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  1. Article ; Online: In utero exposure to arsenite contributes to metabolic and reproductive dysfunction in male offspring of CD-1 mice.

    Rodriguez, Karina F / Mellouk, Namya / Ungewitter, Erica K / Nicol, Barbara / Liu, Chang / Brown, Paula R / Willson, Cynthia J / Yao, Humphrey H-C

    Reproductive toxicology (Elmsford, N.Y.)

    2020  Volume 95, Page(s) 95–103

    Abstract: In utero exposure to arsenite (iAs) is known to increase disease risks later in life. We investigated the effect of in utero exposure to iAs in the drinking water on metabolic and reproductive parameters in male mouse offspring at postnatal and adult ... ...

    Abstract In utero exposure to arsenite (iAs) is known to increase disease risks later in life. We investigated the effect of in utero exposure to iAs in the drinking water on metabolic and reproductive parameters in male mouse offspring at postnatal and adult stages. Pregnant CD-1 mice were exposed to iAs (as sodium arsenite) in the drinking water at 0 (control), 10 ppb (EPA standard for drinking water), and 42.5 ppm (tumor-inducing dose in mice) from embryonic day (E) 10-18. At birth, pups were fostered to unexposed females. Male offspring exposed to 10 ppb in utero exhibited increase in body weight at birth when compared to controls. Male offspring exposed to 42.5 ppm in utero showed a tendency for increased body weight and a smaller anogenital distance. The body weight in iAs-exposed pups continued to increase significantly compared to control at 3 weeks and 11 weeks of age. At 5 months of age, iAs-exposed males exhibited greater body fat content and glucose intolerance. Male offspring exposed to 10 ppb in utero had higher circulating levels of leptin compared to control. In addition, males exposed to 42.5 ppm in utero exhibited decreased total number of pups born compared to controls and lower average number of litters sired over a six-month period. These results indicate that in utero exposure to iAs at either human relevant concentration or tumor-inducing concentration is a potential cause of developmental origin of metabolic and reproductive dysfunction in adult male mice.
    MeSH term(s) Animals ; Arsenites/toxicity ; Body Weight/drug effects ; Female ; Fertility/drug effects ; Glucose/metabolism ; Leptin/blood ; Male ; Maternal-Fetal Exchange ; Mice ; Pregnancy ; Prenatal Exposure Delayed Effects ; Spermatozoa/drug effects ; Testis/drug effects ; Testis/metabolism ; Testis/pathology
    Chemical Substances Arsenites ; Leptin ; Glucose (IY9XDZ35W2) ; arsenite (N5509X556J)
    Language English
    Publishing date 2020-05-17
    Publishing country United States
    Document type Journal Article
    ZDB-ID 639342-1
    ISSN 1873-1708 ; 0890-6238
    ISSN (online) 1873-1708
    ISSN 0890-6238
    DOI 10.1016/j.reprotox.2020.05.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Delta40p53 controls the switch from pluripotency to differentiation by regulating IGF signaling in ESCs.

    Ungewitter, Erica / Scrable, Heidi

    Genes & development

    2010  Volume 24, Issue 21, Page(s) 2408–2419

    Abstract: Δ40p53 is a transactivation-deficient isoform of the tumor suppressor p53. We discovered that Δ40p53, in addition to being highly expressed in embryonic stem cells (ESCs), is the major p53 isoform during early stages of embryogenesis in the mouse. By ... ...

    Abstract Δ40p53 is a transactivation-deficient isoform of the tumor suppressor p53. We discovered that Δ40p53, in addition to being highly expressed in embryonic stem cells (ESCs), is the major p53 isoform during early stages of embryogenesis in the mouse. By altering the dose of Δ40p53 in ESCs, we identified a critical role for this isoform in maintaining the ESC state. Haploinsufficiency for Δ40p53 causes a loss of pluripotency in ESCs and acquisition of a somatic cell cycle, while increased dosage of Δ40p53 prolongs pluripotency and inhibits progression to a more differentiated state. Δ40p53 controls the switch from pluripotent ESCs to differentiated somatic cells by controlling the activity of full-length p53 at critical targets such as Nanog and the IGF-1 receptor (IGF-1R). The IGF axis plays a central role in the switch between pluripotency and differentiation in ESCs-and Δ40p53, by controlling the level of the IGF-1R, acts as a master regulator of this switch. We propose that this is the primary function of Δ40p53 in cells of the early embryo and stem cells, which are the only normal cells in which this isoform is expressed.
    MeSH term(s) Amino Acid Sequence ; Animals ; Blotting, Western ; Cell Cycle ; Cell Differentiation ; Cell Line ; Cell Nucleus/metabolism ; Cell Survival ; Cytoplasm/metabolism ; Embryonic Stem Cells/cytology ; Embryonic Stem Cells/metabolism ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Immunohistochemistry ; Mice ; Mice, 129 Strain ; Mice, Inbred ICR ; Molecular Sequence Data ; Nanog Homeobox Protein ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Pluripotent Stem Cells/cytology ; Pluripotent Stem Cells/metabolism ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Protein Isoforms/physiology ; Receptor, IGF Type 1/genetics ; Receptor, IGF Type 1/physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Tumor Suppressor Protein p53/physiology
    Chemical Substances Homeodomain Proteins ; NANOG protein, human ; Nanog Homeobox Protein ; Protein Isoforms ; Tumor Suppressor Protein p53 ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Receptor, IGF Type 1 (EC 2.7.10.1)
    Language English
    Publishing date 2010-11-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.1987810
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: A new mouse line for cell ablation by diphtheria toxin subunit A controlled by a Cre-dependent FLEx switch.

