DOCSLIB.ORG

Expression Profiling Indicating Low Selenium-Sensitive Microrna

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Expression Profiling Indicating Low Selenium-Sensitive Microrna Downloaded from British Journal of Nutrition (2017), 117, 1212–1221 doi:10.1017/S0007114517001143 © The Authors 2017. This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted https://www.cambridge.org/core re-use, distribution, and reproduction in any medium, provided the original work is properly cited. Expression profiling indicating low selenium-sensitive microRNA levels linked to cell cycle and cell stress response pathways in the CaCo-2 cell line Mark J. McCann1*, Kunjana Rotjanapun2, John E. Hesketh3 and Nicole C. Roy1,4 . IP address: 1Food Nutrition & Health Team, AgResearch Ltd, Grasslands Research Centre, Palmerston North 4442, New Zealand 2Department of Food and Nutritional Sciences, University of Reading, PO Box 226, Whiteknights, Reading RG6 6AP, UK 3Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle Upon Tyne, NE2 4HH, UK 170.106.35.234 4The Riddet Institute, Massey University, Palmerston North 4442, New Zealand (Submitted 8 December 2016 – Final revision received 14 March 2017 – Accepted 11 April 2017 – First published online 2 June 2017) , on 01 Oct 2021 at 16:41:43 Abstract Se is an essential micronutrient for human health, and fluctuations in Se levels and the potential cellular dysfunction associated with it may increase the risk for disease. Although Se has been shown to influence several biological pathways important in health, little is known about the effect of Se on the expression of microRNA (miRNA) molecules regulating these pathways. To explore the potential role of Se-sensitive fi miRNA in regulating pathways linked with colon cancer, we pro led the expression of 800 miRNA in the CaCo-2 human adenocarcinoma cell , subject to the Cambridge Core terms of use, available at line in response to a low-Se (72 h at <40 nM) environment using nCounter direct quantification. These data were then examined using a range of in silico databases to identify experimentally validated miRNA–mRNA interactions and the biological pathways involved. We identified ten Se-sensitive miRNA (hsa-miR-93-5p, hsa-miR-106a-5p, hsa-miR-205-5p, hsa-miR-200c-3p, hsa-miR-99b-5p, hsa-miR-302d-3p, hsa-miR-373-3p, hsa-miR-483-3p, hsa-miR-512-5p and hsa-miR-4454), which regulate 3588 mRNA in key pathways such as the cell cycle, the cellular response to stress, and the canonical Wnt/β-catenin, p53 and ERK/MAPK signalling pathways. Our data show that the effects of low Se on biological pathways may, in part, be due to these ten Se-sensitive miRNA. Dysregulation of the cell cycle and of the stress response pathways due to low Se may influence key genes involved in carcinogenesis. Key words: Selenium: MicroRNA: CaCo-2 cell line: NanoString Se is an essential micronutrient for human health(1,2).Itis regulators of gene expression by affecting translation of mRNA – incorporated as selenocysteine into approximately twenty-five into proteins(21 25). It has been shown that miRNA are critical for Se-containing enzymes (selenoproteins), which have been the appropriate regulation of fundamental cellular pathways proposed to have fundamental roles in oxidative defence pathways, and as such have been implicated in a range of processes that if https://www.cambridge.org/core/terms thyroid hormone production, inflammation and cardiovascular incorrectly regulated can lead to diseases such as cancer(2,5,7). health(3). Se status has also been linked to cancer risk on the basis Furthermore, dietary factors are thought to influence miRNA – of cell, animal and epidemiological studies(4 19), but clinical studies levels and potentially activate abnormal cellular pathways in – involving Se supplementation have been inconclusive(20).This cancer development(26 31), and Se status has been shown to reflects our incomplete understanding of the mechanisms by affect miRNA levels in the CaCo-2 cell line(32). However, the which