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  1. Article ; Online: The enigma of DNA methylation in the mammalian oocyte [version 1; peer review

    Hannah Demond / Gavin Kelsey

    F1000Research, Vol

    4 approved]

    2020  Volume 9

    Abstract: The mammalian genome experiences profound setting and resetting of epigenetic patterns during the life-course. This is understood best for DNA methylation: the specification of germ cells, gametogenesis, and early embryo development are characterised by ... ...

    Abstract The mammalian genome experiences profound setting and resetting of epigenetic patterns during the life-course. This is understood best for DNA methylation: the specification of germ cells, gametogenesis, and early embryo development are characterised by phases of widespread erasure and rewriting of methylation. While mitigating against intergenerational transmission of epigenetic information, these processes must also ensure correct genomic imprinting that depends on faithful and long-term memory of gamete-derived methylation states in the next generation. This underscores the importance of understanding the mechanisms of methylation programming in the germline. De novo methylation in the oocyte is of particular interest because of its intimate association with transcription, which results in a bimodal methylome unique amongst mammalian cells. Moreover, this methylation landscape is entirely set up in a non-dividing cell, making the oocyte a fascinating model system in which to explore mechanistic determinants of methylation. Here, we summarise current knowledge on the oocyte DNA methylome and how it is established, focussing on recent insights from knockout models in the mouse that explore the interplay between methylation and chromatin states. We also highlight some remaining paradoxes and enigmas, in particular the involvement of non-nuclear factors for correct de novo methylation.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2020-02-01T00:00:00Z
    Publisher F1000 Research Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: A lucid interval in a victim of abusive head trauma with multiple parenchymal lacerations.

    Kachelski, Cree / Gavin, Kelsey / Head, Hayden / Horton, Danielle / Anderst, James

    Journal of forensic and legal medicine

    2023  Volume 101, Page(s) 102638

    Abstract: Abusive head trauma (AHT) is a leading cause of abusive deaths in children under age one. AHT can include intracranial hemorrhages, hypoxic ischemic injury, or parenchymal lacerations. Most infants with parenchymal lacerations present with acute ... ...

    Abstract Abusive head trauma (AHT) is a leading cause of abusive deaths in children under age one. AHT can include intracranial hemorrhages, hypoxic ischemic injury, or parenchymal lacerations. Most infants with parenchymal lacerations present with acute neurological symptoms. There has been some published literature on lucid intervals in cases of AHT; however, there has not been a described lucid interval with parenchymal lacerations. Parenchymal lacerations typically present with acute symptomatology such as seizures, alteration in mental status, or increased fussiness/lethargy given the damage to neurons and brain structure. We present a case of a healthy 2-month-old who ultimately was diagnosed with AHT and three parenchymal lacerations and had a 2.5 hour period of normal neurological status prior to acute decompensation.
    MeSH term(s) Infant ; Child ; Humans ; Lacerations ; Child Abuse/diagnosis ; Craniocerebral Trauma/etiology ; Intracranial Hemorrhages ; Magnetic Resonance Imaging/adverse effects
    Language English
    Publishing date 2023-12-26
    Publishing country England
    Document type Case Reports
    ZDB-ID 2268721-X
    ISSN 1878-7487 ; 1752-928X
    ISSN (online) 1878-7487
    ISSN 1752-928X
    DOI 10.1016/j.jflm.2023.102638
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Genomic imprinting beyond DNA methylation

    Courtney W. Hanna / Gavin Kelsey

    Genome Biology, Vol 18, Iss 1, Pp 1-

    a role for maternal histones

    2017  Volume 4

    Abstract: Abstract Inheritance of DNA methylation states from gametes determines genomic imprinting in mammals. A new study shows that repressive chromatin in oocytes can also confer imprinting. ...