    Plummer, Nicholas W / Ungewitter, Erica K / Smith, Kathleen G / Yao, Humphrey H-C / Jensen, Patricia

    Genesis (New York, N.Y. : 2000)

    2017  Volume 55, Issue 10

    Abstract: Recombinase responsive mouse lines expressing diphtheria toxin subunit A (DTA) are well established tools for targeted ablation of genetically defined cell populations. Here we describe a new knock-in allele at the Gt(Rosa)26Sor locus that retains the ... ...

    Abstract Recombinase responsive mouse lines expressing diphtheria toxin subunit A (DTA) are well established tools for targeted ablation of genetically defined cell populations. Here we describe a new knock-in allele at the Gt(Rosa)26Sor locus that retains the best features of previously described DTA alleles-including a CAG promoter, attenuated mutant DTA cDNA, and ubiquitous EGFP labeling-with the addition of a Cre-dependent FLEx switch for tight control of expression. The FLEx switch consists of two pairs of antiparallel lox sites requiring Cre-mediated recombination for inversion of the DTA to the proper orientation for transcription. We demonstrate its utility by Cre-dependent ablation of both a broad domain in the embryonic nervous system and a discrete population of cells in the fetal gonads. We conclude that this new DTA line is useful for targeted ablation of genetically-defined cell populations.
    MeSH term(s) Animals ; Diphtheria Toxin/genetics ; Diphtheria Toxin/metabolism ; Gene Knock-In Techniques/methods ; Gonads/cytology ; Gonads/embryology ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Integrases/genetics ; Integrases/metabolism ; Mice ; Nervous System/cytology ; Nervous System/embryology ; Promoter Regions, Genetic ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism
    Chemical Substances Diphtheria Toxin ; Recombinant Proteins ; Green Fluorescent Proteins (147336-22-9) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
    Language English
    Publishing date 2017-09-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2004544-X
    ISSN 1526-968X ; 1526-954X
    ISSN (online) 1526-968X
    ISSN 1526-954X
    DOI 10.1002/dvg.23067
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Antagonistic pleiotropy and p53.

    Ungewitter, Erica / Scrable, Heidi

    Mechanisms of ageing and development

    2008  Volume 130, Issue 1-2, Page(s) 10–17

    Abstract: George Williams' antagonistic pleiotropy theory of aging proposes that cellular damage and organismal aging are caused by pleiotrophic genes, or genes with multiple phenotypic effects [Williams, G.C., 1957. Pleiotropy, natural selection, and the ... ...

    Abstract George Williams' antagonistic pleiotropy theory of aging proposes that cellular damage and organismal aging are caused by pleiotrophic genes, or genes with multiple phenotypic effects [Williams, G.C., 1957. Pleiotropy, natural selection, and the evolution of senescence. Evolution 11, 398-411]. According to this theory, genes that exhibit antagonistic pleiotropy increase the odds of successful reproduction early in life, but have deleterious effects later in life. The tumor suppressor p53 confers protection against cancer (and death) by interrupting the abnormal proliferation of cells. When control of proliferation is applied to normal stem cells, however, it can impair tissue homeostasis and accelerate aging. We use data from recently developed models of accelerated aging in mice to determine if the deleterious effects of p53 on aging reflect antagonistic pleiotropy of the p53 gene or are attributable to genes that can modify p53 activity but are evolving independently.
    MeSH term(s) Aged ; Aging/physiology ; Animals ; Cell Division/physiology ; Cellular Senescence/physiology ; Evolution, Molecular ; Humans ; Neoplasms/physiopathology ; Stem Cells/cytology ; Stem Cells/physiology ; Tumor Suppressor Protein p53/physiology
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2008-07-01
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 183915-9
    ISSN 1872-6216 ; 0047-6374
    ISSN (online) 1872-6216
    ISSN 0047-6374
    DOI 10.1016/j.mad.2008.06.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Loss of Glis3 causes dysregulation of retrotransposon silencing and germ cell demise in fetal mouse testis.