selenoproteins function in complex interdependent cellular effect of dysregulated miRNA expression, due to a low-Se pathways, how these are regulated, the effect of SNP in Se-sensitive environment, on key pathways in cancer development and genes, which may alter how an individual responds to fluctuations progression is unclear. in Se status, and the differences in experimental design and Colon cancer is the third most common cancer in men and . approaches. Inadequate Se and the potential cellular dysfunction the second most common in women globally(33). The disease is https://doi.org/10.1017/S0007114517001143 associated with it may increase the risk for disease(5,7). Severe characterised by distinct mutations throughout life in key Se deficiency is rare but sub-optimal intake has been suggested to biological cellular functions such as the Wnt/β-catenin, p53, – be prevalent in many parts of the world, and the consequences ERK/MAPK and the DNA mismatch repair pathways(34 39). of inadequate Se status in existing diseases and/or the risk for Several components of these canonical pathways have been – developing disease further is not well understood(5,7). linked with abnormal miRNA activity(40,41) and Se status(42 51). MicroRNA (miRNA) are small non-coding RNA, consisting We hypothesised that there are miRNA whose expression is of nineteen to twenty-five nucleotides, which function as dysregulated in a low-Se environment, and that this dysregulation Abbreviations: miRNA, microRNA; qPCR, quantitative PCR. * Corresponding author: M. J. McCann, email [email protected] Downloaded from Selenium-sensitive microRNA 1213 explains in part the effects of Se status on key biological without 40 nM Se, as described above) on three biological repli- https://www.cambridge.org/core pathways. To investigate this hypothesis, we used cultured cates (with eight technical replicates each). Absorbance of the CaCo-2 cells in a low-Se environment for 72 h before formazan dye produced was measured at 450 and 650 nm using a supplementation with or without 40 nM Se (as sodium selenite). FlexStation 3 Spectrophotometer (Molecular Devices). For all TheconcentrationofSeused(40nM) represents a concentration measurements (including the blank), the background absorbance comparable with plasma levels in people with optimal Se status. It (650 nm) was subtracted from the detection wavelength (450 nm) has been previously shown that 40 nM is adequate to maximise and these corrected values were used for analysis. expression of the Se-sensitive selenoprotein GPX1(18,52).The absolute counts of 800 human miRNA were measured using . IP address: Real-time PCR assay NanoString technology to characterise the miRNA profile in response to a low-Se environment (<40 nM)comparedwith The expression of the Se-sensitive genes, GPX1 and SEPW1, a40-nM Se supplementation. These miRNA data were then was quantified using hydrolysis-probe-based real-time PCR. 170.106.35.234 assessed in silico, only on the basis of experimentally validated After 16 h of low Se or treatment with 40 nM of sodium selenite, miRNA–mRNA interactions for their effects on biological RNA was extracted using the SV Total RNA Isolation System pathways based on the gene ontology and Reactome databases. (Promega) according to the manufacturer’s instructions, with The intent of this study was to discover which miRNA were the quality and quantity of total RNA determined on the basis of , on sensitive to low Se so as to provide a robust data set for further 260:230 and 260:280 absorbance ratios using a NanoDrop 1000 01 Oct 2021 at 16:41:43 functional validation. Spectrophotometer (Thermo Fisher Scientific). A sample value of 1·8–2·0 for each ratio was considered to be of sufficient quality. The High-Capacity RNA-to-cDNA kit (Life Techno- Methods logies) was used to prepare 2 µg of complementary DNA (cDNA) from each RNA sample according to the manufacturer’s Cell culture and chemicals , subject to the Cambridge Core terms of use, available at instructions, and the cDNA samples were