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Genes & development 9건

  1. [해외논문]   Finding the start site: redefining the human initiator element   SCI SCIE

    Kugel, Jennifer F. (Department of Chemistry and Biochemistry, University of Colorado, Boulder, Colorado 80309, USA ) , Goodrich, James A. (Department of Chemistry and Biochemistry, University of Colorado, Boulder, Colorado 80309, USA)
    Genes & development v.31 no.1 ,pp. 1 - 2 , 2017 , 0890-9369 ,

    초록

    In this Outlook, Kugel and Goodrich discuss the findings in a study by Vo ngoc et al. in this issue, which found that transcripts with focused sites of initiation were transcribed from promoters containing a new consensus sequence for the human initiator (Inr) core promoter element. Transcription by RNA polymerase II (Pol II) is dictated in part by core promoter elements, which are DNA sequences flanking the transcription start site (TSS) that help direct the proper initiation of transcription. Taking advantage of recent advances in genome-wide sequencing approaches, Vo ngoc and colleagues (pp. 6–11) identified transcripts with focused sites of initiation and found that many were transcribed from promoters containing a new consensus sequence for the human initiator (Inr) core promoter element.

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    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  2. [해외논문]   Putting PHDs to work: PHF11 clears the way for EXO1 in double-strand break repair   SCI SCIE

    Zahn, Karl E. (Department of Cancer Biology, Department Pathology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA ) , Greenberg, Roger A. (Department of Cancer Biology, Department Pathology, Abramson Family Cancer Research Institute, Basser Research Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA)
    Genes & development v.31 no.1 ,pp. 3 - 5 , 2017 , 0890-9369 ,

    초록

    This Outlook discusses the finding by Gong et al. that PHF11 encodes a previously unknown DNA damage response factor involved in 5′ end resection, ATR signaling, and homologous recombination. In this issue of Genes & Development , Gong and colleagues (pp. 46–58) bring to light a functional role for plant homeodomain finger 11 (PHF11) in 5′ end resection at DNA double-strand breaks (DSBs). Using the proteomics of isolated chromatin segments (PICh) technique to purify deprotected telomeres, PHF11 was enriched as cells mounted a DNA damage response (DDR) against exposed chromosome ends. The study reveals interactions between PHF11 and multiple DNA repair proteins and suggests that PHF11 mediates 5′ end resection by negotiating RPA-coated DNA repair intermediates. This finding provides a novel context for mediator-catalyzed RPA exchanges during the multistep process of homologous recombination (HR).

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  3. [해외논문]   The human initiator is a distinct and abundant element that is precisely positioned in focused core promoters   SCI SCIE

    Vo ngoc, Long (Section of Molecular Biology, University of California at San Diego, La Jolla, California 92093, USA ) , Cassidy, California Jack (Section of Molecular Biology, University of California at San Diego, La Jolla, California 92093, USA ) , Huang, Cassidy Yunjing (Section of Molecular Biology, University of California at San Diego, La Jolla, California 92093, USA ) , Duttke, Sascha H.C. (Section of Molecular Biology, University of California at San Diego, La Jolla, California 92093, USA ) , Kadonaga, James T. (Section of Molecular Biology, University of California at San Diego, La Jolla, California 92093, USA)
    Genes & development v.31 no.1 ,pp. 6 - 11 , 2017 , 0890-9369 ,

    초록

    Vo ngoc et al. show that the human initiator has the consensus of BBCA +1 BW at focused promoters in which transcription initiates at a single site or a narrow cluster of sites. DNA sequence signals in the core promoter, such as the initiator (Inr), direct transcription initiation by RNA polymerase II. Here we show that the human Inr has the consensus of BBCA +1 BW at focused promoters in which transcription initiates at a single site or a narrow cluster of sites. The analysis of 7678 focused transcription start sites revealed 40% with a perfect match to the Inr and 16% with a single mismatch outside of the CA +1 core. TATA-like sequences are underrepresented in Inr promoters. This consensus is a key component of the DNA sequence rules that specify transcription initiation in humans.

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  4. [해외논문]   Loss of maternal Trim28 causes male-predominant early embryonic lethality   SCI SCIE

    Sampath Kumar, Abhishek (Developmental Epigenetics and Disease Group, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology, and Research (A*STAR), Singapore 138673) , Seah, Michelle K.Y. (Developmental Epigenetics and Disease Group, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology, and Research (A*STAR), Singapore 138673) , Ling, Ka Yi (Developmental Epigenetics and Disease Group, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology, and Research (A*STAR), Singapore 138673) , Wang, Yaju (Developmental Epigenetics and Disease Group, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology, and Research (A*STAR), Singapore 138673) , Tan, Joel H.L. (Developmental Epigenetics and Disease Group, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology, and Research (A*STAR), Singapore 138673) , Nitsch, Sandra (Developmental Epigenetics and Disease Group, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology, and Research (A*STAR), Singapore 13) , Lim, Shu Ly , Lorthongpanich, Chanchao , Wollmann, Heike , Low, Diana H.P. , Guccione, Ernesto , Messerschmidt, Daniel M.
    Genes & development v.31 no.1 ,pp. 12 - 17 , 2017 , 0890-9369 ,

