Genomic Responses to Selection for Tame/Aggressive Behaviors in the Silver Fox (Vulpes Vulpes)
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Nuclear and Mitochondrial Genome Defects in Autisms
UC Irvine UC Irvine Previously Published Works Title Nuclear and mitochondrial genome defects in autisms. Permalink https://escholarship.org/uc/item/8vq3278q Journal Annals of the New York Academy of Sciences, 1151(1) ISSN 0077-8923 Authors Smith, Moyra Spence, M Anne Flodman, Pamela Publication Date 2009 DOI 10.1111/j.1749-6632.2008.03571.x License https://creativecommons.org/licenses/by/4.0/ 4.0 Peer reviewed eScholarship.org Powered by the California Digital Library University of California THE YEAR IN HUMAN AND MEDICAL GENETICS 2009 Nuclear and Mitochondrial Genome Defects in Autisms Moyra Smith, M. Anne Spence, and Pamela Flodman Department of Pediatrics, University of California, Irvine, California In this review we will evaluate evidence that altered gene dosage and structure im- pacts neurodevelopment and neural connectivity through deleterious effects on synap- tic structure and function, and evidence that the latter are key contributors to the risk for autism. We will review information on alterations of structure of mitochondrial DNA and abnormal mitochondrial function in autism and indications that interactions of the nuclear and mitochondrial genomes may play a role in autism pathogenesis. In a final section we will present data derived using Affymetrixtm SNP 6.0 microar- ray analysis of DNA of a number of subjects and parents recruited to our autism spectrum disorders project. We include data on two sets of monozygotic twins. Col- lectively these data provide additional evidence of nuclear and mitochondrial genome imbalance in autism and evidence of specific candidate genes in autism. We present data on dosage changes in genes that map on the X chromosomes and the Y chro- mosome. -
A Clinicopathological and Molecular Genetic Analysis of Low-Grade Glioma in Adults
A CLINICOPATHOLOGICAL AND MOLECULAR GENETIC ANALYSIS OF LOW-GRADE GLIOMA IN ADULTS Presented by ANUSHREE SINGH MSc A thesis submitted in partial fulfilment of the requirements of the University of Wolverhampton for the degree of Doctor of Philosophy Brain Tumour Research Centre Research Institute in Healthcare Sciences Faculty of Science and Engineering University of Wolverhampton November 2014 i DECLARATION This work or any part thereof has not previously been presented in any form to the University or to any other body whether for the purposes of assessment, publication or for any other purpose (unless otherwise indicated). Save for any express acknowledgments, references and/or bibliographies cited in the work, I confirm that the intellectual content of the work is the result of my own efforts and of no other person. The right of Anushree Singh to be identified as author of this work is asserted in accordance with ss.77 and 78 of the Copyright, Designs and Patents Act 1988. At this date copyright is owned by the author. Signature: Anushree Date: 30th November 2014 ii ABSTRACT The aim of the study was to identify molecular markers that can determine progression of low grade glioma. This was done using various approaches such as IDH1 and IDH2 mutation analysis, MGMT methylation analysis, copy number analysis using array comparative genomic hybridisation and identification of differentially expressed miRNAs using miRNA microarray analysis. IDH1 mutation was present at a frequency of 71% in low grade glioma and was identified as an independent marker for improved OS in a multivariate analysis, which confirms the previous findings in low grade glioma studies. -
Genetics of Familial Non-Medullary Thyroid Carcinoma (FNMTC)