stored at –20°C until Authenticated CaCo-2 human colon adenocarcinoma cells were required. purchased from the American Type Culture Collection. All cell For real-time PCR analysis, the PrimeTime (Integrated DNA culture reagents and chemicals were purchased from Life Technologies) assays were used. All PCR (no-template controls Technologies unless otherwise stated. The cells were cultured and samples) were prepared as quadruplicate 10 µl reactions before the experiment in Dulbecco’s Modified Eagle’s Medium comprising a 9·0-µl aliquot of master mix (5·0 µlof2× Kapa (DMEM; Sigma-Aldrich), supplemented with 1 % non-essential Probe Fast Mix (KK4703; Kapa Biosystems), 0·5 µlof20× Inte- amino acids, 1 % penicillin–streptomycin solution and 10 % fetal grated DNA Technologies (IDT) gene assay, 3·5 µl of nuclease- bovine serum, and were maintained at 37°C with 5 % CO2 free water (Life Technologies) and 1 µl of cDNA (at a one in ten in a humidified atmosphere. A low-Se medium was prepared dilution in nuclease-free water). The thermal profile used was containing only DMEM, supplemented with 1 % penicillin– as follows: 95°C for 20 s followed by forty cycles of 95°C for streptomycin solution, 5 µg/ml of insulin (Sigma-Aldrich) and 3 s and 60°C for 30 s. The experiment was completed using 5 µg/ml of transferrin (Sigma-Aldrich). a Rotor-Gene 6000 quantitative PCR instrument (Qiagen). The effect of Se supplementation in undifferentiated CaCo-2 These data were normalised to the geometric mean of the β-2 cells was determined in three biologically independent assays. microglobulin (B2M) and the ribosomal protein L19 (RPL19) https://www.cambridge.org/core/terms For each experiment, 5 × 105 CaCo-2 cells were seeded into three reference genes, with the application of the comparative wells of a six-well tissue-culture plate (Corning) and cultured at quantification method with efficiency correction, and expressed 37°C with 5 % CO2 in DMEM-STD in a humidified atmosphere for as fold changes (stressed v.
Load more

Recommended publications
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • Genes with 5' Terminal Oligopyrimidine Tracts Preferentially Escape Global Suppression of Translation by the SARS-Cov-2 NSP1 Protein
    Downloaded from rnajournal.cshlp.org on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press Genes with 5′ terminal oligopyrimidine tracts preferentially escape global suppression of translation by the SARS-CoV-2 Nsp1 protein Shilpa Raoa, Ian Hoskinsa, Tori Tonna, P. Daniela Garciaa, Hakan Ozadama, Elif Sarinay Cenika, Can Cenika,1 a Department of Molecular Biosciences, University of Texas at Austin, Austin, TX 78712, USA 1Corresponding author: [email protected] Key words: SARS-CoV-2, Nsp1, MeTAFlow, translation, ribosome profiling, RNA-Seq, 5′ TOP, Ribo-Seq, gene expression 1 Downloaded from rnajournal.cshlp.org on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press Abstract Viruses rely on the host translation machinery to synthesize their own proteins. Consequently, they have evolved varied mechanisms to co-opt host translation for their survival. SARS-CoV-2 relies on a non-structural protein, Nsp1, for shutting down host translation. However, it is currently unknown how viral proteins and host factors critical for viral replication can escape a global shutdown of host translation. Here, using a novel FACS-based assay called MeTAFlow, we report a dose-dependent reduction in both nascent protein synthesis and mRNA abundance in cells expressing Nsp1. We perform RNA-Seq and matched ribosome profiling experiments to identify gene-specific changes both at the mRNA expression and translation level. We discover that a functionally-coherent subset of human genes are preferentially translated in the context of Nsp1 expression. These genes include the translation machinery components, RNA binding proteins, and others important for viral pathogenicity. Importantly, we uncovered a remarkable enrichment of 5′ terminal oligo-pyrimidine (TOP) tracts among preferentially translated genes.
