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  • 1
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    Molecular biology. RNA interference (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharp, P A -- Zamore, P D -- New York, N.Y. -- Science. 2000 Mar 31;287(5462):2431-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. sharppa@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10766620" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics ; *Caenorhabditis elegans Proteins ; *DNA Transposable Elements ; Female ; *Gene Expression Regulation ; *Gene Silencing ; Genes, Helminth ; Helminth Proteins/genetics/physiology ; Male ; Mutation ; RNA, Double-Stranded/*genetics ; RNA, Helminth/*genetics/metabolism ; RNA, Messenger/*genetics/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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    Promoter directionality is controlled by U1 snRNP and polyadenylation signals (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-06-25
    Description: Transcription of the mammalian genome is pervasive, but productive transcription outside of protein-coding genes is limited by unknown mechanisms. In particular, although RNA polymerase II (RNAPII) initiates divergently from most active gene promoters, productive elongation occurs primarily in the sense-coding direction. Here we show in mouse embryonic stem cells that asymmetric sequence determinants flanking gene transcription start sites control promoter directionality by regulating promoter-proximal cleavage and polyadenylation. We find that upstream antisense RNAs are cleaved and polyadenylated at poly(A) sites (PASs) shortly after initiation. De novo motif analysis shows PAS signals and U1 small nuclear ribonucleoprotein (snRNP) recognition sites to be the most depleted and enriched sequences, respectively, in the sense direction relative to the upstream antisense direction. These U1 snRNP sites and PAS sites are progressively gained and lost, respectively, at the 5' end of coding genes during vertebrate evolution. Functional disruption of U1 snRNP activity results in a dramatic increase in promoter-proximal cleavage events in the sense direction with slight increases in the antisense direction. These data suggest that a U1-PAS axis characterized by low U1 snRNP recognition and a high density of PASs in the upstream antisense region reinforces promoter directionality by promoting early termination in upstream antisense regions, whereas proximal sense PAS signals are suppressed by U1 snRNP. We propose that the U1-PAS axis limits pervasive transcription throughout the genome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3720719/" 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/PMC3720719/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Almada, Albert E -- Wu, Xuebing -- Kriz, Andrea J -- Burge, Christopher B -- Sharp, Phillip A -- GM-085319/GM/NIGMS NIH HHS/ -- P30 CA014051/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R01 CA133404/CA/NCI NIH HHS/ -- R01 GM034277/GM/NIGMS NIH HHS/ -- R01 HG002439/HG/NHGRI NIH HHS/ -- R01-CA133404/CA/NCI NIH HHS/ -- R01-GM34277/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jul 18;499(7458):360-3. doi: 10.1038/nature12349. Epub 2013 Jun 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23792564" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Evolution, Molecular ; Mice ; *Polyadenylation ; *Promoter Regions, Genetic ; RNA Cleavage ; RNA, Antisense/metabolism ; Ribonucleoprotein, U1 Small Nuclear/*metabolism ; *Transcription Elongation, Genetic ; Transcription Termination, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Proliferating cells express mRNAs with shortened 3' untranslated regions and fewer microRNA target sites (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-21
    Description: Messenger RNA (mRNA) stability, localization, and translation are largely determined by sequences in the 3' untranslated region (3'UTR). We found a conserved increase in expression of mRNAs terminating at upstream polyadenylation sites after activation of primary murine CD4+ T lymphocytes. This program, resulting in shorter 3'UTRs, is a characteristic of gene expression during immune cell activation and correlates with proliferation across diverse cell types and tissues. Forced expression of full-length 3'UTRs conferred reduced protein expression. In some cases the reduction in protein expression could be reversed by deletion of predicted microRNA target sites in the variably included region. Our data indicate that gene expression is coordinately regulated, such that states of increased proliferation are associated with widespread reductions in the 3'UTR-based regulatory capacity of mRNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587246/" 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/PMC2587246/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandberg, Rickard -- Neilson, Joel R -- Sarma, Arup -- Sharp, Phillip A -- Burge, Christopher B -- P01 CA042063/CA/NCI NIH HHS/ -- P01 CA042063-22/CA/NCI NIH HHS/ -- P01-CA42063/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R01 GM034277/GM/NIGMS NIH HHS/ -- R01 GM034277-23/GM/NIGMS NIH HHS/ -- R01 HG002439/HG/NHGRI NIH HHS/ -- R01 HG002439-07/HG/NHGRI NIH HHS/ -- R01-GM34277/GM/NIGMS NIH HHS/ -- R01-HG002439/HG/NHGRI NIH HHS/ -- U19 AI056900/AI/NIAID NIH HHS/ -- U19 AI056900-010001/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 20;320(5883):1643-7. doi: 10.1126/science.1155390.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18566288" target="_blank"〉PubMed〈/a〉
    Keywords: *3' Untranslated Regions ; Animals ; CD4-Positive T-Lymphocytes/cytology/immunology/*metabolism ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cells, Cultured ; *Gene Expression Regulation ; Humans ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; MicroRNAs/*metabolism ; Oligonucleotide Array Sequence Analysis ; Polyadenylation ; RNA Splicing ; RNA, Messenger/chemistry/genetics/*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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  • 4