cancers Review Genetics of Familial Non-Medullary Thyroid Carcinoma (FNMTC) Chiara Diquigiovanni * and Elena Bonora Unit of Medical Genetics, Department of Medical and Surgical Sciences, University of Bologna, 40138 Bologna, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-051-208-8418 Simple Summary: Non-medullary thyroid carcinoma (NMTC) originates from thyroid follicular epithelial cells and is considered familial when occurs in two or more first-degree relatives of the patient, in the absence of predisposing environmental factors. Familial NMTC (FNMTC) cases show a high genetic heterogeneity, thus impairing the identification of pivotal molecular changes. In the past years, linkage-based approaches identified several susceptibility loci and variants associated with NMTC risk, however only few genes have been identified. The advent of next-generation sequencing technologies has improved the discovery of new predisposing genes. In this review we report the most significant genes where variants predispose to FNMTC, with the perspective that the integration of these new molecular findings in the clinical data of patients might allow an early detection and tailored therapy of the disease, optimizing patient management. Abstract: Non-medullary thyroid carcinoma (NMTC) is the most frequent endocrine tumor and originates from the follicular epithelial cells of the thyroid. Familial NMTC (FNMTC) has been defined in pedigrees where two or more first-degree relatives of the patient present the disease in absence of other predisposing environmental factors. Compared to sporadic cases, FNMTCs are often multifocal, recurring more frequently and showing an early age at onset with a worse outcome. FNMTC cases Citation: Diquigiovanni, C.; Bonora, E. -
Genetic Influences on Brain Gene Expression in Rats Selected for Tameness and Aggression
Genetic Influences on Brain Gene Expression in Rats Selected for Tameness and Aggression Henrike O. Heyne*,§, Susann Lautenschläger§, Ronald Nelson†, François Besnier†,‡, Maxime Rotival**, Alexander Cagan*, Rimma Kozhemyakina§§, Irina Z. Plyusnina§§, Lyudmila Trut§§, Örjan Carlborg†, Enrico Petretto**, Leonid Kruglyak††,‡‡,***, Svante Pääbo*, Torsten Schöneberg§, Frank W. Albert*,†† * Department of Evolutionary Genetics, Max Planck Institute for Evolutionary Anthropology, Deutscher Platz 6, 04103 Leipzig, Germany § Institute for Biochemistry, University of Leipzig, Medical Faculty, Johannisallee 30, 04103 Leipzig † Swedish University of Agricultural Sciences, Department of Clinical Sciences, Division of Computational Genetics, Mailing address: Box 7078 SE-75007 Uppsala Sweden ‡ Section of Population Genetics and Ecology, Institute of Marine Research, Bergen, Norway, Havforskningsinstituttet, Postboks 1870, Nordnes 5817, Bergen Norway ** MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK §§ Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 630090 Novosibirsk, Russia †† Department of Human Genetics, University of California, Los Angeles, Gonda Center, 695 Charles E. Young Drive South, Los Angeles, CA 90095, USA ‡‡ Department of Biological Chemistry, University of California, Los Angeles, Gonda Center, 695 Charles E. Young Drive South, Los Angeles, CA 90095, USA *** Howard Hughes Medical Institute, University of California, Los Angeles, Gonda Center, 695 Charles E. Young Drive South, Los Angeles, CA 90095, USA deceased: I.Z.P. Irina Z. Plyusnina . 1 ABSTRACT Inter-individual differences in many behaviors are partly due to genetic differences, but the identification of the genes and variants that influence behavior remains challenging. Here, we studied an F2 intercross of two outbred lines of rats selected for tame and aggressive behavior towards humans for more than 64 generations. -
The Putative Tumor Suppressor Gene GLTSCR2 Induces PTEN-Modulated Cell Death
