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  • Female  (4)
  • Mutation  (3)
  • Binding Sites
  • American Association for the Advancement of Science (AAAS)  (6)
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  • 1
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    Extent of chromatin spreading determined by roX RNA recruitment of MSL proteins (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-11-26
    Description: The untranslated roX1 and roX2 RNAs are components of the Drosophila male-specific lethal (MSL) complex, which modifies histones to up-regulate transcription of the male X chromosome. roX genes are normally located on the X chromosome, and roX transgenes can misdirect the dosage compensation machinery to spread locally on other chromosomes. Here we define MSL protein abundance as a determinant of whether the MSL complex will spread in cis from an autosomal roX transgene. The number of expressed roX genes in a nucleus was inversely correlated with spreading from roX transgenes. We suggest a model in which MSL proteins assemble into active complexes by binding nascent roX transcripts. When MSL protein/roX RNA ratios are high, assembly will be efficient, and complexes may be completed while still tethered to the DNA template. We propose that this local production of MSL complexes determines the extent of spreading into flanking chromatin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Yongkyu -- Kelley, Richard L -- Oh, Hyangyee -- Kuroda, Mitzi I -- Meller, Victoria H -- GM45744/GM/NIGMS NIH HHS/ -- GM58427/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Nov 22;298(5598):1620-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12446910" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/*metabolism ; Chromosomes/metabolism ; DNA, Complementary ; DNA-Binding Proteins ; *Dosage Compensation, Genetic ; Drosophila/*genetics/metabolism ; *Drosophila Proteins ; Gene Expression Regulation ; Mutation ; Nuclear Proteins/genetics/*metabolism ; RNA, Messenger/*genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic ; Transgenes ; X Chromosome/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Epigenetic aspects of X-chromosome dosage compensation (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-08-11
    Description: The X chromosomes of mammals and fruit flies exhibit unusual properties that have evolved to deal with the different dosages of X-linked genes in males (XY) and females (XX). The X chromosome dosage-compensation mechanisms discovered in these species are evolutionarily unrelated, but exhibit surprising parallels in their regulatory strategies. These features include the importance of noncoding RNAs, and epigenetic spreading of chromatin-modifying activities. Sex chromosomes have posed a fascinating puzzle for biologists. The dissimilar organization, gene content, and regulation of the X and Y chromosomes are thought to reflect selective forces acting on original pairs of identical chromosomes (1-3). The result in many organisms is a male-specific Y chromosome that has lost most of its original genetic content, and a difference in dosage of the X chromosome in males (XY) and females (XX).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Y -- Kuroda, M I -- New York, N.Y. -- Science. 2001 Aug 10;293(5532):1083-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11498577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/metabolism ; *Dosage Compensation, Genetic ; Drosophila/genetics ; Evolution, Molecular ; Female ; Genomic Imprinting ; Histones/metabolism ; Humans ; Male ; Mammals/genetics ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; RNA-Binding Proteins/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; X Chromosome/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    CHD1 motor protein is required for deposition of histone variant H3.3 into chromatin in vivo (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-25