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    Transcription factor trapping by RNA in gene regulatory elements (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-10-31
    Description: Transcription factors (TFs) bind specific sequences in promoter-proximal and -distal DNA elements to regulate gene transcription. RNA is transcribed from both of these DNA elements, and some DNA binding TFs bind RNA. Hence, RNA transcribed from regulatory elements may contribute to stable TF occupancy at these sites. We show that the ubiquitously expressed TF Yin-Yang 1 (YY1) binds to both gene regulatory elements and their associated RNA species across the entire genome. Reduced transcription of regulatory elements diminishes YY1 occupancy, whereas artificial tethering of RNA enhances YY1 occupancy at these elements. We propose that RNA makes a modest but important contribution to the maintenance of certain TFs at gene regulatory elements and suggest that transcription of regulatory elements produces a positive-feedback loop that contributes to the stability of gene expression programs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720525/" 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/PMC4720525/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sigova, Alla A -- Abraham, Brian J -- Ji, Xiong -- Molinie, Benoit -- Hannett, Nancy M -- Guo, Yang Eric -- Jangi, Mohini -- Giallourakis, Cosmas C -- Sharp, Phillip A -- Young, Richard A -- HG002668/HG/NHGRI NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2015 Nov 20;350(6263):978-81. doi: 10.1126/science.aad3346. Epub 2015 Oct 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. ; Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. ; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. David H. Koch Institute for Integrative Cancer Research, Cambridge, MA 02140, USA. ; Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. young@wi.mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26516199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cell Line ; Consensus Sequence ; DNA/metabolism ; Embryonic Stem Cells/metabolism ; *Enhancer Elements, Genetic ; *Gene Expression Regulation ; Mice ; *Promoter Regions, Genetic ; RNA, Messenger/*metabolism ; *Transcription, Genetic ; YY1 Transcription Factor/*metabolism
    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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  • 5
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    The adenovirus major late transcription factor activates the rat gamma-fibrinogen promoter (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-30
    Description: The major late transcription factor (MLTF) is a 46-kilodalton polypeptide that specifically binds to and activates transcription from the major late promoter of adenovirus. The presence of this promoter-specific transcription factor in uninfected HeLa cell extracts suggests that MLTF is also involved in the transcription of cellular genes. This report demonstrates that MLTF specifically stimulates transcription of the rat gamma-fibrinogen gene through a high-affinity binding site. Stimulation of transcription by MLTF was not dependent on the exact position of the MLTF binding site with respect either to the transcription initiation site or to adjacent promoter elements. These results suggest that one of the cellular functions of MLTF is to control gamma-fibrinogen gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chodosh, L A -- Carthew, R W -- Morgan, J G -- Crabtree, G R -- Sharp, P A -- P01-CA42063/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):684-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3672119" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviruses, Human/*genetics ; Animals ; DNA-Binding Proteins/*genetics ; Fibrinogen/*genetics ; *Gene Expression Regulation ; *Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; Rats ; Regulatory Sequences, Nucleic Acid ; Transcription Factors/*genetics ; Transcription, Genetic ; Viral Proteins/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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  • 6
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    Measurement of suppressor transfer RNA activity (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-08-26
    Description: Transfer RNA (tRNA) suppression of nonsense mutations in prokaryotic systems has been widely used to study the structure and function of different prokaryotic genes. Through genetic engineering techniques, it is now possible to introduce suppressor (Su+) tRNA molecules into mammalian cells. A quantitative assay of the suppressor tRNA activity in these mammalian cells is described; it is based on the amount of tRNA-mediated readthrough of a terminating codon in the influenza virus NS1 gene after the cells are infected with virus. Suppressor activity in L cells continuously expressing Su+ (tRNAtyr) was 3.5 percent and that in CV-1 cells infected with an SV40- Su+ (tRNAtyr) recombinant was 22.5 percent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, J F -- Capecchi, M -- Laski, F A -- RajBhandary, U L -- Sharp, P A -- Palese, P -- AI-11823/AI/NIAID NIH HHS/ -- AI-18998/AI/NIAID NIH HHS/ -- GM17151/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Aug 26;221(4613):873-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6308765" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Eukaryotic Cells/physiology ; Genes, Viral ; Mice ; Orthomyxoviridae/genetics ; Peptide Chain Termination, Translational ; Protein Biosynthesis ; RNA, Transfer/*genetics ; Simian virus 40/genetics ; *Suppression, Genetic
    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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