    Ungewitter, Erica K / Rotgers, Emmi / Kang, Hong Soon / Lichti-Kaiser, Kristin / Li, Leping / Grimm, Sara A / Jetten, Anton M / Yao, Humphrey H-C

    Scientific reports

    2018  Volume 8, Issue 1, Page(s) 9662

    Abstract: Fetal germ cell development is regulated by an elaborate combination of cell-extrinsic and cell-intrinsic signals. Here we identify a novel role for the Krüppel-like transcription factor Gli-Similar 3 (Glis3) in male germ cell development in the mouse ... ...

    Abstract Fetal germ cell development is regulated by an elaborate combination of cell-extrinsic and cell-intrinsic signals. Here we identify a novel role for the Krüppel-like transcription factor Gli-Similar 3 (Glis3) in male germ cell development in the mouse embryos. Glis3 is expressed in male germ cells during the brief window of time prior to initiation of piRNA-dependent retrotransposon surveillance. Disruption of Glis3 function led to a widespread reduction in retrotransposon silencing factors, aberrant retrotransposon expression and pronounced germ cell loss. Experimental induction of precocious Glis3 expression in vivo before its normal expression resulted in premature expression of several piRNA pathway members, suggesting that GLIS3 is necessary for the activation of the retrotransposon silencing programs. Our findings reveal an unexpected role for GLIS3 in the development of male germ cells and point to a central role for GLIS3 in the control of retrotransposon silencing in the fetal germline.
    MeSH term(s) Animals ; Cell Survival/genetics ; DNA-Binding Proteins ; Fetus/cytology ; Gene Expression Regulation ; Gene Knockout Techniques ; Gene Silencing ; Male ; Mice ; Phenotype ; Repressor Proteins/deficiency ; Repressor Proteins/genetics ; Retroelements/genetics ; Spermatozoa/metabolism ; Testis/cytology ; Trans-Activators/deficiency ; Trans-Activators/genetics
    Chemical Substances DNA-Binding Proteins ; Glis3 protein, mouse ; Repressor Proteins ; Retroelements ; Trans-Activators
    Language English
    Publishing date 2018-06-25
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-018-27843-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: From the Cover: Teratogenic Effects of in Utero Exposure to Di-(2-Ethylhexyl)-Phthalate (DEHP) in B6:129S4 Mice.

    Ungewitter, Erica / Rotgers, Emmi / Bantukul, Tanika / Kawakami, Yasuhiko / Kissling, Grace E / Yao, Humphrey Hung-Chang

    Toxicological sciences : an official journal of the Society of Toxicology

    2016  Volume 157, Issue 1, Page(s) 8–19

    Abstract: Intrauterine exposure to phthalates is known to cause disorders of male reproductive function including androgen insufficiency, decreased fertility, and germ cell defects in rodents. In this study, we set out to investigate the effects of intrauterine ... ...

    Abstract Intrauterine exposure to phthalates is known to cause disorders of male reproductive function including androgen insufficiency, decreased fertility, and germ cell defects in rodents. In this study, we set out to investigate the effects of intrauterine exposure to di-(2-ethylhexyl)-phthalate (DEHP) on fetal development of the B6:129S4 mouse strain. Time-mated pregnant C57BL/6 dams were exposed to 0, 5, 250, or 500 mg/kg DEHP with corn oil as the vehicle via oral gavage from embryonic days (E)7 to 16. Survival and gross morphology of the pups were analyzed one day after the last treatment. Anogenital distance (AGD) and testicular cell functions were examined in male embryos to confirm the known effects of phthalate exposure. DEHP exposure significantly reduced the survival rate of fetuses in the 250 and 500 mg/kg dosage groups compared with the control and 5 mg/kg groups. Exposure to 250 and 500 mg/kg DEHP was teratogenic and induced exencephaly and limb malformations such as polydactyly in the B6:126S4 embryos. No gross malformations were observed in control or 5 mg/kg DEHP groups. In male embryos, exposure to both 5 and 250 mg/kg DEHP in utero was sufficient to induce the formation of multinucleated germ cells in the testes and widespread changes in mRNA expression of germ cell, interstitium and Sertoli cell-associated genes. These findings reveal that intrauterine DEHP exposure has a strong teratogenic, and lethal impact on the fetuses of B6:129S4 mouse strain.
    MeSH term(s) Abnormalities, Drug-Induced ; Animals ; Diethylhexyl Phthalate/toxicity ; Dose-Response Relationship, Drug ; Female ; Fetal Death ; Fetal Development/drug effects ; Gene Expression Regulation, Developmental/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Pregnancy ; Teratogens/toxicity ; Testis/cytology ; Testis/drug effects ; Testis/embryology
    Chemical Substances Teratogens ; Diethylhexyl Phthalate (C42K0PH13C)
    Language English
    Publishing date 2016-11-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1420885-4
    ISSN 1096-0929 ; 1096-6080
    ISSN (online) 1096-0929
    ISSN 1096-6080
    DOI 10.1093/toxsci/kfx019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Response to "Comment on 'Effects of in Utero Exposure to Arsenic during the Second Half of Gestation on Reproductive End Points and Metabolic Parameters in Female CD-1 Mice'".