    [Show full text]
  • Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets
    Research JAMA Neurology | Original Investigation Identification of Candidate Parkinson Disease Genes by Integrating Genome-Wide Association Study, Expression, and Epigenetic Data Sets Demis A. Kia, MBBS; David Zhang, MSc; Sebastian Guelfi, PhD; Claudia Manzoni, PhD; Leon Hubbard, PhD; Regina H. Reynolds, MSc; Juan Botía, PhD; Mina Ryten, MD; Raffaele Ferrari, PhD; Patrick A. Lewis, PhD; Nigel Williams, PhD; Daniah Trabzuni, PhD; John Hardy, PhD; Nicholas W. Wood, PhD; for the United Kingdom Brain Expression Consortium (UKBEC) and the International Parkinson’s Disease Genomics Consortium (IPDGC) Supplemental content IMPORTANCE Substantial genome-wide association study (GWAS) work in Parkinson disease (PD) has led to the discovery of an increasing number of loci shown reliably to be associated with increased risk of disease. Improved understanding of the underlying genes and mechanisms at these loci will be key to understanding the pathogenesis of PD. OBJECTIVE To investigate what genes and genomic processes underlie the risk of sporadic PD. DESIGN AND SETTING This genetic association study used the bioinformatic tools Coloc and transcriptome-wide association study (TWAS) to integrate PD case-control GWAS data published in 2017 with expression data (from Braineac, the Genotype-Tissue Expression [GTEx], and CommonMind) and methylation data (derived from UK Parkinson brain samples) to uncover putative gene expression and splicing mechanisms associated with PD GWAS signals. Candidate genes were further characterized using cell-type specificity, weighted gene coexpression networks, and weighted protein-protein interaction networks. MAIN OUTCOMES AND MEASURES It was hypothesized a priori that some genes underlying PD loci would alter PD risk through changes to expression, splicing, or methylation.
    [Show full text]
  • Genetic Studies of Human Hereditary Skin Disorders: Ectodermal Dysplasias and Alopecias
    Genetic Studies of Human Hereditary Skin Disorders: Ectodermal Dysplasias and Alopecias by Muhammad Tariq Department of Biochemistry Faculty of Biological Sciences Quaid-I-Azam University Islamabad, Pakistan 2009 Genetic Studies of Human Hereditary Skin Disorders: Ectodermal Dysplasias and Alopecias A thesis submitted in the partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biochemistry/ Molecular Biology by Muhammad Tariq Department of Biochemistry Faculty of Biological Sciences Quaid-I-Azam University Islamabad, Pakistan 2009 In the name of Allah, the Most Gracious, the Most Merciful He is the One who created the heavens and the earth, truthfully. Whenever He says, "Be," it is. His word is the absolute truth. All sovereignty belongs to Him the day the horn is blown. Knower of all secrets and declarations, He is the Most Wise, the Cognizant. (Al-Quran 6:73) Dedicated to My sweet & beloved parents & brothers Declaration I hereby declared that the work presented in this thesis is my own effort and hard work and it is written and composed by me. No part of this thesis has been previously published or presented for any other degree or certificate. Muhammad Tariq Contents CONTENTS Title Page No. Preface Acknowledgements I List of Abbreviations III List of Tables VII List of Figures XI Summary XIX List of Publications XXIII Chapter 1: Introduction 1 Human Skin 1 Epidermis 2 Dermis 2 Hypodermis 2 Ectodermal Appendages 2 Hair 2 Nail 3 Tooth 4 Sweat Glands 5 Genetic Studies of Human Hereditary Skin
    [Show full text]
  • Identification of Molecular Targets in Head and Neck Squamous Cell Carcinomas Based on Genome-Wide Gene Expression Profiling
    1489-1497 7/11/07 18:41 Page 1489 ONCOLOGY REPORTS 18: 1489-1497, 2007 Identification of molecular targets in head and neck squamous cell carcinomas based on genome-wide gene expression profiling SATOYA SHIMIZU1,2, NAOHIKO SEKI2, TAKASHI SUGIMOTO2, SHIGETOSHI HORIGUCHI1, HIDEKI TANZAWA3, TOYOYUKI HANAZAWA1 and YOSHITAKA OKAMOTO1 Departments of 1Otorhinolaryngology, 2Functional Genomics and 3Clinical Molecular Biology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan Received May 21, 2007; Accepted June 28, 2007 Abstract. DNA amplifications activate oncogenes and are patients and metastases develop in 15-25% of patients (1). hallmarks of nearly all advanced cancers including head and Many factors, such as TNM stage, pathological grade and neck squamous cell carcinoma (HNSCC). Some oncogenes tumor site, influence the prognosis of HNSCC but are not show both DNA copy number gain and mRNA overexpression. sufficient to predict outcome. In addition, treatment often Chromosomal comparative genomic hybridization and oligo- results in impairment of functions such as speech and nucleotide microarrays were used to examine 8 HNSCC cell swallowing, cosmetic disfiguration and mental pain. These lines and a plot of gene expression levels relative to their inflictions significantly erode quality of life. To overcome this position on the chromosome was produced. Three highly situation, there is a need to find novel biomarkers that classify up-regulated genes, NT5C3, ANLN and INHBA, were patients into prognostic groups, to aid identification of high- identified on chromosome 7p14. These genes were subjected risk patients who may benefit from different treatments. to quantitative real-time RT-PCR on cDNA and genomic Comparative genomic hybridization (CGH) has facilitated DNA derived from 8 HNSCC cell lines.