    초록

    Kumar et al. show that the Y-linked gene Rbmy1a1 is highly methylated in mature sperm and resists DNA demethylation post-fertilization. Aberrant hypomethylation of the Rbmy1a1 promoter results in its ectopic activation, causing male-specific peri-implantation lethality. Global DNA demethylation is a hallmark of embryonic epigenetic reprogramming. However, embryos engage noncanonical DNA methylation maintenance mechanisms to ensure inheritance of exceptional epigenetic germline features to the soma. Besides the paradigmatic genomic imprints, these exceptions remain ill-defined, and the mechanisms ensuring demethylation resistance in the light of global reprogramming remain poorly understood. Here we show that the Y-linked gene Rbmy1a1 is highly methylated in mature sperm and resists DNA demethylation post-fertilization. Aberrant hypomethylation of the Rbmy1a1 promoter results in its ectopic activation, causing male-specific peri-implantation lethality. Rbmy1a1 is a novel target of the TRIM28 complex, which is required to protect its repressive epigenetic state during embryonic epigenetic reprogramming.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  5. [해외논문]   Translation reprogramming is an evolutionarily conserved driver of phenotypic plasticity and therapeutic resistance in melanoma   SCI SCIE

    Falletta, Paola (Ludwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom) , Sanchez-del-Campo, Luis (Ludwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom) , Chauhan, Jagat (Ludwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom) , Effern, Maike (Department of Clinical Chemistry and Clinical Pharmacology, Unit for RNA Biology, University Hospital of Bonn, D-53127 Bonn, Germany) , Kenyon, Amy (Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, John Radcliffe Hospital, Headington, Oxford OX3 9DS, United Kingdom) , Kershaw, Christopher J. (Division of Molecular and Cellular Function, School of Biological Sciences, Faculty of Biology, Medicine, and Health, The University of Manchester, Manchester M13 9PT, United Kingdom) , Siddaway, Robert (Ludwig Institute for Cancer Research, Nuffield Department of Cl) , Lisle, Richard , Freter, Rasmus , Daniels, Matthew J. , Lu, Xin , Tuting, Thomas , Middleton, Mark , Buffa, Francesca M. , Willis, Anne E. , Pavitt, Graham , Ronai, Ze'ev A. , Sauka-Spengler, Tatjana , Holzel, Michael , Goding, Colin R.
    Genes & development v.31 no.1 ,pp. 18 - 33 , 2017 , 0890-9369 ,

    초록

    In this study, Falletta et al. show that microenvironmental cues, including inflammation-mediated resistance to adoptive T-cell immunotherapy, transcriptionally repress MITF via ATF4 in response to inhibition of translation initiation factor eIF2B. Their results suggest that translation reprogramming, an evolutionarily conserved starvation response, has been hijacked by microenvironmental stress signals in melanoma to drive phenotypic plasticity and invasion and determine therapeutic outcome. The intratumor microenvironment generates phenotypically distinct but interconvertible malignant cell subpopulations that fuel metastatic spread and therapeutic resistance. Whether different microenvironmental cues impose invasive or therapy-resistant phenotypes via a common mechanism is unknown. In melanoma, low expression of the lineage survival oncogene microphthalmia-associated transcription factor (MITF) correlates with invasion, senescence, and drug resistance. However, how MITF is suppressed in vivo and how MITF-low cells in tumors escape senescence are poorly understood. Here we show that microenvironmental cues, including inflammation-mediated resistance to adoptive T-cell immunotherapy, transcriptionally repress MITF via ATF4 in response to inhibition of translation initiation factor eIF2B. ATF4, a key transcription mediator of the integrated stress response, also activates AXL and suppresses senescence to impose the MITF-low/AXL-high drug-resistant phenotype observed in human tumors. However, unexpectedly, without translation reprogramming an ATF4-high/MITF-low state is insufficient to drive invasion. Importantly, translation reprogramming dramatically enhances tumorigenesis and is linked to a previously unexplained gene expression program associated with anti-PD-1 immunotherapy resistance. Since we show that inhibition of eIF2B also drives neural crest migration and yeast invasiveness, our results suggest that translation reprogramming, an evolutionarily conserved starvation response, has been hijacked by microenvironmental stress signals in melanoma to drive phenotypic plasticity and invasion and determine therapeutic outcome.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  6. [해외논문]   The PIDDosome activates p53 in response to supernumerary centrosomes   SCI SCIE

