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The Temperature-Dependent Retention of Introns in GPI8 Transcripts Contributes to a Drooping and Fragile Shoot Phenotype in Rice
International Journal of Molecular Sciences Article The Temperature-Dependent Retention of Introns in GPI8 Transcripts Contributes to a Drooping and Fragile Shoot Phenotype in Rice Bo Zhao 1,2, Yongyan Tang 1,2, Baocai Zhang 3, Pingzhi Wu 1, Meiru Li 1, Xinlan Xu 1, Guojiang Wu 1, Huawu Jiang 1 and Yaping Chen 1,* 1 Key Laboratory of Plant Resources Conservation and Sustainable Utilization, South China Botanical Garden, Innovation Academy for Seed Design, Chinese Academy of Sciences, Guangzhou 510650, China; [email protected] (B.Z.); [email protected] (Y.T.); [email protected] (P.W.); [email protected] (M.L.); [email protected] (X.X.); [email protected] (G.W.); [email protected] (H.J.) 2 University of Chinese Academy of Sciences, Beijing 100049, China 3 State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China; [email protected] * Correspondence: [email protected]; Tel.: +86-20-37252750 Received: 14 November 2019; Accepted: 30 December 2019; Published: 31 December 2019 Abstract: Attachment of glycosylphosphatidylinositols (GPIs) to the C-termini of proteins is one of the most common posttranslational modifications in eukaryotic cells. GPI8/PIG-K is the catalytic subunit of the GPI transamidase complex catalyzing the transfer en bloc GPI to proteins. In this study, a T-DNA insertional mutant of rice with temperature-dependent drooping and fragile (df ) shoots phenotype was isolated. The insertion site of the T-DNA fragment was 879 bp downstream of the stop codon of the OsGPI8 gene, which caused introns retention in the gene transcripts, especially at higher temperatures. -
ESM1 As a Marker of Macrotrabecular-Massive Hepatocellular Carcinoma
Author Manuscript Published OnlineFirst on July 29, 2019; DOI: 10.1158/1078-0432.CCR-19-0859 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. ESM1 as a marker of macrotrabecular-massive hepatocellular carcinoma. Julien Calderaro1,2,3, Léa Meunier4, Cong Trung Nguyen2,3, Marouane Boubaya5, Stefano Caruso4, Alain Luciani2,3,6, Giuliana Amaddeo2,3,7, Hélène Regnault7, Jean-Charles Nault4,8,9 , Justine Cohen1,2,Frédéric Oberti10, Sophie Michalak11, Mohamed Bouattour12, Valérie Vilgrain18, Georges Philippe Pageaux14, Jeanne Ramos15, Nathalie Barget16, Boris Guiu17, Valérie Paradis13, Christophe Aubé19, Alexis Laurent20, Jean-Michel Pawlotsky2,3,22, Nathalie Ganne-Carrié4,8,9, Jessica Zucman-Rossi4,22,23, Olivier Seror24, Marianne Ziol4,9,25. 1. Assistance Publique-Hôpitaux de Paris, Département Pathologie, CHU Henri Mondor, F-94000 Créteil, France. 2. Université Paris-Est Créteil, Faculté de Médecine, Créteil, France. 3. Inserm, U955, Team 18, Créteil, France. 4. INSERM UMR-1162, génomique fonctionnelle des tumeurs solides, 75010, Paris, France 5. Unité de Recherche Clinique, AP-HP, Hôpital Universitaire Avicenne, Bobigny, France. 6. Assistance Publique-Hôpitaux de Paris, Service de Radiologie, CHU Henri Mondor, F-94000 Créteil, France 7. Assistance Publique-Hôpitaux de Paris, Service d'Hépatologie, CHU Henri Mondor, F-94000 Créteil, France. 8. Service d’Hépatologie, Groupe hospitalier Paris-Seine-Saint Denis, Hôpital Jean Verdier, AP-HP, 93143 Bondy, France, 9. Université Paris 13, Sorbonne Paris-Cité, Bobigny, France 10. Hépato-gastroentérologie et oncologie digestive, Centre Hospitalier Universitaire d'Angers, France. 11. Service d'Anatomie et de Cytologie Pathologiques, Centre Hospitalier Universitaire d'Angers, France. 12. Assistance Publique-Hôpitaux de Paris, Service d’Oncologie Digestive, Hôpital Universitaire Beaujon, France. -
Environmental Influences on Endothelial Gene Expression
