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mRNA processing factors in plasma cells [Immunology] (2012)

Benson, M. J., Ai&jnodot;o, T., Chang, X., Gagnon, J., Pape, U. J., Anantharaman, V., Aravind, L., Pursiheimo, J.–P., Oberdoerffer, S., Liu, X. S., Lahesmaa, R., Lahdesmaki, H., Rao, A.

National Academy of Sciences

In: PNAS - Proceedings of the National Academy of Sciences

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Publication Date: 2012-10-03

Description: B cells and plasma cells possess distinct RNA processing environments that respectively promote the expression of membrane-associated Ig by B cells versus the secretion of Ig by plasma cells. Through a combination of transcriptional profiling and screening using a lentiviral short-hairpin RNA interference library, we show that both the splicing...

Print ISSN: 0027-8424

Electronic ISSN: 1091-6490

Topics: Biology , Medicine , Natural Sciences in General

Published by National Academy of Sciences

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CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing (2011)

S. Shukla ; E. Kavak ; M. Gregory ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 479(7371): 74-9. doi: 10.1038/nature10442.

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Publication Date: 2011-10-04

Description: Alternative splicing of pre-messenger RNA is a key feature of transcriptome expansion in eukaryotic cells, yet its regulation is poorly understood. Spliceosome assembly occurs co-transcriptionally, raising the possibility that DNA structure may directly influence alternative splicing. Supporting such an association, recent reports have identified distinct histone methylation patterns, elevated nucleosome occupancy and enriched DNA methylation at exons relative to introns. Moreover, the rate of transcription elongation has been linked to alternative splicing. Here we provide the first evidence that a DNA-binding protein, CCCTC-binding factor (CTCF), can promote inclusion of weak upstream exons by mediating local RNA polymerase II pausing both in a mammalian model system for alternative splicing, CD45, and genome-wide. We further show that CTCF binding to CD45 exon 5 is inhibited by DNA methylation, leading to reciprocal effects on exon 5 inclusion. These findings provide a mechanistic basis for developmental regulation of splicing outcome through heritable epigenetic marks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shukla, Sanjeev -- Kavak, Ersen -- Gregory, Melissa -- Imashimizu, Masahiko -- Shutinoski, Bojan -- Kashlev, Mikhail -- Oberdoerffer, Philipp -- Sandberg, Rickard -- Oberdoerffer, Shalini -- Intramural NIH HHS/ -- England -- Nature. 2011 Nov 3;479(7371):74-9. doi: 10.1038/nature10442.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Mouse Cancer Genetics Program, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21964334" target="_blank"〉PubMed〈/a〉

Keywords: *Alternative Splicing ; Animals ; Antigens, CD45/genetics ; Cell Line ; Cells, Cultured ; *DNA Methylation ; Epigenesis, Genetic ; Exons/genetics ; Genome, Human/genetics ; Humans ; Mice ; Protein Binding ; RNA Polymerase II/*metabolism ; RNA Splice Sites/genetics ; RNA, Messenger/genetics/metabolism ; Repressor Proteins/*metabolism ; Saccharomyces cerevisiae/enzymology ; *Transcription, Genetic/genetics

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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Dietary restriction: standing up for sirtuins (2010)

J. A. Baur ; D. Chen ; E. N. Chini ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 329(5995): 1012-3; author reply 1013-4. doi: 10.1126/science.329.5995.1012.

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Publication Date: 2010-08-28

Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985480/" 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/PMC3985480/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baur, Joseph A -- Chen, Danica -- Chini, Eduardo N -- Chua, Katrin -- Cohen, Haim Y -- de Cabo, Rafael -- Deng, Chuxia -- Dimmeler, Stefanie -- Gius, David -- Guarente, Leonard P -- Helfand, Stephen L -- Imai, Shin-Ichiro -- Itoh, Hiroshi -- Kadowaki, Takashi -- Koya, Daisuke -- Leeuwenburgh, Christiaan -- McBurney, Michael -- Nabeshima, Yo-Ichi -- Neri, Christian -- Oberdoerffer, Philipp -- Pestell, Richard G -- Rogina, Blanka -- Sadoshima, Junichi -- Sartorelli, Vittorio -- Serrano, Manuel -- Sinclair, David A -- Steegborn, Clemens -- Tatar, Marc -- Tissenbaum, Heidi A -- Tong, Qiang -- Tsubota, Kazuo -- Vaquero, Alejandro -- Verdin, Eric -- P01 AG027916/AG/NIA NIH HHS/ -- R00 AG031182/AG/NIA NIH HHS/ -- R01 AG019719/AG/NIA NIH HHS/ -- R01 AG023039/AG/NIA NIH HHS/ -- R01 AG023088/AG/NIA NIH HHS/ -- R01 AG023088-08/AG/NIA NIH HHS/ -- R01 AG024360/AG/NIA NIH HHS/ -- R01 AG028730/AG/NIA NIH HHS/ -- R01 AG028730-05/AG/NIA NIH HHS/ -- R01 HL067724/HL/NHLBI NIH HHS/ -- R01 HL091469/HL/NHLBI NIH HHS/ -- R01 HL102738/HL/NHLBI NIH HHS/ -- R37 AG024360/AG/NIA NIH HHS/ -- Z99 DK999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1012-3; author reply 1013-4. doi: 10.1126/science.329.5995.1012.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798296" target="_blank"〉PubMed〈/a〉

Keywords: Aging/*physiology ; Animals ; *Caloric Restriction ; Humans ; *Longevity ; Signal Transduction ; Sirtuins/*physiology

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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Controlled DNA double-strand break induction in mice reveals post-damage transcriptome stability (2016)

Kim, J., Sturgill, D., Tran, A. D., Sinclair, D. A., Oberdoerffer, P.

Oxford University Press

In: Nucleic Acids Research

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Publication Date: 2016-04-21

Description: DNA double-strand breaks (DSBs) and their repair can cause extensive epigenetic changes. As a result, DSBs have been proposed to promote transcriptional and, ultimately, physiological dysfunction via both cell-intrinsic and cell-non-autonomous pathways. Studying the consequences of DSBs in higher organisms has, however, been hindered by a scarcity of tools for controlled DSB induction. Here, we describe a mouse model that allows for both tissue-specific and temporally controlled DSB formation at ~140 defined genomic loci. Using this model, we show that DSBs promote a DNA damage signaling-dependent decrease in gene expression in primary cells specifically at break-bearing genes, which is reversed upon DSB repair. Importantly, we demonstrate that restoration of gene expression can occur independently of cell cycle progression, underlining its relevance for normal tissue maintenance. Consistent with this, we observe no evidence for persistent transcriptional repression in response to a multi-day course of continuous DSB formation and repair in mouse lymphocytes in vivo . Together, our findings reveal an unexpected capacity of primary cells to maintain transcriptome integrity in response to DSBs, pointing to a limited role for DNA damage as a mediator of cell-autonomous epigenetic dysfunction.

Keywords: Repair

Print ISSN: 0305-1048

Electronic ISSN: 1362-4962

Topics: Biology

Published by Oxford University Press

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