    Rodriguez, Karina F / Ungewitter, Erica K / Crespo-Mejias, Yasmin / Liu, Chang / Nicol, Barbara / Kissling, Grace E / Yao, Humphrey Hung-Chang

    Environmental health perspectives

    2016  Volume 124, Issue 3, Page(s) A46–7

    MeSH term(s) Animals ; Arsenic ; Arsenites ; Female ; Mice ; Prenatal Exposure Delayed Effects ; Reproduction
    Chemical Substances Arsenites ; Arsenic (N712M78A8G)
    Language English
    Publishing date 2016-03
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 195189-0
    ISSN 1552-9924 ; 0091-6765 ; 1078-0475
    ISSN (online) 1552-9924
    ISSN 0091-6765 ; 1078-0475
    DOI 10.1289/ehp.1511181
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Effects of in Utero Exposure to Arsenic during the Second Half of Gestation on Reproductive End Points and Metabolic Parameters in Female CD-1 Mice.

    Rodriguez, Karina F / Ungewitter, Erica K / Crespo-Mejias, Yasmin / Liu, Chang / Nicol, Barbara / Kissling, Grace E / Yao, Humphrey Hung-Chang

    Environmental health perspectives

    2016  Volume 124, Issue 3, Page(s) 336–343

    Abstract: Background: Mice exposed to high levels of arsenic in utero have increased susceptibility to tumors such as hepatic and pulmonary carcinomas when they reach adulthood. However, the effects of in utero arsenic exposure on general physiological functions ... ...

    Abstract Background: Mice exposed to high levels of arsenic in utero have increased susceptibility to tumors such as hepatic and pulmonary carcinomas when they reach adulthood. However, the effects of in utero arsenic exposure on general physiological functions such as reproduction and metabolism remain unclear.
    Objectives: We evaluated the effects of in utero exposure to inorganic arsenic at the U.S. Environmental Protection Agency (EPA) drinking water standard (10 ppb) and at tumor-inducing levels (42.5 ppm) on reproductive end points and metabolic parameters when the exposed females reached adulthood.
    Methods: Pregnant CD-1 mice were exposed to sodium arsenite [none (control), 10 ppb, or 42.5 ppm] in drinking water from gestational day 10 to birth, the window of organ formation. At birth, exposed offspring were fostered to unexposed dams. We examined reproductive end points (age at vaginal opening, reproductive hormone levels, estrous cyclicity, and fertility) and metabolic parameters (body weight changes, hormone levels, body fat content, and glucose tolerance) in the exposed females when they reached adulthood.
    Results: Arsenic-exposed females (10 ppb and 42.5 ppm) exhibited early onset of vaginal opening. Fertility was not affected when females were exposed to the 10-ppb dose. However, the number of litters per female was decreased in females exposed to 42.5 ppm of arsenic in utero. In both 10-ppb and 42.5-ppm groups, arsenic-exposed females had significantly greater body weight gain, body fat content, and glucose intolerance.
    Conclusion: Our findings revealed unexpected effects of in utero exposure to arsenic: exposure to both a human-relevant low dose and a tumor-inducing level led to early onset of vaginal opening and to obesity in female CD-1 mice.
    MeSH term(s) Adipose Tissue/drug effects ; Animals ; Arsenites/toxicity ; Blood Glucose/metabolism ; Drinking Water/chemistry ; Environmental Pollutants/toxicity ; Estrous Cycle/drug effects ; Female ; Fertility/drug effects ; Gonadotropins/blood ; Mice ; Pregnancy ; Prenatal Exposure Delayed Effects/metabolism ; Prenatal Exposure Delayed Effects/physiopathology ; Reproduction/drug effects ; Sexual Maturation/drug effects ; Sodium Compounds/toxicity ; Vagina/drug effects ; Vagina/physiology
    Chemical Substances Arsenites ; Blood Glucose ; Drinking Water ; Environmental Pollutants ; Gonadotropins ; Sodium Compounds ; sodium arsenite (48OVY2OC72)
    Language English
    Publishing date 2016-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
    ZDB-ID 195189-0
    ISSN 1552-9924 ; 0091-6765 ; 1078-0475
    ISSN (online) 1552-9924
    ISSN 0091-6765 ; 1078-0475
    DOI 10.1289/ehp.1509703
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Running on empty: how p53 controls INS/IGF signaling and affects life span.