ENDOTHELIAL CELL GENE EXPRESSION John Matthew Jeff Herbert Supervisors: Prof. Roy Bicknell and Dr. Victoria Heath PhD thesis University of Birmingham August 2012 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. ABSTRACT Tumour angiogenesis is a vital process in the pathology of tumour development and metastasis. Targeting markers of tumour endothelium provide a means of targeted destruction of a tumours oxygen and nutrient supply via destruction of tumour vasculature, which in turn ultimately leads to beneficial consequences to patients. Although current anti -angiogenic and vascular targeting strategies help patients, more potently in combination with chemo therapy, there is still a need for more tumour endothelial marker discoveries as current treatments have cardiovascular and other side effects. For the first time, the analyses of in-vivo biotinylation of an embryonic system is performed to obtain putative vascular targets. Also for the first time, deep sequencing is applied to freshly isolated tumour and normal endothelial cells from lung, colon and bladder tissues for the identification of pan-vascular-targets. Integration of the proteomic, deep sequencing, public cDNA libraries and microarrays, delivers 5,892 putative vascular targets to the science community. -
Integrative Genome Analysis of Somatic P53 Mutant Osteosarcomas Identifies Ets2-Dependent Regulation of Small Nucleolar Rnas by Mutant P53 Protein
Downloaded from genesdev.cshlp.org on September 30, 2021 - Published by Cold Spring Harbor Laboratory Press Integrative genome analysis of somatic p53 mutant osteosarcomas identifies Ets2-dependent regulation of small nucleolar RNAs by mutant p53 protein Rasoul Pourebrahim,1 Yun Zhang,1 Bin Liu,1 Ruli Gao,1 Shunbin Xiong,1 Patrick P. Lin,2 Mark J. McArthur,3 Michael C. Ostrowski,4 and Guillermina Lozano1 1Department of Genetics, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA; 2Department of Orthopedic Oncology, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA; 3Department of Veterinary Medicine and Surgery, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA; 4Department of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio 43210, USA TP53 is the most frequently mutated gene in human cancer. Many mutant p53 proteins exert oncogenic gain-of- function (GOF) properties that contribute to metastasis, but the mechanisms mediating these functions remain poorly defined in vivo. To elucidate how mutant p53 GOF drives metastasis, we developed a traceable somatic os- teosarcoma mouse model that is initiated with either a single p53 mutation (p53R172H) or p53 loss in osteoblasts. Our study confirmed that p53 mutant mice developed osteosarcomas with increased metastasis as compared with p53-null mice. Comprehensive transcriptome RNA sequencing (RNA-seq) analysis of 16 tumors identified a cluster of small nucleolar RNAs (snoRNAs) that are highly up-regulated in p53 mutant tumors. Regulatory element analysis of these deregulated snoRNA genes identified strong enrichment of a common Ets2 transcription factor-binding site. Homozygous deletion of Ets2 in p53 mutant mice resulted in strong down-regulation of snoRNAs and reversed the prometastatic phenotype of mutant p53 but had no effect on osteosarcoma development, which remained 100% penetrant. -
Mapping the Genetic Architecture of Gene Regulation in Whole Blood
Mapping the Genetic Architecture of Gene Regulation in Whole Blood Katharina Schramm1,2., Carola Marzi3,4,5., Claudia Schurmann6., Maren Carstensen7,8., Eva Reinmaa9,10, Reiner Biffar11, Gertrud Eckstein1, Christian Gieger12, Hans-Jo¨ rgen Grabe13, Georg Homuth6, Gabriele Kastenmu¨ ller14, Reedik Ma¨gi10, Andres Metspalu9,10, Evelin Mihailov10,15, Annette Peters2, Astrid Petersmann16, Michael Roden7,8,17, Konstantin Strauch12,18, Karsten Suhre14,19, Alexander Teumer6,UweVo¨ lker6, Henry Vo¨ lzke20, Rui Wang-Sattler3,4, Melanie Waldenberger3,4, Thomas Meitinger1,2,21, Thomas Illig22, Christian Herder7,8., Harald Grallert3,4,5., Holger Prokisch1,2*. 1 Institute of Human Genetics, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany, 2 Institute of Human Genetics, Technical University Munich, Mu¨nchen, Germany, 3 Research Unit of Molecular Epidemiology, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany, 4 Institute of Epidemiology II, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany, 5 German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany, 6 Interfaculty Institute for Genetics and Functional Genomics, Department of Functional Genomics, University Medicine Greifswald, Greifswald, Germany, 7 Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University Du¨sseldorf, Du¨sseldorf, Germany, 8 German Center for Diabetes Research (DZD e.V.), -