    Fava, Luca L. (Division of Developmental Immunology, Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria) , Schuler, Fabian (Division of Developmental Immunology, Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria) , Sladky, Valentina (Division of Developmental Immunology, Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria) , Haschka, Manuel D. (Division of Developmental Immunology, Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria) , Soratroi, Claudia (Division of Developmental Immunology, Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria) , Eiterer, Lisa (Division of Developmental Immunology, Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria) , Demetz, Egon (Department of Internal Medicine VI, Infectious Diseases, Immunology, Rheumatology, Pneumology, Medical University of Innsbruck, 6020 Innsbruck, Austria) , Weiss, Guenter (Department of Internal Medicine VI, Infectious Diseases, Immunology, Rheumatology, Pneumology, Medical University of Innsbruck, 6020 Innsbruck, Austria) , Geley, Stephan (Division of Molecular Pathophysiolog) , Nigg, Erich A. , Villunger, Andreas
    Genes & development v.31 no.1 ,pp. 34 - 45 , 2017 , 0890-9369 ,

    초록

    In this study, Fava et al. show that an increase in the number of mature centrosomes (the main microtubule-organizing centers in animal cells), generated by disrupting cytokinesis or forcing centrosome overduplication, triggers the activation of the PIDDosome multiprotein complex, leading to Caspase-2-mediated MDM2 cleavage, p53 stabilization, and p21-dependent cell cycle arrest. Centrosomes, the main microtubule-organizing centers in animal cells, are replicated exactly once during the cell division cycle to form the poles of the mitotic spindle. Supernumerary centrosomes can lead to aberrant cell division and have been causally linked to chromosomal instability and cancer. Here, we report that an increase in the number of mature centrosomes, generated by disrupting cytokinesis or forcing centrosome overduplication, triggers the activation of the PIDDosome multiprotein complex, leading to Caspase-2-mediated MDM2 cleavage, p53 stabilization, and p21-dependent cell cycle arrest. This pathway also restrains the extent of developmentally scheduled polyploidization by regulating p53 levels in hepatocytes during liver organogenesis. Taken together, the PIDDosome acts as a first barrier, engaging p53 to halt the proliferation of cells carrying more than one mature centrosome to maintain genome integrity.

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    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  7. [해외논문]   PHF11 promotes DSB resection, ATR signaling, and HR   SCI SCIE

    Gong, Yi (Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, New York 10065, USA) , Handa, Naofumi (Department of Microbiology and Molecular Genetics, University of California at Davis, Davis, California 95616, USA ) , Kowalczykowski, Stephen C. (Department of Microbiology and Molecular Genetics, University of California at Davis, Davis, California 95616, USA ) , de Lange, Titia (Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, New York 10065, USA;)
    Genes & development v.31 no.1 ,pp. 46 - 58 , 2017 , 0890-9369 ,

    초록

    Here, de Lange and colleagues report that PHF11 (plant homeodomain finger 11) encodes a previously unknown DNA damage response factor involved in 5′ end resection, ATR signaling, and homologous recombination. Biochemical experiments demonstrated that PHF11 stimulates EXO1 by overcoming its inhibition by RPA, suggesting that PHF11 acts (in part) by promoting 5′ end resection at RPA-bound sites of DNA damage. Resection of double-strand breaks (DSBs) plays a critical role in their detection and appropriate repair. The 3′ ssDNA protrusion formed through resection activates the ATR-dependent DNA damage response (DDR) and is required for DSB repair by homologous recombination (HR). Here we report that PHF11 (plant homeodomain finger 11) encodes a previously unknown DDR factor involved in 5′ end resection, ATR signaling, and HR. PHF11 was identified based on its association with deprotected telomeres and localized to sites of DNA damage in S phase. Depletion of PHF11 diminished the ATR signaling response to telomere dysfunction and genome-wide DNA damage, reduced end resection at sites of DNA damage, resulted in compromised HR and misrejoining of S-phase DSBs, and increased the sensitivity to DNA-damaging agents. PHF11 interacted with the ssDNA-binding protein RPA and was found in a complex with several nucleases, including the 5′ dsDNA exonuclease EXO1. Biochemical experiments demonstrated that PHF11 stimulates EXO1 by overcoming its inhibition by RPA, suggesting that PHF11 acts (in part) by promoting 5′ end resection at RPA-bound sites of DNA damage. These findings reveal a role for PHF11 in DSB resection, DNA damage signaling, and DSB repair.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  8. [해외논문]   Targeted CRISPR disruption reveals a role for RNase MRP RNA in human preribosomal RNA processing   SCI SCIE