    Scrable, Heidi / Medrano, Silvia / Ungewitter, Erica

    Experimental gerontology

    2008  Volume 44, Issue 1-2, Page(s) 93–100

    Abstract: In higher organisms dependent on the regenerative ability of tissue stem cells to maintain tissue integrity throughout adulthood, the failure of stem cells to replace worn out, dead, or damaged cells is seen as one mechanism that limits life span. In ... ...

    Abstract In higher organisms dependent on the regenerative ability of tissue stem cells to maintain tissue integrity throughout adulthood, the failure of stem cells to replace worn out, dead, or damaged cells is seen as one mechanism that limits life span. In these organisms, tumor suppressors such as p53 are central participants in the control of longevity because they regulate stem cell proliferation. Several recent reports have identified p53 as a longevity gene in organisms such as Caenorhabditis elegans and Drosophila melanogaster, which lack proliferative stem cells in all but the germline and have relatively short life spans. This has forced us to reevaluate the role of p53 in the control of life span. We discuss how p53 might regulate longevity in both long- and short-lived species by controlling the activity of insulin-like molecules that operate in proliferating and non-proliferating compartments of adult somatic tissues. We also discuss the hierarchical structure of life span regulation where loss of p53 has life span extending effects. Finally, we suggest a molecular mechanism by which p53 might facilitate the response to severe nutrient deprivation that allows metabolically active cells to survive periods of starvation. Paradoxically, loss of p53 function in these cells would compromise life span.
    MeSH term(s) Animals ; Caenorhabditis elegans ; Cell Proliferation ; Cell Survival ; Drosophila melanogaster ; Humans ; Insulin/metabolism ; Life Expectancy ; Mice ; Oxidative Stress ; Signal Transduction/physiology ; Somatomedins/metabolism ; Starvation/metabolism ; Stem Cells/physiology ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Insulin ; Somatomedins ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2008-06-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 390992-x
    ISSN 1873-6815 ; 0531-5565
    ISSN (online) 1873-6815
    ISSN 0531-5565
    DOI 10.1016/j.exger.2008.05.017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Loss of Glis3 causes dysregulation of retrotransposon silencing and germ cell demise in fetal mouse testis

    Erica K. Ungewitter / Emmi Rotgers / Hong Soon Kang / Kristin Lichti-Kaiser / Leping Li / Sara A. Grimm / Anton M. Jetten / Humphrey H.-C. Yao

    Scientific Reports, Vol 8, Iss 1, Pp 1-

    2018  Volume 10

    Abstract: Abstract Fetal germ cell development is regulated by an elaborate combination of cell-extrinsic and cell-intrinsic signals. Here we identify a novel role for the Krüppel-like transcription factor Gli-Similar 3 (Glis3) in male germ cell development in the ...

    Abstract Abstract Fetal germ cell development is regulated by an elaborate combination of cell-extrinsic and cell-intrinsic signals. Here we identify a novel role for the Krüppel-like transcription factor Gli-Similar 3 (Glis3) in male germ cell development in the mouse embryos. Glis3 is expressed in male germ cells during the brief window of time prior to initiation of piRNA-dependent retrotransposon surveillance. Disruption of Glis3 function led to a widespread reduction in retrotransposon silencing factors, aberrant retrotransposon expression and pronounced germ cell loss. Experimental induction of precocious Glis3 expression in vivo before its normal expression resulted in premature expression of several piRNA pathway members, suggesting that GLIS3 is necessary for the activation of the retrotransposon silencing programs. Our findings reveal an unexpected role for GLIS3 in the development of male germ cells and point to a central role for GLIS3 in the control of retrotransposon silencing in the fetal germline.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2018-06-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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