Alterations of Genetic Variants and Transcriptomic Features of Response to Tamoxifen in the Breast Cancer Cell Line
Alterations of Genetic Variants and Transcriptomic Features of Response to Tamoxifen in the Breast Cancer Cell Line Mahnaz Nezamivand-Chegini Shiraz University Hamed Kharrati-Koopaee Shiraz University https://orcid.org/0000-0003-2345-6919 seyed taghi Heydari ( [email protected] ) Shiraz University of Medical Sciences https://orcid.org/0000-0001-7711-1137 Hasan Giahi Shiraz University Ali Dehshahri Shiraz University of Medical Sciences Mehdi Dianatpour Shiraz University of Medical Sciences Kamran Bagheri Lankarani Shiraz University of Medical Sciences Research Keywords: Tamoxifen, breast cancer, genetic variants, RNA-seq. Posted Date: August 17th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-783422/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/33 Abstract Background Breast cancer is one of the most important causes of mortality in the world, and Tamoxifen therapy is known as a medication strategy for estrogen receptor-positive breast cancer. In current study, two hypotheses of Tamoxifen consumption in breast cancer cell line (MCF7) were investigated. First, the effect of Tamoxifen on genes expression prole at transcriptome level was evaluated between the control and treated samples. Second, due to the fact that Tamoxifen is known as a mutagenic factor, there may be an association between the alterations of genetic variants and Tamoxifen treatment, which can impact on the drug response. Methods In current study, the whole-transcriptome (RNA-seq) dataset of four investigations (19 samples) were derived from European Bioinformatics Institute (EBI). At transcriptome level, the effect of Tamoxifen was investigated on gene expression prole between control and treatment samples. -
Cacybp (NM 009786) Mouse Tagged ORF Clone Product Data
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for MR202748 Cacybp (NM_009786) Mouse Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: Cacybp (NM_009786) Mouse Tagged ORF Clone Tag: Myc-DDK Symbol: Cacybp Synonyms: SIP Vector: pCMV6-Entry (PS100001) E. coli Selection: Kanamycin (25 ug/mL) Cell Selection: Neomycin ORF Nucleotide >MR202748 ORF sequence Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGGCTTCCGTTTTGGAAGAGTTGCAGAAAGACCTAGAAGAGGTCAAAGTATTGCTGGAAAAGTCCACTA GGAAAAGACTACGTGATACTCTTACAAGTGAAAAGTCCAAGATTGAGACGGAACTCAAGAACAAGATGCA ACAGAAGTCGCAGAAGAAACCAGAACTTGATAATGAAAAGCCAGCTGCTGTGGTTGCTCCTCTTACAACA GGATACACCGTGAAAATCAGTAATTATGGATGGGATCAGTCAGATAAGTTTGTGAAAATCTACATTACCT TGACTGGCGTCCATCAGGTGCCCACTGAGAACGTGCAGGTGCACTTCACAGAGAGGTCATTTGATCTTCT GGTAAAAAACCTCAATGGCAAGAATTACTCCATGATTGTGAACAATCTTTTGAAACCTATCTCTGTGGAA AGCAGTTCAAAAAAAGTCAAGACTGATACAGTAATTATTCTATGTAGAAAGAAAGCAGAAAACACAAGAT GGGACTACTTAACACAGGTGGAAAAGGAATGCAAAGAGAAAGAAAAGCCTTCCTACGACACGGAGGCAGA CCCTAGTGAGGGATTAATGAATGTTCTAAAGAAAATTTATGAAGACGGAGACGATGATATGAAGCGAACC ATTAATAAAGCGTGGGTGGAATCCAGAGAGAAGCAAGCCAGAGAAGACACGGAATTT ACGCGTACGCGGCCGCTCGAGCAGAAACTCATCTCAGAAGAGGATCTGGCAGCAAATGATATCCTGGATT ACAAGGATGACGACGATAAGGTTTAA This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online -
Warsaw Breakage Syndrome DDX11 Helicase Acts Jointly with RAD17 in the Repair of Bulky Lesions and Replication Through Abasic Sites
