Human microRNA-155 on Chromosome 21 Differentially Interacts with Its Polymorphic Target in the AGTR1 3′ Untranslated Region: A Mechanism for Functional Single-Nucleotide Polymorphisms Related to Phenotypes

Animal microRNAs (miRNAs) regulate gene expression through base pairing to their targets within the 3′ untranslated region (UTR) of protein-coding genes. Single-nucleotide polymorphisms (SNPs) located within such target sites can affect miRNA regulation. We mapped annotated SNPs onto a collection of...

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Published inAmerican journal of human genetics Vol. 81; no. 2; pp. 405 - 413
Main Authors Sethupathy, Praveen, Borel, Christelle, Gagnebin, Maryline, Grant, Gregory R., Deutsch, Samuel, Elton, Terry S., Hatzigeorgiou, Artemis G., Antonarakis, Stylianos E.
Format Journal Article
LanguageEnglish
Published Chicago, IL Elsevier Inc 01.08.2007
University of Chicago Press
American Society of Human Genetics
Subjects
3' Untranslated Regions
Base Sequence
Biological and medical sciences
Chromosomes, Human, Pair 21
Down Syndrome - genetics
Fundamental and applied biological sciences. Psychology
General aspects. Genetic counseling
Genetics of eukaryotes. Biological and molecular evolution
Humans
Hypertension - genetics
Medical genetics
Medical sciences
MicroRNAs - genetics
Molecular and cellular biology
Molecular Sequence Data
Phenotype
Polymorphism, Single Nucleotide
Receptor, Angiotensin, Type 1 - genetics
Reproducibility of Results
Human
Chromosome G21
Genetics
Phenotype
Single nucleotide polymorphism
Mechanism
Online AccessGet full text
ISSN0002-9297
1537-6605
DOI10.1086/519979

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Abstract Animal microRNAs (miRNAs) regulate gene expression through base pairing to their targets within the 3′ untranslated region (UTR) of protein-coding genes. Single-nucleotide polymorphisms (SNPs) located within such target sites can affect miRNA regulation. We mapped annotated SNPs onto a collection of experimentally supported human miRNA targets. Of the 143 experimentally supported human target sites, 9 contain 12 SNPs. We further experimentally investigated one of these target sites for hsa-miR-155, within the 3′ UTR of the human AGTR1 gene that contains SNP rs5186. Using reporter silencing assays, we show that hsa-miR-155 down-regulates the expression of only the 1166A, and not the 1166C, allele of rs5186. Remarkably, the 1166C allele has been associated with hypertension in many studies. Thus, the 1166C allele may be functionally associated with hypertension by abrogating regulation by hsa-miR-155, thereby elevating AGTR1 levels. Since hsa-miR-155 is on chromosome 21, we hypothesize that the observed lower blood pressure in trisomy 21 is partially caused by the overexpression of hsa-miR-155 leading to allele-specific underexpression of AGTR1. Indeed, we have shown in fibroblasts from monozygotic twins discordant for trisomy 21 that levels of AGTR1 protein are lower in trisomy 21.
AbstractList Animal microRNAs (miRNAs) regulate gene expression through base pairing to their targets within the 3' untranslated region (UTR) of protein-coding genes. Single-nucleotide polymorphisms (SNPs) located within such target sites can affect miRNA regulation. We mapped annotated SNPs onto a collection of experimentally supported human miRNA targets. Of the 143 experimentally supported human target sites, 9 contain 12 SNPs. We further experimentally investigated one of these target sites for hsa-miR-155, within the 3' UTR of the human AGTR1 gene that contains SNP rs5186. Using reporter silencing assays, we show that hsa-miR-155 down-regulates the expression of only the 1166A, and not the 1166C, allele of rs5186. Remarkably, the 1166C allele has been associated with hypertension in many studies. Thus, the 1166C allele may be functionally associated with hypertension by abrogating regulation by hsa-miR-155, thereby elevating AGTR1 levels. Since hsa-miR-155 is on chromosome 21, we hypothesize that the observed lower blood pressure in trisomy 21 is partially caused by the overexpression of hsa-miR-155 leading to allele-specific underexpression of AGTR1. Indeed, we have shown in fibroblasts from monozygotic twins discordant for trisomy 21 that levels of AGTR1 protein are lower in trisomy 21.