    Abstract Abstract Inheritance of DNA methylation states from gametes determines genomic imprinting in mammals. A new study shows that repressive chromatin in oocytes can also confer imprinting.
    Keywords Biology (General) ; QH301-705.5 ; Genetics ; QH426-470
    Language English
    Publishing date 2017-09-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Single-cell multi-omic analysis profiles defective genome activation and epigenetic reprogramming associated with human pre-implantation embryo arrest

    Jose Ramon Hernandez Mora / Claudia Buhigas / Stephen Clark / Raquel Del Gallego Bonilla / Dagne Daskeviciute / Ana Monteagudo-Sánchez / Maria Eugenia Poo-Llanillo / Jose Vicente Medrano / Carlos Simón / Marcos Meseguer / Gavin Kelsey / David Monk

    Cell Reports, Vol 42, Iss 2, Pp 112100- (2023)

    2023  

    Abstract: Summary: During pre-implantation stages of mammalian development, maternally stored material promotes both the erasure of the sperm and oocyte epigenetic profiles and is responsible for concomitant genome activation. Here, we have utilized single-cell ... ...

    Abstract Summary: During pre-implantation stages of mammalian development, maternally stored material promotes both the erasure of the sperm and oocyte epigenetic profiles and is responsible for concomitant genome activation. Here, we have utilized single-cell methylome and transcriptome sequencing (scM&T-seq) to quantify both mRNA expression and DNA methylation in oocytes and a developmental series of human embryos at single-cell resolution. We fully characterize embryonic genome activation and maternal transcript degradation and map key epigenetic reprogramming events in developmentally high-quality embryos. By comparing these signatures with early embryos that have undergone spontaneous cleavage-stage arrest, as determined by time-lapse imaging, we identify embryos that fail to appropriately activate their genomes or undergo epigenetic reprogramming. Our results indicate that a failure to successfully accomplish these essential milestones impedes the developmental potential of pre-implantation embryos and is likely to have important implications, similar to aneuploidy, for the success of assisted reproductive cycles.
    Keywords CP: Stem cell research ; Biology (General) ; QH301-705.5
    Subject code 572
    Language English
    Publishing date 2023-02-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Culture Medium and Sex Drive Epigenetic Reprogramming in Preimplantation Bovine Embryos

    Sebastian Canovas / Elena Ivanova / Meriem Hamdi / Fernando Perez-Sanz / Dimitrios Rizos / Gavin Kelsey / Pilar Coy

    International Journal of Molecular Sciences, Vol 22, Iss 6426, p

    2021  Volume 6426

    Abstract: Assisted reproductive technologies impact transcriptome and epigenome of embryos and can result in long-term phenotypic consequences. Whole-genome DNA methylation profiles from individual bovine blastocysts in vivo- and in vitro-derived (using three ... ...

    Abstract Assisted reproductive technologies impact transcriptome and epigenome of embryos and can result in long-term phenotypic consequences. Whole-genome DNA methylation profiles from individual bovine blastocysts in vivo- and in vitro-derived (using three sources of protein: reproductive fluids, blood serum and bovine serum albumin) were generated. The impact of in vitro culture on DNA methylation was analyzed, and sex-specific methylation differences at blastocyst stage were uncovered. In vivo embryos showed the highest levels of methylation (29.5%), close to those produced in vitro with serum, whilst embryos produced in vitro with reproductive fluids or albumin showed less global methylation (25–25.4%). During repetitive element analysis, the serum group was the most affected. DNA methylation differences between in vivo and in vitro groups were more frequent in the first intron than in CpGi in promoters. Moreover, hierarchical cluster analysis showed that sex produced a stronger bias in the results than embryo origin. For each group, distance between male and female embryos varied, with in vivo blastocyst showing a lesser distance. Between the sexually dimorphic methylated tiles, which were biased to X-chromosome, critical factors for reproduction, developmental process, cell proliferation and DNA methylation machinery were included. These results support the idea that blastocysts show sexually-dimorphic DNA methylation patterns, and the known picture about the blastocyst methylome should be reconsidered.
    Keywords embryo ; DNA methylation ; epigenetic ; preimplantation ; sexual dimorphism ; bovine ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 570
    Language English
    Publishing date 2021-06-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Leptin Signaling in the Ovary of Diet-Induced Obese Mice Regulates Activation of NOD-Like Receptor Protein 3 Inflammasome

    Marek Adamowski / Karolina Wołodko / Joana Oliveira / Juan Castillo-Fernandez / Daniel Murta / Gavin Kelsey / António M. Galvão

    Frontiers in Cell and Developmental Biology, Vol

    2021  Volume 9

    Abstract: Obesity leads to ovarian dysfunction and the establishment of local leptin resistance. The aim of our study was to characterize the levels of NOD-like receptor protein 3 (NLRP3) inflammasome activation in ovaries and liver of mice during obesity ... ...

