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  • 1
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    New class of gene-termini-associated human RNAs suggests a novel RNA copying mechanism (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-31
    Description: Small (〈200 nucleotide) RNA (sRNA) profiling of human cells using various technologies demonstrates unexpected complexity of sRNAs with hundreds of thousands of sRNA species present. Genetic and in vitro studies show that these RNAs are not merely degradation products of longer transcripts but could indeed have a function. Furthermore, profiling of RNAs, including the sRNAs, can reveal not only novel transcripts, but also make clear predictions about the existence and properties of novel biochemical pathways operating in a cell. For example, sRNA profiling in human cells indicated the existence of an unknown capping mechanism operating on cleaved RNA, a biochemical component of which was later identified. Here we show that human cells contain a novel type of sRNA that has non-genomically encoded 5' poly(U) tails. The presence of these RNAs at the termini of genes, specifically at the very 3' ends of known mRNAs, strongly argues for the presence of a yet uncharacterized endogenous biochemical pathway in cells that can copy RNA. We show that this pathway can operate on multiple genes, with specific enrichment towards transcript-encoding components of the translational machinery. Finally, we show that genes are also flanked by sense, 3' polyadenylated sRNAs that are likely to be capped.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058539/" 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/PMC3058539/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kapranov, Philipp -- Ozsolak, Fatih -- Kim, Sang Woo -- Foissac, Sylvain -- Lipson, Doron -- Hart, Chris -- Roels, Steve -- Borel, Christelle -- Antonarakis, Stylianos E -- Monaghan, A Paula -- John, Bino -- Milos, Patrice M -- GM079756/GM/NIGMS NIH HHS/ -- MH60774/MH/NIMH NIH HHS/ -- R01 GM079756/GM/NIGMS NIH HHS/ -- R01 GM079756-01A1/GM/NIGMS NIH HHS/ -- R01 GM079756-02/GM/NIGMS NIH HHS/ -- R01 GM079756-03/GM/NIGMS NIH HHS/ -- R01 HG005230/HG/NHGRI NIH HHS/ -- England -- Nature. 2010 Jul 29;466(7306):642-6. doi: 10.1038/nature09190.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Helicos BioSciences Corporation, 1 Kendall Sq. Ste B7301 Cambridge, Massachusetts 02139-1671, USA. philippk08@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671709" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Genes/*genetics ; HeLa Cells ; Humans ; Models, Genetic ; Nucleotides/genetics ; Poly A/genetics/metabolism ; Poly U/genetics/metabolism ; RNA/biosynthesis/*classification/genetics/*metabolism ; RNA, Antisense/classification/genetics/metabolism ; Templates, 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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  • 2
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    Direct RNA sequencing (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-09-25
    Description: Our understanding of human biology and disease is ultimately dependent on a complete understanding of the genome and its functions. The recent application of microarray and sequencing technologies to transcriptomics has changed the simplistic view of transcriptomes to a more complicated view of genome-wide transcription where a large fraction of transcripts emanates from unannotated parts of genomes, and underlined our limited knowledge of the dynamic state of transcription. Most of this broad body of knowledge was obtained indirectly because current transcriptome analysis methods typically require RNA to be converted to complementary DNA (cDNA) before measurements, even though the cDNA synthesis step introduces multiple biases and artefacts that interfere with both the proper characterization and quantification of transcripts. Furthermore, cDNA synthesis is not particularly suitable for the analysis of short, degraded and/or small quantity RNA samples. Here we report direct single molecule RNA sequencing without prior conversion of RNA to cDNA. We applied this technology to sequence femtomole quantities of poly(A)(+) Saccharomyces cerevisiae RNA using a surface coated with poly(dT) oligonucleotides to capture the RNAs at their natural poly(A) tails and initiate sequencing by synthesis. We observed transcript 3' end heterogeneity and polyadenylated small nucleolar RNAs. This study provides a path to high-throughput and low-cost direct RNA sequencing and achieving the ultimate goal of a comprehensive and bias-free understanding of transcriptomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ozsolak, Fatih -- Platt, Adam R -- Jones, Dan R -- Reifenberger, Jeffrey G -- Sass, Lauryn E -- McInerney, Peter -- Thompson, John F -- Bowers, Jayson -- Jarosz, Mirna -- Milos, Patrice M -- R01 HG005230/HG/NHGRI NIH HHS/ -- England -- Nature. 2009 Oct 8;461(7265):814-8. doi: 10.1038/nature08390. Epub 2009 Sep 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Helicos BioSciences Corporation, One Kendall Square, Cambridge, Massachusetts 02139, USA. fatihozsolak@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19776739" target="_blank"〉PubMed〈/a〉