Warsaw breakage syndrome DDX11 helicase acts jointly with RAD17 in the repair of bulky lesions and replication through abasic sites Takuya Abea,b,1, Masato Ookaa,b,1, Ryotaro Kawasumia, Keiji Miyatab, Minoru Takatac, Kouji Hirotab, and Dana Branzeia,d,2 aDNA Repair lab, IFOM, Fondazione Italiana per la Ricerca sul Cancro Institute of Molecular Oncology, 20139 Milan, Italy; bDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Hachioji-shi, 192-0397 Tokyo, Japan; cLaboratory of DNA Damage Signaling, Radiation Biology Center, Kyoto University, 606-8501 Kyoto, Japan; and dIstituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche, 27100 Pavia, Italy Edited by Philip C. Hanawalt, Stanford University, Stanford, CA, and approved June 28, 2018 (received for review February 21, 2018) Warsaw breakage syndrome, a developmental disorder caused by genes result in impaired ability of cells to deal with certain mutations in the DDX11/ChlR1 helicase, shows cellular features of forms of DNA damage, such as endogenous formaldehyde (9), genome instability similar to Fanconi anemia (FA). Here we report and lead to a hereditary disorder, FA, characterized by bone that DDX11-deficient avian DT40 cells exhibit interstrand crosslink marrow failure, developmental abnormalities, and predisposition (ICL)-induced chromatid breakage, with DDX11 functioning as to cancer. backup for the FA pathway in regard to ICL repair. Importantly, The central components of the FA pathway, FANCD2 and we establish that DDX11 acts jointly with the 9-1-1 checkpoint FANCI, interact with each other (10), and are monoubiquitylated – clamp and its loader, RAD17, primarily in a postreplicative fashion, by the FA core complex. -
Assessment Genetics Mutations in Genes AMELX, ENAM, MMP20 and FAM83H in Inducate Amelogenesis Imperfecta Syndrome Shahin Asadi*
Haematology Open Access Open Journal Review Assessment Genetics Mutations in Genes AMELX, ENAM, MMP20 and FAM83H in Inducate Amelogenesis Imperfecta Syndrome Shahin Asadi* Director of the Division of Medical Genetics and Molecular Research, Molecular Medicine, Genetics Harvard University, USA *Correspondence to: Shahin Asadi; Director of the Division of Medical Genetics and Molecular Research, Molecular Medicine, Genetics Harvard University, USA; E-mail: [email protected] Received: March 28th, 2019; Revised: March 29th, 2019; Accepted: March 29th, 2019; Published: March 30th, 2019 Citation: Carlos TJ, Ignacio HD, Xavier SI, Ariel LE. Assessment genetics mutations in genes AMELX,ENAM, MMP20 and FAM83H in inducate amelogenesis imperfecta syndrome. Haemat Open A Open J. 2019; I(1): 5-8. ABSTRACT Defective amelogenesis syndrome is a genetic disorder in the development of teeth. The researchers described at least 14 types of incomplete amelogenesis disorders. Mutations in the AMELX, ENAM, MMP20, and FAM83H genes can cause malformation of the amelogenesis syndrome. Keywords: Amelogenesis syndrome, AMELX, ENAM, MMP20, FAM83H genes, Teeth disorders.. GENERALIZATIONS OF INCOMPLETE AMELOGENESIS cific dental disorders and hereditary patterns. Additionally, incomplete SYNDROME amelogenesis syndrome can occur alone without any other symptoms or symptoms, or it can occur as part of a syndrome that affects different Defective amelogenesis syndrome is a genetic disorder in the develop- parts of the body.2 ment of teeth. This condition causes the teeth to be abnormally small, colored, pitted or perforated, and are prone to wear and breakage. Other Figure 2. Another view of dental disorders in amelogenesis syndrome dental disorders may also occur in incomplete amelogenesis syndrome. These defects, which vary among people affected, can affect the teeth (the child) and permanent teeth (adults).1 Figure 1. -
Supplementary Data
SUPPLEMENTARY DATA A cyclin D1-dependent transcriptional program predicts clinical outcome in mantle cell lymphoma Santiago Demajo et al. 1 SUPPLEMENTARY DATA INDEX Supplementary Methods p. 3 Supplementary References p. 8 Supplementary Tables (S1 to S5) p. 9 Supplementary Figures (S1 to S15) p. 17 2 SUPPLEMENTARY METHODS Western blot, immunoprecipitation, and qRT-PCR Western blot (WB) analysis was performed as previously described (1), using cyclin D1 (Santa Cruz Biotechnology, sc-753, RRID:AB_2070433) and tubulin (Sigma-Aldrich, T5168, RRID:AB_477579) antibodies. Co-immunoprecipitation assays were performed as described before (2), using