    Abstract Obesity leads to ovarian dysfunction and the establishment of local leptin resistance. The aim of our study was to characterize the levels of NOD-like receptor protein 3 (NLRP3) inflammasome activation in ovaries and liver of mice during obesity progression. Furthermore, we tested the putative role of leptin on NLRP3 regulation in those organs. C57BL/6J female mice were treated with equine chorionic gonadotropin (eCG) or human chorionic gonadotropin (hCG) for estrous cycle synchronization and ovary collection. In diet-induced obesity (DIO) protocol, mice were fed chow diet (CD) or high-fat diet (HFD) for 4 or 16 weeks, whereas in the hyperleptinemic model (LEPT), mice were injected with leptin for 16 days (16 L) or saline (16 C). Finally, the genetic obese leptin-deficient ob/ob (+/? and −/−) mice were fed CD for 4 week. Either ovaries and liver were collected, as well as cumulus cells (CCs) after superovulation from DIO and LEPT. The estrus cycle synchronization protocol showed increased protein levels of NLRP3 and interleukin (IL)-18 in diestrus, with this stage used for further sample collections. In DIO, protein expression of NLRP3 inflammasome components was increased in 4 week HFD, but decreased in 16 week HFD. Moreover, NLRP3 and IL-1β were upregulated in 16 L and downregulated in ob/ob. Transcriptome analysis of CC showed common genes between LEPT and 4 week HFD modulating NLRP3 inflammasome. Liver analysis showed NLRP3 protein upregulation after 16 week HFD in DIO, but also its downregulation in ob/ob−/−. We showed the link between leptin signaling and NLRP3 inflammasome activation in the ovary throughout obesity progression in mice, elucidating the molecular mechanisms underpinning ovarian failure in maternal obesity.
    Keywords ovary ; inflammation ; obesity ; NLRP3 inflammasome ; leptin ; Biology (General) ; QH301-705.5
    Subject code 630
    Language English
    Publishing date 2021-11-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: A DNMT3A PWWP mutation leads to methylation of bivalent chromatin and growth retardation in mice

    Gintarė Sendžikaitė / Courtney W. Hanna / Kathleen R. Stewart-Morgan / Elena Ivanova / Gavin Kelsey

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 16

    Abstract: PWWP domains of DNMT3A and DNMT3B are proposed to interact with H3K36me3. Here the authors present a mouse model carrying a D329A point mutation in the DNMT3A PWWP domain and find this causes dominant postnatal growth retardation, with aberrant ... ...

    Abstract PWWP domains of DNMT3A and DNMT3B are proposed to interact with H3K36me3. Here the authors present a mouse model carrying a D329A point mutation in the DNMT3A PWWP domain and find this causes dominant postnatal growth retardation, with aberrant progressive gain of DNA methylation across domains marked by H3K27me3 in adult tissues.
    Keywords Science ; Q
    Language English
    Publishing date 2019-04-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: A DNMT3A PWWP mutation leads to methylation of bivalent chromatin and growth retardation in mice

    Gintarė Sendžikaitė / Courtney W. Hanna / Kathleen R. Stewart-Morgan / Elena Ivanova / Gavin Kelsey

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 16

    Abstract: PWWP domains of DNMT3A and DNMT3B are proposed to interact with H3K36me3. Here the authors present a mouse model carrying a D329A point mutation in the DNMT3A PWWP domain and find this causes dominant postnatal growth retardation, with aberrant ... ...