    Description: The organization of chromatin affects all aspects of nuclear DNA metabolism in eukaryotes. H3.3 is an evolutionarily conserved histone variant and a key substrate for replication-independent chromatin assembly. Elimination of chromatin remodeling factor CHD1 in Drosophila embryos abolishes incorporation of H3.3 into the male pronucleus, renders the paternal genome unable to participate in zygotic mitoses, and leads to the development of haploid embryos. Furthermore, CHD1, but not ISWI, interacts with HIRA in cytoplasmic extracts. Our findings establish CHD1 as a major factor in replacement histone metabolism in the nucleus and reveal a critical role for CHD1 in the earliest developmental instances of genome-scale, replication-independent nucleosome assembly. Furthermore, our results point to the general requirement of adenosine triphosphate (ATP)-utilizing motor proteins for histone deposition in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014568/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014568/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Konev, Alexander Y -- Tribus, Martin -- Park, Sung Yeon -- Podhraski, Valerie -- Lim, Chin Yan -- Emelyanov, Alexander V -- Vershilova, Elena -- Pirrotta, Vincenzo -- Kadonaga, James T -- Lusser, Alexandra -- Fyodorov, Dmitry V -- GM58272/GM/NIGMS NIH HHS/ -- GM74233/GM/NIGMS NIH HHS/ -- R01 GM074233/GM/NIGMS NIH HHS/ -- Y 275/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2007 Aug 24;317(5841):1087-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717186" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Cell Cycle Proteins/metabolism ; Chromatin/*metabolism ; *Chromatin Assembly and Disassembly ; DNA-Binding Proteins/genetics/*metabolism ; Drosophila/embryology/genetics/metabolism/*physiology ; Drosophila Proteins/genetics/*metabolism ; Embryo, Nonmammalian/physiology ; Embryonic Development ; Female ; Haploidy ; Histone Chaperones ; Histones/*metabolism ; Male ; Mutation ; Nucleosomes/metabolism ; Protamines/metabolism ; Spermatozoa/physiology ; Transcription Factors/genetics/*metabolism ; Transgenes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Evidence of a pluripotent human embryonic stem cell line derived from a cloned blastocyst (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-14
    Description: Somatic cell nuclear transfer (SCNT) technology has recently been used to generate animals with a common genetic composition. In this study, we report the derivation of a pluripotent embryonic stem (ES) cell line (SCNT-hES-1) from a cloned human blastocyst. The SCNT-hES-1 cells displayed typical ES cell morphology and cell surface markers and were capable of differentiating into embryoid bodies in vitro and of forming teratomas in vivo containing cell derivatives from all three embryonic germ layers in severe combined immunodeficient mice. After continuous proliferation for more than 70 passages, SCNT-hES-1 cells maintained normal karyotypes and were genetically identical to the somatic nuclear donor cells. Although we cannot completely exclude the possibility that the cells had a parthenogenetic origin, imprinting analyses support a SCNT origin of the derived human ES cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, Woo Suk -- Ryu, Young June -- Park, Jong Hyuk -- Park, Eul Soon -- Lee, Eu Gene -- Koo, Ja Min -- Jeon, Hyun Yong -- Lee, Byeong Chun -- Kang, Sung Keun -- Kim, Sun Jong -- Ahn, Curie -- Hwang, Jung Hye -- Park, Ky Young -- Cibelli, Jose B -- Moon, Shin Yong -- New York, N.Y. -- Science. 2004 Mar 12;303(5664):1669-74. Epub 2004 Feb 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉College of Veterinary Medicine, Seoul National University, Seoul 151-742, Korea. hwangws@snu.ac.kr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14963337" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Blastocyst/*cytology ; Cell Differentiation ; *Cell Line ; *Cloning, Organism ; Culture Media ; Culture Techniques ; DNA Fingerprinting ; Embryo, Mammalian/*cytology ; Female ; Genomic Imprinting ; Humans ; Karyotyping ; Male ; Mice ; Mice, SCID ; Nuclear Transfer Techniques ; Oocyte Donation ; Ovarian Follicle/cytology ; Parthenogenesis ; Pluripotent Stem Cells/chemistry/*cytology ; Reverse Transcriptase Polymerase Chain Reaction ; Tandem Repeat Sequences ; Teratoma/etiology/pathology ; Testicular Neoplasms/etiology/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    EGF-like growth factors as mediators of LH action in the ovulatory follicle (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-17