Animal microRNAs (miRNAs) regulate gene expression through base pairing to their targets within the 3′ untranslated region (UTR) of protein-coding genes. Single-nucleotide polymorphisms (SNPs) located within such target sites can affect miRNA regulation. We mapped annotated SNPs onto a collection of experimentally supported human miRNA targets. Of the 143 experimentally supported human target sites, 9 contain 12 SNPs. We further experimentally investigated one of these target sites for hsa-miR-155, within the 3′ UTR of the human AGTR1 gene that contains SNP rs5186. Using reporter silencing assays, we show that hsa-miR-155 down-regulates the expression of only the 1166A, and not the 1166C, allele of rs5186. Remarkably, the 1166C allele has been associated with hypertension in many studies. Thus, the 1166C allele may be functionally associated with hypertension by abrogating regulation by hsa-miR-155, thereby elevating AGTR1 levels. Since hsa-miR-155 is on chromosome 21, we hypothesize that the observed lower blood pressure in trisomy 21 is partially caused by the overexpression of hsa-miR-155 leading to allele-specific underexpression of AGTR1. Indeed, we have shown in fibroblasts from monozygotic twins discordant for trisomy 21 that levels of AGTR1 protein are lower in trisomy 21.
Animal microRNAs (miRNAs) regulate gene expression through base pairing to their targets within the 3' untranslated region (UTR) of protein-coding genes. Single-nucleotide polymorphisms (SNPs) located within such target sites can affect miRNA regulation. We mapped annotated SNPs onto a collection of experimentally supported human miRNA targets. Of the 143 experimentally supported human target sites, 9 contain 12 SNPs. We further experimentally investigated one of these target sites for hsa-miR-155, within the 3' UTR of the human AGTR1 gene that contains SNP rs5186. Using reporter silencing assays, we show that hsa-miR-155 down-regulates the expression of only the 1166A, and not the 1166C, allele of rs5186. Remarkably, the 1166C allele has been associated with hypertension in many studies. Thus, the 1166C allele may be functionally associated with hypertension by abrogating regulation by hsa-miR-155, thereby elevating AGTR1 levels. Since hsa-miR-155 is on chromosome 21, we hypothesize that the observed lower blood pressure in trisomy 21 is partially caused by the overexpression of hsa-miR-155 leading to allele-specific underexpression of AGTR1. Indeed, we have shown in fibroblasts from monozygotic twins discordant for trisomy 21 that levels of AGTR1 protein are lower in trisomy 21.Animal microRNAs (miRNAs) regulate gene expression through base pairing to their targets within the 3' untranslated region (UTR) of protein-coding genes. Single-nucleotide polymorphisms (SNPs) located within such target sites can affect miRNA regulation. We mapped annotated SNPs onto a collection of experimentally supported human miRNA targets. Of the 143 experimentally supported human target sites, 9 contain 12 SNPs. We further experimentally investigated one of these target sites for hsa-miR-155, within the 3' UTR of the human AGTR1 gene that contains SNP rs5186. Using reporter silencing assays, we show that hsa-miR-155 down-regulates the expression of only the 1166A, and not the 1166C, allele of rs5186. Remarkably, the 1166C allele has been associated with hypertension in many studies. Thus, the 1166C allele may be functionally associated with hypertension by abrogating regulation by hsa-miR-155, thereby elevating AGTR1 levels. Since hsa-miR-155 is on chromosome 21, we hypothesize that the observed lower blood pressure in trisomy 21 is partially caused by the overexpression of hsa-miR-155 leading to allele-specific underexpression of AGTR1. Indeed, we have shown in fibroblasts from monozygotic twins discordant for trisomy 21 that levels of AGTR1 protein are lower in trisomy 21.
Animal microRNAs (miRNAs) regulate gene expression through base pairing to their targets within the 3′ untranslated region (UTR) of protein-coding genes. Single-nucleotide polymorphisms (SNPs) located within such target sites can affect miRNA regulation. We mapped annotated SNPs onto a collection of experimentally supported human miRNA targets. Of the 143 experimentally supported human target sites, 9 contain 12 SNPs. We further experimentally investigated one of these target sites for hsa-miR-155, within the 3′ UTR of the human AGTR1 gene that contains SNP rs5186. Using reporter silencing assays, we show that hsa-miR-155 down-regulates the expression of only the 1166A, and not the 1166C, allele of rs5186. Remarkably, the 1166C allele has been associated with hypertension in many studies. Thus, the 1166C allele may be functionally associated with hypertension by abrogating regulation by hsa-miR-155, thereby elevating AGTR1 levels. Since hsa-miR-155 is on chromosome 21, we hypothesize that the observed lower blood pressure in trisomy 21 is partially caused by the overexpression of hsa-miR-155 leading to allele-specific underexpression of AGTR1. Indeed, we have shown in fibroblasts from monozygotic twins discordant for trisomy 21 that levels of AGTR1 protein are lower in trisomy 21.
Author Borel, Christelle
Grant, Gregory R.
Hatzigeorgiou, Artemis G.
Sethupathy, Praveen
Antonarakis, Stylianos E.
Deutsch, Samuel
Elton, Terry S.
