a repressor such as Ssm1 was not discovered earlier might be that the target recognition sequences are short and, because of the redundancy of the system, were not found. We do not know whether, in analogy with Zfp57 (Takikawa et al, 2013), Ssm1b targets imprinted genes.…”

Section: Discussionmentioning

confidence: 99%

Identification of Ssm1b, a novel modifier of DNA methylation, and its expression during mouse embryogenesis

et al. 2014

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The strain-specific modifier Ssm1 is responsible for the straindependent methylation of particular E. coli gpt-containing transgenic sequences. Here, we identify Ssm1 as the KRAB-zinc finger (ZF) gene 2610305D13Rik located on distal chromosome 4. Ssm1b is a member of a gene family with an unusual array of three ZFs. Ssm1 family members in C57BL/6 (B6) and DBA/2 (D2) mice have various amino acid changes in their ZF domain and in the linker between the KRAB and ZF domains. Ssm1b is expressed up to E8.5; its target transgene gains partial methylation by this stage as well. At E9.5, Ssm1b mRNA is no longer expressed but by then its target has become completely methylated. By contrast, in D2 embryos the transgene is essentially unmethylated. Methylation during B6 embryonic development depends on Dnmt3b but not Mecp2. In differentiating B6 embryonic stem cells methylation spreads from gpt to a co-integrated neo gene that has a similarly high CpG content as gpt, but neo alone is not methylated. In adult B6 mice, Ssm1b is expressed in ovaries, but in other organs only other members of the Ssm1 family are expressed. Interestingly, the transgene becomes methylated when crossed into some, but not other, wild mice that were kept outbred in the laboratory. Thus, polymorphisms for the methylation patterns seen among laboratory inbred strains are also found in a free-living population. This may imply that mice that do not have the Ssm1b gene may use another member of the Ssm1 family to control the potentially harmful expression of certain endogenous or exogenous genes.

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Section: Discussionmentioning

confidence: 99%

Identification of Ssm1b, a novel modifier of DNA methylation, and its expression during mouse embryogenesis

et al. 2014

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“…ZFP57-directed heterochromatin-like complexes are also likely to preserve methylation of imprinted gDMRs during human pre-implantation embryogenesis (Takikawa et al 2013), which undergoes a rapid loss of methylation that is almost complete by the third embryonic division with residual methylation diminishing further by the blastocyst stage (Guo et al 2014;Smith et al 2014). However, ZFP57 is unlikely to be the only factor that specifically preserves methylation at imprinted gDMRs.…”

Section: Comparison Of Imprinting Mechanisms In Animalsmentioning

confidence: 99%

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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“…KAP1-mediated DNA methylation is important for genomic imprinting and epigenetic reprogramming during embryogenesis [59][60][61][62][63] . Studies have demonstrated that ZFP57, a KRAB-ZFP important for maintaining DNA methylation at the imprinted loci, recruits KAP1 to imprinting control regions (ICRs) to interact with NP95, a protein responsible for recruiting DNMTs to hemimethylated DNA, resulting in the maintenance of genomic imprinting at ICRs [59,61] .…”

Section: Dna Methylationmentioning

confidence: 99%

“…It is worth noting that among these dysregulated genes in hippocampus, some are imprinted genes [103] . We speculate that Kap1 is also required for the maintenance of a set of specific imprinted genes because many recent studies have demonstrated that KAP1 mediates DNA methylation by recruiting DNMTs to ICRs during early embryogenesis [59,61,62] . More than maintaining normal cellular physiological functions, KAP1 also regulates several pathways in response to different stresses.…”

Section: Implications Of Kap1 In Cellular Physiologymentioning

confidence: 99%

KAPtain in charge of multiple missions: Emerging roles of KAP1

Cheng

Kuo

Ann

2014

WJBC

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from conditional knockout mouse models reveal that KAP1-deficiency significantly impairs vital physiological processes, such as immune maturation, stress vulnerability, hepatic metabolism, gamete development and erythropoiesis. In this review, we summarize and evaluate current literatures involving the biochemical and physiological functions of KAP1. In addition, increasing studies on the clinical relevance of KAP1 in cancer will also be discussed. Key words: KRAB domain-associated protein 1; Transcriptional co-repressor; Post-translational modification; Chromatin remodeling; KRAB-containing zinc finger protein Core tip: This review article primarily summarizes the current findings of KAP1/TRIM28/TIF1β, with focuses on its biochemical and physiological functions. Both the canonical transcriptional co-repressor function and the transcriptional-independent roles of KAP1 are discussed in detail. We highlight the post-translational modifications and the compartmentalized localization of KAP1 and suggest that the function of KAP1 could be spatial and temporal regulated in multiple physiological circumstances. Finally, we summarize the clinical relevance of KAP1 in cancer and discuss the possibility to translate the mechanistic studies of KAP1 to human pathophysiology in the future. Abstract KAP1/TRIM28/TIF1β was identified nearly twenty years ago as a universal transcriptional co-repressor because it interacts with a large KRAB-containing zinc finger protein (KRAB-ZFP) transcription factor family. Many studies demonstrate that KAP1 affects gene expression by regulating the transcription of KRAB-ZFP-specific loci, trans-repressing as a transcriptional co-repressor or epigenetically modulating chromatin structure. Emerging evidence suggests that KAP1 also functions independent of gene regulation by serving as a SUMO/ubiquitin E3 ligase or signaling scaffold protein to mediate signal transduction. KAP1 is subjected to multiple post-translational modifications (PTMs), including serine/tyrosine phosphorylation, SUMOylation, and acetylation, which coordinately regulate KAP1 function and its protein abundance. KAP1 is involved in multiple aspects of cellular activities, including DNA damage response, virus replication, cytokine production and stem cell pluripotency. Moreover, knockout of KAP1 results in embryonic lethality, indicating that KAP1 is crucial for embryonic development and possibly impacts a wide-range of (patho)physiological manifestations. Indeed, studies World J Biol Chem 2014 August 26; 5(3): 308-320 ISSN 1949-8454 (online)

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Human and mouse ZFP57 proteins are functionally interchangeable in maintaining genomic imprinting at multiple imprinted regions in mouse ES cells

Cited by 29 publications

References 20 publications

Identification of Ssm1b, a novel modifier of DNA methylation, and its expression during mouse embryogenesis

Identification of Ssm1b, a novel modifier of DNA methylation, and its expression during mouse embryogenesis

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

KAPtain in charge of multiple missions: Emerging roles of KAP1

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