Cell Death and Differentiation (2007) 14, 1872–1879 & 2007 Nature Publishing Group All rights reserved 1350-9047/07 $30.00 www.nature.com/cdd The putative tumor suppressor gene GLTSCR2 induces PTEN-modulated cell death J-H Yim1,2, Y-J Kim1,2, J-H Ko1,2, Y-E Cho1,2, S-M Kim1,2, J-Y Kim1,2, S Lee1,2 and J-H Park*,1,2 Glioma tumor suppressor candidate region gene 2 (GLTSCR2/PICT-1) is localized within the well-known 1.4-Mb tumor suppressive region of chromosome 19q, which is frequently altered in various human tumors, including diffuse gliomas. Aside from its localization on the chromosome, several lines of evidence, such as PTEN phosphorylation, support that GLTSCR2 partakes in the suppression of tumor growth and development. However, much remains unknown about the molecular mechanisms of the tumor suppressive activity of GLTSCR2. The purpose of this study was to investigate the molecular mechanisms of GLTSCR2 in cell death pathways in association with its binding partner PTEN. In this work, we show that GLTSCR2 is a nucleus-localized protein with a discrete globular expression pattern. In addition to phosphorylating PTEN, GLTSCR2 induces caspase-independent PTEN-modulated apoptotic cell death when overexpressed. However, the cytotoxic activity of GLTSCR2 is independent of its ability to phosphorylate PTEN, suggesting that the GLTSCR2-induced cell death pathway is divergent from PTEN-induced death pathways. Our results suggest that the induction of PTEN-modulated apoptosis is one of the putative mechanisms of tumor suppressive activity -
Tepzz¥ 6Z54za T
(19) TZZ¥ ZZ_T (11) EP 3 260 540 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 27.12.2017 Bulletin 2017/52 C12N 15/113 (2010.01) A61K 9/127 (2006.01) A61K 31/713 (2006.01) C12Q 1/68 (2006.01) (21) Application number: 17000579.7 (22) Date of filing: 12.11.2011 (84) Designated Contracting States: • Sarma, Kavitha AL AT BE BG CH CY CZ DE DK EE ES FI FR GB Philadelphia, PA 19146 (US) GR HR HU IE IS IT LI LT LU LV MC MK MT NL NO • Borowsky, Mark PL PT RO RS SE SI SK SM TR Needham, MA 02494 (US) • Ohsumi, Toshiro Kendrick (30) Priority: 12.11.2010 US 412862 P Cambridge, MA 02141 (US) 20.12.2010 US 201061425174 P 28.07.2011 US 201161512754 P (74) Representative: Clegg, Richard Ian et al Mewburn Ellis LLP (62) Document number(s) of the earlier application(s) in City Tower accordance with Art. 76 EPC: 40 Basinghall Street 11840099.3 / 2 638 163 London EC2V 5DE (GB) (71) Applicant: The General Hospital Corporation Remarks: Boston, MA 02114 (US) •Thecomplete document including Reference Tables and the Sequence Listing can be downloaded from (72) Inventors: the EPO website • Lee, Jeannie T •This application was filed on 05-04-2017 as a Boston, MA 02114 (US) divisional application to the application mentioned • Zhao, Jing under INID code 62. San Diego, CA 92122 (US) •Claims filed after the date of receipt of the divisional application (Rule 68(4) EPC). (54) POLYCOMB-ASSOCIATED NON-CODING RNAS (57) This invention relates to long non-coding RNAs (IncRNAs), libraries of those ncRNAs that bind chromatin modifiers, such as Polycomb Repressive Complex 2, inhibitory nucleic acids and methods and compositions for targeting IncRNAs. -
CXCR4 Pathway Retards Muscle Atrophy During Cancer Cachexia
Oncogene (2016) 35, 6212–6222 © 2016 Macmillan Publishers Limited, part of Springer Nature. All rights reserved 0950-9232/16 www.nature.com/onc ORIGINAL ARTICLE Activation of the SDF1/CXCR4 pathway retards muscle atrophy during cancer cachexia GB Martinelli1, D Olivari1, AD Re Cecconi1, L Talamini1, L Ottoboni2, SH Lecker3, C Stretch4, VE Baracos4, OF Bathe5, A Resovi6, R Giavazzi1, L Cervo7 and R Piccirillo1 Cancer cachexia is a life-threatening syndrome that affects most patients with advanced cancers and causes severe body weight loss, with rapid depletion of skeletal muscle. No treatment is available. We analyzed microarray data sets to identify a subset of genes whose expression is specifically altered in cachectic muscles of Yoshida hepatoma-bearing rodents but not in those with diabetes, disuse, uremia or fasting. Ingenuity Pathways Analysis indicated that three genes belonging to the C-X-C motif chemokine receptor 4 (CXCR4) pathway were downregulated only in muscles atrophying because of cancer: stromal cell-derived factor 1 (SDF1), adenylate cyclase 7 (ADCY7), and p21 protein-activated kinase 1 (PAK1). Notably, we found that, in the Rectus Abdominis muscle of cancer patients, the expression of SDF1 and CXCR4 was inversely correlated with that of two ubiquitin ligases induced in muscle wasting, atrogin-1 and MuRF1, suggesting a possible clinical relevance of this pathway. The expression of all main SDF1 isoforms (α, β, γ) also declined in Tibialis Anterior muscle from cachectic mice bearing murine colon adenocarcinoma or human renal cancer and drugs with anticachexia properties restored their expression. Overexpressing genes of this pathway (that is, SDF1 or CXCR4) in cachectic muscles increased the fiber area by 20%, protecting them from wasting. -
Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like, -
Genome-Wide Association and Transcriptome Studies Identify Candidate Genes and Pathways for Feed Conversion Ratio in Pigs
Miao et al. BMC Genomics (2021) 22:294 https://doi.org/10.1186/s12864-021-07570-w RESEARCH ARTICLE Open Access Genome-wide association and transcriptome studies identify candidate genes and pathways for feed conversion ratio in pigs Yuanxin Miao1,2,3, Quanshun Mei1,2, Chuanke Fu1,2, Mingxing Liao1,2,4, Yan Liu1,2, Xuewen Xu1,2, Xinyun Li1,2, Shuhong Zhao1,2 and Tao Xiang1,2* Abstract Background: The feed conversion ratio (FCR) is an important productive trait that greatly affects profits in the pig industry. Elucidating the genetic mechanisms underpinning FCR may promote more efficient improvement of FCR through artificial selection. In this study, we integrated a genome-wide association study (GWAS) with transcriptome analyses of different tissues in Yorkshire pigs (YY) with the aim of identifying key genes and signalling pathways associated with FCR. Results: A total of 61 significant single nucleotide polymorphisms (SNPs) were detected by GWAS in YY. All of these SNPs were located on porcine chromosome (SSC) 5, and the covered region was considered a quantitative trait locus (QTL) region for FCR. Some genes distributed around these significant SNPs were considered as candidates for regulating FCR, including TPH2, FAR2, IRAK3, YARS2, GRIP1, FRS2, CNOT2 and TRHDE. According to transcriptome analyses in the hypothalamus, TPH2 exhibits the potential to regulate intestinal motility through serotonergic synapse and oxytocin signalling pathways. In addition, GRIP1 may be involved in glutamatergic and GABAergic signalling pathways, which regulate FCR by affecting appetite in pigs. Moreover, GRIP1, FRS2, CNOT2,andTRHDE may regulate metabolism in various tissues through a thyroid hormone signalling pathway. -
Identification of Gene Modules Associated with Warfarin Dosage by a Genome-Wide DNA Methylation Study
ORIGINAL ARTICLES Department of Clinical Pharmacology1, Xiangya Hospital, Institute of Clinical Pharmacology2, Central South University, Hunan Key Laboratory of Pharmacogenetics; Changsha; Department of Cardio-Thoracic Surgery3, the Second Xiangya Hospital of Central South University, Changsha; Key Laboratory of Bio-resources and Eco-environment4 (Ministry of Education), College of Life Science, Sichuan University, Chengdu, China Identification of gene modules associated with warfarin dosage by a genome-wide DNA methylation study ZHIYING LUO1, 2, RONG LIU1, 2, BAO SUN1, 2, XINMING ZHOU3, ZHAOQIAN LIU1, 2, HONGHAO ZHOU1, 2, HENG XU4, XI LI1,2,*,#, WEI ZHANG1,2,*,# Received December 12, 2017, accepted January 10, 2018 *Corresponding authors: Prof. Wei Zhang, Xi Li, Department of Clinical Pharmacology, Xiangya Hospital, Central South University, 110 Xiangya Rode, Kaifu district, Changsha, Hunan 410008, China [email protected]; [email protected] #Wei Zhang and Xi Li contributed equally to this study. Pharmazie 73: 288–293 (2018) doi: 10.1691/ph.2018.7319 Objective: To identify warfarin dose-associated DNA methylation changes, we conducted the first genomewide DNA methylation association study. Method: A total of 22 patients