    [Show full text]
  • A Concise Review of Human Brain Methylome During Aging and Neurodegenerative Diseases
    BMB Rep. 2019; 52(10): 577-588 BMB www.bmbreports.org Reports Invited Mini Review A concise review of human brain methylome during aging and neurodegenerative diseases Renuka Prasad G & Eek-hoon Jho* Department of Life Science, University of Seoul, Seoul 02504, Korea DNA methylation at CpG sites is an essential epigenetic mark position of carbon in the cytosine within CG dinucleotides that regulates gene expression during mammalian development with resultant formation of 5mC. The symmetrical CG and diseases. Methylome refers to the entire set of methylation dinucleotides are also called as CpG, due to the presence of modifications present in the whole genome. Over the last phosphodiester bond between cytosine and guanine. The several years, an increasing number of reports on brain DNA human genome contains short lengths of DNA (∼1,000 bp) in methylome reported the association between aberrant which CpG is commonly located (∼1 per 10 bp) in methylation and the abnormalities in the expression of critical unmethylated form and referred as CpG islands; they genes known to have critical roles during aging and neuro- commonly overlap with the transcription start sites (TSSs) of degenerative diseases. Consequently, the role of methylation genes. In human DNA, 5mC is present in approximately 1.5% in understanding neurodegenerative diseases has been under of the whole genome and CpG base pairs are 5-fold enriched focus. This review outlines the current knowledge of the human in CpG islands than other regions of the genome (3, 4). CpG brain DNA methylomes during aging and neurodegenerative islands have the following salient features. In the human diseases.
    [Show full text]
  • Use of IBM Watson to Identify Additional RNA-Binding Proteins
    Acta Neuropathol DOI 10.1007/s00401-017-1785-8 ORIGINAL PAPER Artifcial intelligence in neurodegenerative disease research: use of IBM Watson to identify additional RNA‑binding proteins altered in amyotrophic lateral sclerosis Nadine Bakkar1 · Tina Kovalik1 · Ileana Lorenzini1 · Scott Spangler2 · Alix Lacoste3 · Kyle Sponaugle1 · Philip Ferrante1 · Elenee Argentinis3 · Rita Sattler1 · Robert Bowser1 Received: 29 September 2017 / Revised: 4 November 2017 / Accepted: 4 November 2017 © The Author(s) 2017. This article is an open access publication Abstract Amyotrophic lateral sclerosis (ALS) is a dev- to controls. Overall, we successfully used IBM Watson to astating neurodegenerative disease with no efective treat- help identify additional RBPs altered in ALS, highlighting ments. Numerous RNA-binding proteins (RBPs) have been the use of artifcial intelligence tools to accelerate scientifc shown to be altered in ALS, with mutations in 11 RBPs discovery in ALS and possibly other complex neurological causing familial forms of the disease, and 6 more RBPs disorders. showing abnormal expression/distribution in ALS albeit without any known mutations. RBP dysregulation is widely Keywords Amyotrophic lateral sclerosis · RNA-binding accepted as a contributing factor in ALS pathobiology. There protein · Artifcial intelligence · Protein aggregation · are at least 1542 RBPs in the human genome; therefore, Motor neuron other unidentifed RBPs may also be linked to the patho- genesis of ALS. We used IBM ­Watson® to sieve through all RBPs in the genome and identify new RBPs linked to ALS Introduction (ALS-RBPs). IBM Watson extracted features from pub- lished literature to create semantic similarities and identify Amyotrophic lateral sclerosis (ALS) is characterized by new connections between entities of interest.