    Goldfarb, Katherine C. (Department of Chemistry and Biochemistry, BioFrontiers Institute, University of Colorado at Boulder, Boulder, Colorado 80302, USA) , Cech, Thomas R. (Department of Chemistry and Biochemistry, BioFrontiers Institute, University of Colorado at Boulder, Boulder, Colorado 80302, USA;)
    Genes & development v.31 no.1 ,pp. 59 - 71 , 2017 , 0890-9369 ,

    초록

    In this study, Goldfarb et al. used CRISPR–Cas9 genome editing to eliminate MRP RNA—a ribonucleoprotein complex with an RNA subunit that is conserved across eukarya—in the majority of cells. Analysis by RNA FISH, Northerns, and RNA sequencing demonstrates an accumulation of ribosomal RNA precursor and thus establishes a role for RNase MRP in human pre-rRNA processing. MRP RNA is an abundant, essential noncoding RNA whose functions have been proposed in yeast but are incompletely understood in humans. Mutations in the genomic locus for MRP RNA cause pleiotropic human diseases, including cartilage hair hypoplasia (CHH). Here we applied CRISPR–Cas9 genome editing to disrupt the endogenous human MRP RNA locus, thereby attaining what has eluded RNAi and RNase H experiments: elimination of MRP RNA in the majority of cells. The resulting accumulation of ribosomal RNA (rRNA) precursor—analyzed by RNA fluorescent in situ hybridization (FISH), Northern blots, and RNA sequencing—implicates MRP RNA in pre-rRNA processing. Amelioration of pre-rRNA imbalance is achieved through rescue of MRP RNA levels by ectopic expression. Furthermore, affinity-purified MRP ribonucleoprotein (RNP) from HeLa cells cleaves the human pre-rRNA in vitro at at least one site used in cells, while RNP isolated from cells with CRISPR-edited MRP loci loses this activity, and ectopic MRP RNA expression restores cleavage activity. Thus, a role for RNase MRP in human pre-rRNA processing is established. As demonstrated here, targeted CRISPR disruption is a valuable tool for functional studies of essential noncoding RNAs that are resistant to RNAi and RNase H-based degradation.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  9. [해외논문]   Live-cell analysis of DNA methylation during sexual reproduction in Arabidopsis reveals context and sex-specific dynamics controlled by noncanonical RdDM   SCI SCIE

    Ingouff, Mathieu (Epigenetic Regulations and Seed Development, UMR232, Institut de Recherche pour le Dééééveloppement (IRD), Universitééééé) , Selles, Benjamin (de Montpellier, 34394 Montpellier, France) , Michaud, Caroline (Epigenetic Regulations and Seed Development, UMR232, Institut de Recherche pour le Dééééveloppement (IRD), Universitééééé) , Vu, Thiet M. (de Montpellier, 34394 Montpellier, France) , Berger, Fré (Epigenetic Regulations and Seed Development, UMR232, Institut de Recherche pour le Dééééveloppement (IRD), Universitééééé) , dé (de Montpellier, 34394 Montpellier, France) , é (Gregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, 1030 Vienna, Austria) , ric (Gregor Mendel Institute, Austrian Academy of Sciences, Vienna BioCenter, 1030 Vienna, Austria) , Schorn, Andrea J. (Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA) , Autran, Daphné (Epigenetic Regulations and Seed Developmen) , é , é , , Van Durme, Matthias , Nowack, Moritz K. , Martienssen, Robert A. , Grimanelli, Daniel
    Genes & development v.31 no.1 ,pp. 72 - 83 , 2017 , 0890-9369 ,

    초록

    In this Resource/Methodology, Ingouff et al. developed a new method to investigate DNA methylation reprogramming in plants. Using Arabidopsis , the authors developed sensors that reported CG and non-CG methylation with single-cell resolution. Cytosine methylation is a key epigenetic mark in many organisms, important for both transcriptional control and genome integrity. While relatively stable during somatic growth, DNA methylation is reprogrammed genome-wide during mammalian reproduction. Reprogramming is essential for zygotic totipotency and to prevent transgenerational inheritance of epimutations. However, the extent of DNA methylation reprogramming in plants remains unclear. Here, we developed sensors reporting with single-cell resolution CG and non-CG methylation in Arabidopsis. Live imaging during reproduction revealed distinct and sex-specific dynamics for both contexts. We found that CHH methylation in the egg cell depends on DOMAINS REARRANGED METHYLASE 2 (DRM2) and RNA polymerase V (Pol V), two main actors of RNA-directed DNA methylation, but does not depend on Pol IV. Our sensors provide insight into global DNA methylation dynamics at the single-cell level with high temporal resolution and offer a powerful tool to track CG and non-CG methylation both during development and in response to environmental cues in all organisms with methylated DNA, as we illustrate in mouse embryonic stem cells.

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