Gagnebin, Maryline
AuthorAffiliation From the Department of Genetics (P.S.; A.G.H.) and Penn Center for Bioinformatics (P.S.; G.R.G.; A.G.H.), School of Medicine, and Department of Computer and Information Sciences, School of Engineering and Applied Sciences (A.G.H.), University of Pennsylvania, Philadelphia; Department of Genetic Medicine and Development, University of Geneva Medical School and University Hospitals of Geneva, Geneva, Switzerland (C.B.; M.G., S.D.; S.E.A.); and Davis Heart and Lung Research Institute, The Ohio State University, Columbus (T.S.E.)
AuthorAffiliation_xml – name: From the Department of Genetics (P.S.; A.G.H.) and Penn Center for Bioinformatics (P.S.; G.R.G.; A.G.H.), School of Medicine, and Department of Computer and Information Sciences, School of Engineering and Applied Sciences (A.G.H.), University of Pennsylvania, Philadelphia; Department of Genetic Medicine and Development, University of Geneva Medical School and University Hospitals of Geneva, Geneva, Switzerland (C.B.; M.G., S.D.; S.E.A.); and Davis Heart and Lung Research Institute, The Ohio State University, Columbus (T.S.E.)
Author_xml – sequence: 1
  givenname: Praveen
  surname: Sethupathy
  fullname: Sethupathy, Praveen
  organization: Department of Genetics, University of Pennsylvania, Philadelphia
– sequence: 2
  givenname: Christelle
  surname: Borel
  fullname: Borel, Christelle
  organization: Department of Genetic Medicine and Development, University of Geneva Medical School and University Hospitals of Geneva, Geneva, Switzerland
– sequence: 3
  givenname: Maryline
  surname: Gagnebin
  fullname: Gagnebin, Maryline
  organization: Department of Genetic Medicine and Development, University of Geneva Medical School and University Hospitals of Geneva, Geneva, Switzerland
– sequence: 4
  givenname: Gregory R.
  surname: Grant
  fullname: Grant, Gregory R.
  organization: Penn Center for Bioinformatics, University of Pennsylvania, Philadelphia
– sequence: 5
  givenname: Samuel
  surname: Deutsch
  fullname: Deutsch, Samuel
  organization: Department of Genetic Medicine and Development, University of Geneva Medical School and University Hospitals of Geneva, Geneva, Switzerland
– sequence: 6
  givenname: Terry S.
  surname: Elton
  fullname: Elton, Terry S.
  organization: and Davis Heart and Lung Research Institute, The Ohio State University, Columbus
– sequence: 7
  givenname: Artemis G.
  surname: Hatzigeorgiou
  fullname: Hatzigeorgiou, Artemis G.
  organization: Department of Genetics, University of Pennsylvania, Philadelphia
– sequence: 8
  givenname: Stylianos E.
  surname: Antonarakis
  fullname: Antonarakis, Stylianos E.
  email: artemis@fleming.gr
  organization: Department of Genetic Medicine and Development, University of Geneva Medical School and University Hospitals of Geneva, Geneva, Switzerland
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https://www.ncbi.nlm.nih.gov/pubmed/17668390$$D View this record in MEDLINE/PubMed
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Keywords Human
Chromosome G21
Genetics
Phenotype
Single nucleotide polymorphism
Mechanism
Language English
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These two authors contributed equally to this work.
Present affiliation: Institute of Molecular Oncology, Biomedical Sciences Research Center “Alexander Fleming.”
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Snippet Animal microRNAs (miRNAs) regulate gene expression through base pairing to their targets within the 3′ untranslated region (UTR) of protein-coding genes....
Animal microRNAs (miRNAs) regulate gene expression through base pairing to their targets within the 3' untranslated region (UTR) of protein-coding genes....
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SourceType Open Access Repository
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Enrichment Source
Publisher
StartPage 405
SubjectTerms 3' Untranslated Regions
Base Sequence
Biological and medical sciences
Chromosomes, Human, Pair 21
Down Syndrome - genetics
Fundamental and applied biological sciences. Psychology
General aspects. Genetic counseling
Genetics of eukaryotes. Biological and molecular evolution
Humans
Hypertension - genetics
Medical genetics
Medical sciences
MicroRNAs - genetics
Molecular and cellular biology
Molecular Sequence Data
Phenotype
Polymorphism, Single Nucleotide
Receptor, Angiotensin, Type 1 - genetics
Reproducibility of Results
Title Human microRNA-155 on Chromosome 21 Differentially Interacts with Its Polymorphic Target in the AGTR1 3′ Untranslated Region: A Mechanism for Functional Single-Nucleotide Polymorphisms Related to Phenotypes
URI https://dx.doi.org/10.1086/519979
https://www.ncbi.nlm.nih.gov/pubmed/17668390
https://www.proquest.com/docview/68107423
https://pubmed.ncbi.nlm.nih.gov/PMC1950808
Volume 81
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