    [Show full text]
  • Proteomicsdb: a Multi-Omics and Multi-Organism Resource for Life Science
    Published online 30 October 2019 Nucleic Acids Research, 2020, Vol. 48, Database issue D1153–D1163 doi: 10.1093/nar/gkz974 ProteomicsDB: a multi-omics and multi-organism resource for life science research Patroklos Samaras 1, Tobias Schmidt 1,MartinFrejno1, Siegfried Gessulat1,2, Maria Reinecke1,3,4, Anna Jarzab1, Jana Zecha1, Julia Mergner1, Piero Giansanti1, Hans-Christian Ehrlich2, Stephan Aiche2, Johannes Rank5,6, Harald Kienegger5,6, Helmut Krcmar5,6, Bernhard Kuster1,7,* and Mathias Wilhelm1,* 1Chair of Proteomics and Bioanalytics, Technical University of Munich (TUM), Freising, Bavaria, Germany, 2Innovation Center Network, SAP SE, Potsdam, Germany, 3German Cancer Consortium (DKTK), Partner Site Munich, Munich, Germany, 4German Cancer Research Center (DKFZ), Heidelberg, Germany, 5Chair for Information Systems, Technical University of Munich (TUM), Garching, Germany, 6SAP University Competence Center, Technical University of Munich (TUM), Garching, Germany and 7Bavarian Biomolecular Mass Spectrometry Center (BayBioMS), Technical University of Munich (TUM), Freising, Bavaria, Germany Received September 14, 2019; Revised October 11, 2019; Editorial Decision October 11, 2019; Accepted October 15, 2019 ABSTRACT INTRODUCTION ProteomicsDB (https://www.ProteomicsDB.org) ProteomicsDB (https://www.ProteomicsDB.org) is an in- started as a protein-centric in-memory database for memory database initially developed for the exploration of the exploration of large collections of quantitative large quantities of quantitative human mass spectrometry- mass spectrometry-based proteomics data. The based proteomics data including the first draft of the hu- data types and contents grew over time to include man proteome (1). Among many features, it allows the real- time exploration and retrieval of protein abundance values RNA-Seq expression data, drug-target interactions across different tissues, cell lines, and body fluids via inter- and cell line viability data.
    [Show full text]
  • Foraging Shifts and Visual Pre Adaptation in Ecologically Diverse Bats
    See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/340654059 Foraging shifts and visual preadaptation in ecologically diverse bats Article in Molecular Ecology · April 2020 DOI: 10.1111/mec.15445 CITATIONS READS 0 153 9 authors, including: Kalina T. J. Davies Laurel R Yohe Queen Mary, University of London Yale University 40 PUBLICATIONS 254 CITATIONS 24 PUBLICATIONS 93 CITATIONS SEE PROFILE SEE PROFILE Edgardo M. Rengifo Elizabeth R Dumont University of São Paulo University of California, Merced 13 PUBLICATIONS 28 CITATIONS 115 PUBLICATIONS 3,143 CITATIONS SEE PROFILE SEE PROFILE Some of the authors of this publication are also working on these related projects: Ecology of the Greater horseshoe bat View project BAT 1K View project All content following this page was uploaded by Liliana M. Davalos on 14 May 2020. The user has requested enhancement of the downloaded file. Received: 17 October 2019 | Revised: 28 February 2020 | Accepted: 31 March 2020 DOI: 10.1111/mec.15445 ORIGINAL ARTICLE Foraging shifts and visual pre adaptation in ecologically diverse bats Kalina T. J. Davies1 | Laurel R. Yohe2,3 | Jesus Almonte4 | Miluska K. R. Sánchez5 | Edgardo M. Rengifo6,7 | Elizabeth R. Dumont8 | Karen E. Sears9 | Liliana M. Dávalos2,10 | Stephen J. Rossiter1 1School of Biological and Chemical Sciences, Queen Mary University of London, London, UK 2Department of Ecology and Evolution, State University of New York at Stony Brook, Stony Brook, USA 3Department of Geology & Geophysics, Yale University,
    [Show full text]
  • A Concise Review of Human Brain Methylome During Aging and Neurodegenerative Diseases