cyclin D1 antibody (Santa Cruz Biotechnology, sc-8396, RRID:AB_627344) or control IgG (Santa Cruz Biotechnology, sc-2025, RRID:AB_737182) followed by protein G- magnetic beads (Invitrogen) incubation and elution with Glycine 100mM pH=2.5. Co-IP experiments were performed within five weeks after cell thawing. Cyclin D1 (Santa Cruz Biotechnology, sc-753), E2F4 (Bethyl, A302-134A, RRID:AB_1720353), FOXM1 (Santa Cruz Biotechnology, sc-502, RRID:AB_631523), and CBP (Santa Cruz Biotechnology, sc-7300, RRID:AB_626817) antibodies were used for WB detection. In figure 1A and supplementary figure S2A, the same blot was probed with cyclin D1 and tubulin antibodies by cutting the membrane. In figure 2H, cyclin D1 and CBP blots correspond to the same membrane while E2F4 and FOXM1 blots correspond to an independent membrane. Image acquisition was performed with ImageQuant LAS 4000 mini (GE Healthcare). Image processing and quantification were performed with Multi Gauge software (Fujifilm). For qRT-PCR analysis, cDNA was generated from 1 µg RNA with qScript cDNA Synthesis kit (Quantabio). qRT–PCR reaction was performed using SYBR green (Roche). -
Variation in Protein Coding Genes Identifies Information
bioRxiv preprint doi: https://doi.org/10.1101/679456; this version posted June 21, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Animal complexity and information flow 1 1 2 3 4 5 Variation in protein coding genes identifies information flow as a contributor to 6 animal complexity 7 8 Jack Dean, Daniela Lopes Cardoso and Colin Sharpe* 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Institute of Biological and Biomedical Sciences 25 School of Biological Science 26 University of Portsmouth, 27 Portsmouth, UK 28 PO16 7YH 29 30 * Author for correspondence 31 [email protected] 32 33 Orcid numbers: 34 DLC: 0000-0003-2683-1745 35 CS: 0000-0002-5022-0840 36 37 38 39 40 41 42 43 44 45 46 47 48 49 Abstract bioRxiv preprint doi: https://doi.org/10.1101/679456; this version posted June 21, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Animal complexity and information flow 2 1 Across the metazoans there is a trend towards greater organismal complexity. How 2 complexity is generated, however, is uncertain. Since C.elegans and humans have 3 approximately the same number of genes, the explanation will depend on how genes are 4 used, rather than their absolute number. -
Discovery of Genes by Phylocsf Supplemental
Supplemental Materials for Discovery of high-confidence human protein-coding genes and exons by whole-genome PhyloCSF helps elucidate 118 GWAS loci Supplemental Methods ....................................................................................................................... 2 Supplemental annotation methods ........................................................................................................... 2 Manual annotation overview ...................................................................................................................................... 2 Summary diagram for the workflow used in this study ................................................................................. 3 Transcriptomics analysis ............................................................................................................................................. 3 Comparative annotation ............................................................................................................................................... 4 Overlap of novel annotations with transposon sequences ........................................................................... 6 Assessing the novelty of annotations ...................................................................................................................... 7 Additional considerations for the annotation of PCCRs in other species ............................................... 7 PhyloCSF and browser tracks ....................................................................................................................