    Abstract PWWP domains of DNMT3A and DNMT3B are proposed to interact with H3K36me3. Here the authors present a mouse model carrying a D329A point mutation in the DNMT3A PWWP domain and find this causes dominant postnatal growth retardation, with aberrant progressive gain of DNA methylation across domains marked by H3K27me3 in adult tissues.
    Keywords Science ; Q
    Language English
    Publishing date 2019-04-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: FOXA2 controls the anti-oxidant response in FH-deficient cells

    Connor Rogerson / Marco Sciacovelli / Lucas A. Maddalena / Andromachi Pouikli / Marc Segarra-Mondejar / Lorea Valcarcel-Jimenez / Christina Schmidt / Ming Yang / Elena Ivanova / Joshua Kent / Ariane Mora / Danya Cheeseman / Jason S. Carroll / Gavin Kelsey / Christian Frezza

    Cell Reports, Vol 42, Iss 7, Pp 112751- (2023)

    2023  

    Abstract: Summary: Hereditary leiomyomatosis and renal cell cancer (HLRCC) is a cancer syndrome caused by inactivating germline mutations in fumarate hydratase (FH) and subsequent accumulation of fumarate. Fumarate accumulation leads to profound epigenetic changes ...

    Abstract Summary: Hereditary leiomyomatosis and renal cell cancer (HLRCC) is a cancer syndrome caused by inactivating germline mutations in fumarate hydratase (FH) and subsequent accumulation of fumarate. Fumarate accumulation leads to profound epigenetic changes and the activation of an anti-oxidant response via nuclear translocation of the transcription factor NRF2. The extent to which chromatin remodeling shapes this anti-oxidant response is currently unknown. Here, we explored the effects of FH loss on the chromatin landscape to identify transcription factor networks involved in the remodeled chromatin landscape of FH-deficient cells. We identify FOXA2 as a key transcription factor that regulates anti-oxidant response genes and subsequent metabolic rewiring cooperating without direct interaction with the anti-oxidant regulator NRF2. The identification of FOXA2 as an anti-oxidant regulator provides additional insights into the molecular mechanisms behind cell responses to fumarate accumulation and potentially provides further avenues for therapeutic intervention for HLRCC.
    Keywords CP: Molecular biology ; CP: Cancer ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2023-07-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article: DNA Methylation in Embryo Development: Epigenetic Impact of ART (Assisted Reproductive Technologies)

    Canovas, Sebastian / Gavin Kelsey / Pablo J. Ross / Pilar Coy

    BioEssays. 2017 Nov., v. 39, no. 11

    2017  

    Abstract: DNA methylation can be considered a component of epigenetic memory with a critical role during embryo development, and which undergoes dramatic reprogramming after fertilization. Though it has been a focus of research for many years, the reprogramming ... ...

    Abstract DNA methylation can be considered a component of epigenetic memory with a critical role during embryo development, and which undergoes dramatic reprogramming after fertilization. Though it has been a focus of research for many years, the reprogramming mechanism is still not fully understood. Recent results suggest that absence of maintenance at DNA replication is a major factor, and that there is an unexpected role for TET3‐mediated oxidation of 5mC to 5hmC in guarding against de novo methylation. Base‐resolution and genome‐wide profiling methods are enabling more comprehensive assessments of the extent to which ART might impair DNA methylation reprogramming, and which sequence elements are most vulnerable. Indeed, as we also review here, studies showing the effect of culture media, ovarian stimulation or embryo transfer on the methylation pattern of embryos emphasize the need to face ART‐associated defects and search for strategies to mitigate adverse effects on the health of ART‐derived children.
    Keywords adverse effects ; animal ovaries ; children ; culture media ; DNA methylation ; DNA replication ; embryo transfer ; embryogenesis ; epigenetics ; oxidation
    Language English
    Dates of publication 2017-11
    Size p. .
    Publishing place John Wiley & Sons, Ltd
    Document type Article
    Note REVIEW
    ZDB-ID 50140-2
    ISSN 1521-1878 ; 0265-9247
    ISSN (online) 1521-1878
    ISSN 0265-9247
    DOI 10.1002/bies.201700106
    Database NAL-Catalogue (AGRICOLA)

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