    BMB Rep. 2019; 52(10): 577-588 BMB www.bmbreports.org Reports Invited Mini Review A concise review of human brain methylome during aging and neurodegenerative diseases Renuka Prasad G & Eek-hoon Jho* Department of Life Science, University of Seoul, Seoul 02504, Korea DNA methylation at CpG sites is an essential epigenetic mark position of carbon in the cytosine within CG dinucleotides that regulates gene expression during mammalian development with resultant formation of 5mC. The symmetrical CG and diseases. Methylome refers to the entire set of methylation dinucleotides are also called as CpG, due to the presence of modifications present in the whole genome. Over the last phosphodiester bond between cytosine and guanine. The several years, an increasing number of reports on brain DNA human genome contains short lengths of DNA (∼1,000 bp) in methylome reported the association between aberrant which CpG is commonly located (∼1 per 10 bp) in methylation and the abnormalities in the expression of critical unmethylated form and referred as CpG islands; they genes known to have critical roles during aging and neuro- commonly overlap with the transcription start sites (TSSs) of degenerative diseases. Consequently, the role of methylation genes. In human DNA, 5mC is present in approximately 1.5% in understanding neurodegenerative diseases has been under of the whole genome and CpG base pairs are 5-fold enriched focus. This review outlines the current knowledge of the human in CpG islands than other regions of the genome (3, 4). CpG brain DNA methylomes during aging and neurodegenerative islands have the following salient features. In the human diseases.
    [Show full text]
  • Sequence, Structure and Context Preferences of Human RNA
    bioRxiv preprint doi: https://doi.org/10.1101/201996; this version posted October 12, 2017. 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. Sequence, Structure and Context Preferences of Human RNA Binding Proteins Daniel Dominguez§,1, Peter Freese§,2, Maria Alexis§,2, Amanda Su1, Myles Hochman1, Tsultrim Palden1, Cassandra Bazile1, Nicole J Lambert1, Eric L Van Nostrand3,4, Gabriel A. Pratt3,4,5, Gene W. Yeo3,4,6,7, Brenton R. Graveley8, Christopher B. Burge1,9,* 1. Department of Biology, MIT, Cambridge MA 2. Program in Computational and Systems Biology, MIT, Cambridge MA 3. Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 4. Institute for Genomic Medicine, University of California at San Diego, La Jolla, CA 5. Bioinformatics and Systems Biology Graduate Program, University of California San Diego, La Jolla, CA 6. Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 7. Molecular Engineering Laboratory. A*STAR, Singapore 8. Department of Genetics and Genome Sciences, Institute for Systems Genomics, Univ. Connecticut Health, Farmington, CT 9. Department of Biological Engineering, MIT, Cambridge MA * Address correspondence to: [email protected] 1 of 61 bioRxiv preprint doi: https://doi.org/10.1101/201996; this version posted October 12, 2017. 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.
    [Show full text]
  • Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress
    University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations Fall 2010 Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress Renuka Nayak University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Computational Biology Commons, and the Genomics Commons Recommended Citation Nayak, Renuka, "Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress" (2010). Publicly Accessible Penn Dissertations. 1559. https://repository.upenn.edu/edissertations/1559 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/1559 For more information, please contact [email protected]. Coexpression Networks Based on Natural Variation in Human Gene Expression at Baseline and Under Stress Abstract Genes interact in networks to orchestrate cellular processes. Here, we used coexpression networks based on natural variation in gene expression to study the functions and interactions of human genes. We asked how these networks change in response to stress. First, we studied human coexpression networks at baseline. We constructed networks by identifying correlations in expression levels of 8.9 million gene pairs in immortalized B cells from 295 individuals comprising three independent samples. The resulting networks allowed us to infer interactions between biological processes. We used the network to predict the functions of poorly-characterized human genes, and provided some experimental support. Examining genes implicated in disease, we found that IFIH1, a diabetes susceptibility gene, interacts with YES1, which affects glucose transport. Genes predisposing to the same diseases are clustered non-randomly in the network, suggesting that the network may be used to identify candidate genes that influence disease susceptibility.
    [Show full text]