    Keywords: DNA, Complementary/genetics ; Gene Expression Profiling/methods ; Oligoribonucleotides/genetics ; Polymerase Chain Reaction ; RNA/*analysis/*genetics/isolation & purification ; RNA, Fungal/analysis/genetics/isolation & purification ; Saccharomyces cerevisiae/genetics ; Sequence Analysis, RNA/*methods ; Templates, 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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    The Lkb1 metabolic sensor maintains haematopoietic stem cell survival (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-03
    Description: Haematopoietic stem cells (HSCs) can convert between growth states that have marked differences in bioenergetic needs. Although often quiescent in adults, these cells become proliferative upon physiological demand. Balancing HSC energetics in response to nutrient availability and growth state is poorly understood, yet essential for the dynamism of the haematopoietic system. Here we show that the Lkb1 tumour suppressor is critical for the maintenance of energy homeostasis in haematopoietic cells. Lkb1 inactivation in adult mice causes loss of HSC quiescence followed by rapid depletion of all haematopoietic subpopulations. Lkb1-deficient bone marrow cells exhibit mitochondrial defects, alterations in lipid and nucleotide metabolism, and depletion of cellular ATP. The haematopoietic effects are largely independent of Lkb1 regulation of AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) signalling. Instead, these data define a central role for Lkb1 in restricting HSC entry into cell cycle and in broadly maintaining energy homeostasis in haematopoietic cells through a novel metabolic checkpoint.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037591/" 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/PMC3037591/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurumurthy, Sushma -- Xie, Stephanie Z -- Alagesan, Brinda -- Kim, Judith -- Yusuf, Rushdia Z -- Saez, Borja -- Tzatsos, Alexandros -- Ozsolak, Fatih -- Milos, Patrice -- Ferrari, Francesco -- Park, Peter J -- Shirihai, Orian S -- Scadden, David T -- Bardeesy, Nabeel -- DK050234/DK/NIDDK NIH HHS/ -- R01 DK050234/DK/NIDDK NIH HHS/ -- R01 DK050234-12/DK/NIDDK NIH HHS/ -- R01 DK050234-13/DK/NIDDK NIH HHS/ -- R01 HG005230/HG/NHGRI NIH HHS/ -- R01 HG005230-01/HG/NHGRI NIH HHS/ -- U01 CA141576-01/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 2;468(7324):659-63. doi: 10.1038/nature09572.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Center and Center for Regenerative Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21124451" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Apoptosis ; Autophagy ; Bone Marrow/metabolism/pathology ; Cell Cycle ; Cell Proliferation ; Cell Survival ; *Energy Metabolism ; Enzyme Activation ; Female ; Hematopoiesis ; Hematopoietic Stem Cells/*cytology/*metabolism/pathology ; Homeostasis ; Lipid Metabolism ; Male ; Membrane Potential, Mitochondrial ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism/pathology ; Multiprotein Complexes ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Proteins/antagonists & inhibitors/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Tumor Suppressor Proteins/deficiency/genetics/metabolism
    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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  • 4
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    RNA sequencing of pancreatic circulating tumour cells implicates WNT signalling in metastasis (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-07-06
    Description: Circulating tumour cells (CTCs) shed into blood from primary cancers include putative precursors that initiate distal metastases. Although these cells are extraordinarily rare, they may identify cellular pathways contributing to the blood-borne dissemination of cancer. Here, we adapted a microfluidic device for efficient capture of CTCs from an endogenous mouse pancreatic cancer model and subjected CTCs to single-molecule RNA sequencing, identifying Wnt2 as a candidate gene enriched in CTCs. Expression of WNT2 in pancreatic cancer cells suppresses anoikis, enhances anchorage-independent sphere formation, and increases metastatic propensity in vivo. This effect is correlated with fibronectin upregulation and suppressed by inhibition of MAP3K7 (also known as TAK1) kinase. In humans, formation of non-adherent tumour spheres by pancreatic cancer cells is associated with upregulation of multiple WNT genes, and pancreatic CTCs revealed enrichment