    Description: Before ovulation in mammals, a cascade of events resembling an inflammatory and/or tissue remodeling process is triggered by luteinizing hormone (LH) in the ovarian follicle. Many LH effects, however, are thought to be indirect because of the restricted expression of its receptor. Here, we demonstrate that LH stimulation induces the transient and sequential expression of the epidermal growth factor (EGF) family members amphiregulin, epiregulin, and beta-cellulin. Incubation of follicles with these growth factors recapitulates the morphological and biochemical events triggered by LH, including cumulus expansion and oocyte maturation. Thus, these EGF-related growth factors are paracrine mediators that propagate the LH signal throughout the follicle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Jy-Young -- Su, You-Qiang -- Ariga, Miyako -- Law, Evelyn -- Jin, S-L Catherine -- Conti, Marco -- HD20788/HD/NICHD NIH HHS/ -- HD31398/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2004 Jan 30;303(5658):682-4. Epub 2004 Jan 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Reproductive Biology and Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14726596" target="_blank"〉PubMed〈/a〉
    Keywords: Amphiregulin ; Animals ; Betacellulin ; Chorionic Gonadotropin/pharmacology ; EGF Family of Proteins ; Epidermal Growth Factor/genetics/*metabolism ; Epiregulin ; Female ; Gene Expression Regulation ; Glycoproteins/genetics/*metabolism ; Granulosa Cells/metabolism ; Intercellular Signaling Peptides and Proteins/genetics/*metabolism ; Luteinizing Hormone/pharmacology/*physiology ; Meiosis ; Mice ; Mice, Inbred C57BL ; Oocytes/physiology ; Organ Culture Techniques ; Ovarian Follicle/*physiology ; Ovulation/*physiology ; Paracrine Communication ; RNA, Messenger/genetics/metabolism ; Receptor, Epidermal Growth Factor/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Abscisic acid inhibits type 2C protein phosphatases via the PYR/PYL family of START proteins (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: Type 2C protein phosphatases (PP2Cs) are vitally involved in abscisic acid (ABA) signaling. Here, we show that a synthetic growth inhibitor called pyrabactin functions as a selective ABA agonist. Pyrabactin acts through PYRABACTIN RESISTANCE 1 (PYR1), the founding member of a family of START proteins called PYR/PYLs, which are necessary for both pyrabactin and ABA signaling in vivo. We show that ABA binds to PYR1, which in turn binds to and inhibits PP2Cs. We conclude that PYR/PYLs are ABA receptors functioning at the apex of a negative regulatory pathway that controls ABA signaling by inhibiting PP2Cs. Our results illustrate the power of the chemical genetic approach for sidestepping genetic redundancy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2827199/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2827199/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Sang-Youl -- Fung, Pauline -- Nishimura, Noriyuki -- Jensen, Davin R -- Fujii, Hiroaki -- Zhao, Yang -- Lumba, Shelley -- Santiago, Julia -- Rodrigues, Americo -- Chow, Tsz-Fung F -- Alfred, Simon E -- Bonetta, Dario -- Finkelstein, Ruth -- Provart, Nicholas J -- Desveaux, Darrell -- Rodriguez, Pedro L -- McCourt, Peter -- Zhu, Jian-Kang -- Schroeder, Julian I -- Volkman, Brian F -- Cutler, Sean R -- 01GM59138/GM/NIGMS NIH HHS/ -- R01 GM060396/GM/NIGMS NIH HHS/ -- R01 GM060396-08/GM/NIGMS NIH HHS/ -- R01GM060396/GM/NIGMS NIH HHS/ -- U54GM074901/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 22;324(5930):1068-71. doi: 10.1126/science.1173041. Epub 2009 Apr 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Botany and Plant Sciences, University of California at Riverside, Riverside, CA 92521, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407142" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/agonists/*metabolism ; Arabidopsis/enzymology/genetics/growth & development/*metabolism ; Arabidopsis Proteins/*antagonists & inhibitors/genetics/*metabolism ; Genes, Plant ; Germination/drug effects ; Ligands ; Membrane Transport Proteins/genetics/*metabolism ; Mutation ; Naphthalenes/chemistry/metabolism/*pharmacology ; Phosphoprotein Phosphatases/*antagonists & inhibitors/metabolism ; Protein Binding ; Recombinant Fusion Proteins/metabolism ; Seeds/growth & development/metabolism ; Signal Transduction ; Sulfonamides/chemistry/metabolism/*pharmacology ; Two-Hybrid System Techniques
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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