who required an extreme warfarin dosage from VKORC1 -1639AA & CYP2C9*1*1 genotype group were enrolled in this study. The Illumina Infinium Human- Methylation450 platform was used to perform genome-scale DNA methylation profiling, identifying differentially methylated CpG sites by a nonparametric test. WGCNA was used to analyze the association between gene modules and extreme warfarin dosage. Results: For a total of 378,313 CpG sites that passed the quality control processes, we identified eight differentially methylated CpG probes (p<0.05) showing altered DNA methylation level (>20%) between two extreme dose groups. -
Independent Centromere Formation in a Capricious, Gene-Free Domain of Chromosome 13Q21 in Old World Monkeys and Pigs
Open Access Research2006CardoneetVolume al. 7, Issue 10, Article R91 Independent centromere formation in a capricious, gene-free comment domain of chromosome 13q21 in Old World monkeys and pigs Maria Francesca Cardone*, Alicia Alonso†, Michele Pazienza*, Mario Ventura*, Gabriella Montemurro*, Lucia Carbone*, Pieter J de Jong‡, Roscoe Stanyon§, Pietro D'Addabbo*, Nicoletta Archidiacono*, Xinwei She¶, Evan E Eichler¶, Peter E Warburton† and Mariano Rocchi* reviews Addresses: *Department of Genetics and Microbiology, University of Bari, Bari, Italy. †Department of Human Genetics, Mount Sinai School of Medicine, New York, New York 10029, USA. ‡Children's Hospital Oakland Research Institute, Oakland, California 94609, USA. §Department of Animal Biology and Genetics 'Leo Pardi', University of Florence, Florence, Italy. ¶Howard Hughes Medical Institute, Department of Genome Sciences, University of Washington School of Medicine, Seattle, Washington 98195, USA. Correspondence: Mariano Rocchi. Email: [email protected] Published: 13 October 2006 Received: 3 May 2006 reports Revised: 31 July 2006 Genome Biology 2006, 7:R91 (doi:10.1186/gb-2006-7-10-r91) Accepted: 13 October 2006 The electronic version of this article is the complete one and can be found online at http://genomebiology.com/2006/7/10/R91 © 2006 Cardone et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which deposited research permits unrestricted -
Advances in Prognostic Methylation Biomarkers for Prostate Cancer
cancers Review Advances in Prognostic Methylation Biomarkers for Prostate Cancer 1 1,2 1,2, 1,2, , Dilys Lam , Susan Clark , Clare Stirzaker y and Ruth Pidsley * y 1 Epigenetics Research Laboratory, Genomics and Epigenetics Division, Garvan Institute of Medical Research, Sydney, New South Wales 2010, Australia; [email protected] (D.L.); [email protected] (S.C.); [email protected] (C.S.) 2 St. Vincent’s Clinical School, University of New South Wales, Sydney, New South Wales 2010, Australia * Correspondence: [email protected]; Tel.: +61-2-92958315 These authors have contributed equally. y Received: 22 September 2020; Accepted: 13 October 2020; Published: 15 October 2020 Simple Summary: Prostate cancer is a major cause of cancer-related death in men worldwide. There is an urgent clinical need for improved prognostic biomarkers to better predict the likely outcome and course of the disease and thus inform the clinical management of these patients. Currently, clinically recognised prognostic markers lack sensitivity and specificity in distinguishing aggressive from indolent disease, particularly in patients with localised, intermediate grade prostate cancer. Thus, there is major interest in identifying new molecular biomarkers to complement existing standard clinicopathological markers. DNA methylation is a frequent alteration in the cancer genome and offers potential as a reliable and robust biomarker. In this review, we provide a comprehensive overview of the current state of DNA methylation biomarker studies in prostate cancer prognosis. We highlight advances in this field that have enabled the discovery of novel prognostic genes and discuss the potential of methylation biomarkers for noninvasive liquid-biopsy testing.