for WNT signalling in 5 out of 11 cases. Thus, molecular analysis of CTCs may identify candidate therapeutic targets to prevent the distal spread of cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408856/" 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/PMC3408856/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Min -- Ting, David T -- Stott, Shannon L -- Wittner, Ben S -- Ozsolak, Fatih -- Paul, Suchismita -- Ciciliano, Jordan C -- Smas, Malgorzata E -- Winokur, Daniel -- Gilman, Anna J -- Ulman, Matthew J -- Xega, Kristina -- Contino, Gianmarco -- Alagesan, Brinda -- Brannigan, Brian W -- Milos, Patrice M -- Ryan, David P -- Sequist, Lecia V -- Bardeesy, Nabeel -- Ramaswamy, Sridhar -- Toner, Mehmet -- Maheswaran, Shyamala -- Haber, Daniel A -- 5K12CA87723-09/CA/NCI NIH HHS/ -- 5R01EB008047/EB/NIBIB NIH HHS/ -- CA129933/CA/NCI NIH HHS/ -- P01 CA117969/CA/NCI NIH HHS/ -- R01 CA129933/CA/NCI NIH HHS/ -- U01 EB012493/EB/NIBIB NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jul 26;487(7408):510-3. doi: 10.1038/nature11217.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763454" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival ; Contact Inhibition ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic/*genetics ; Genes, Neoplasm/genetics ; Humans ; MAP Kinase Kinase Kinases/antagonists & inhibitors ; Mice ; Neoplasm Metastasis/*genetics ; Neoplastic Cells, Circulating/*metabolism ; Pancreatic Neoplasms/*genetics/*pathology ; RNA, Messenger/analysis/biosynthesis ; Sequence Analysis, RNA ; Wnt Proteins/genetics/*metabolism ; Wnt Signaling Pathway/*genetics ; Wnt2 Protein/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Htt CAG repeat expansion confers pleiotropic gains of mutant huntingtin function in chromatin regulation (2015)
    Oxford University Press
    Details
    Publication Date: 2015-04-04
    Description: The CAG repeat expansion in the Huntington's disease gene HTT extends a polyglutamine tract in mutant huntingtin that enhances its ability to facilitate polycomb repressive complex 2 (PRC2). To gain insight into this dominant gain of function, we mapped histone modifications genome-wide across an isogenic panel of mouse embryonic stem cell (ESC) and neuronal progenitor cell (NPC) lines, comparing the effects of Htt null and different size Htt CAG mutations. We found that Htt is required in ESC for the proper deposition of histone H3K27me3 at a subset of ‘bivalent’ loci but in NPC it is needed at ‘bivalent’ loci for both the proper maintenance and the appropriate removal of this mark. In contrast, Htt CAG size, though changing histone H3K27me3, is prominently associated with altered histone H3K4me3 at ‘active’ loci. The sets of ESC and NPC genes with altered histone marks delineated by the lack of huntingtin or the presence of mutant huntingtin, though distinct, are enriched in similar pathways with apoptosis specifically highlighted for the CAG mutation. Thus, the manner by which huntingtin function facilitates PRC2 may afford mutant huntingtin with multiple opportunities to impinge upon the broader machinery that orchestrates developmentally appropriate chromatin status.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 6
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    An in-depth map of polyadenylation sites in cancer (2012)
    Oxford University Press
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    Publication Date: 2012-09-27
    Description: We present a comprehensive map of over 1 million polyadenylation sites and quantify their usage in major cancers and tumor cell lines using direct RNA sequencing. We built the Expression and Polyadenylation Database to enable the visualization of the polyadenylation maps in various cancers and to facilitate the discovery of novel genes and gene isoforms that are potentially important to tumorigenesis. Analyses of polyadenylation sites indicate that a large fraction (~30%) of mRNAs contain alternative polyadenylation sites in their 3' untranslated regions, independent of the cell type. The shortest 3' untranslated region isoforms are preferentially upregulated in cancer tissues, genome-wide. Candidate targets of alternative polyadenylation-mediated upregulation of short isoforms include POLR2K, and signaling cascades of cell–cell and cell–extracellular matrix contact, particularly involving regulators of Rho GTPases. Polyadenylation maps also helped to improve 3' untranslated region annotations and identify candidate regulatory marks such as sequence motifs, H3K36Me3 and Pabpc1 that are isoform dependent and occur in a position-specific manner. In summary, these results highlight the need to go beyond monitoring only the cumulative transcript levels for a gene, to separately analysing the expression of its RNA isoforms.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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