Regulatory regions responsive to oxidative stress in the promoter of the human DNA glycosylase gene NEIL2

Reactive oxygen species (ROS) generated endogenously or from exogenous sources produce mutagenic DNA lesions. If not repaired, these lesions could lead to genomic instability and, potentially, to cancer development. NEIL2 (EC 4.2.99.18), a mammalian base excision repair (BER) protein and ortholog of...

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Veröffentlicht in:Mutagenesis 2010-03, Vol.25 (2), p.171-177
Hauptverfasser: Kinslow, Carla J., El-Zein, Randa A., Rondelli, Catherine M., Hill, Courtney E., Wickliffe, Jeffrey K., Abdel-Rahman, Sherif Z.
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container_issue 2
container_start_page 171
container_title Mutagenesis
container_volume 25
creator Kinslow, Carla J.
El-Zein, Randa A.
Rondelli, Catherine M.
Hill, Courtney E.
Wickliffe, Jeffrey K.
Abdel-Rahman, Sherif Z.
description Reactive oxygen species (ROS) generated endogenously or from exogenous sources produce mutagenic DNA lesions. If not repaired, these lesions could lead to genomic instability and, potentially, to cancer development. NEIL2 (EC 4.2.99.18), a mammalian base excision repair (BER) protein and ortholog of the bacterial Fpg/Nei, excises oxidized DNA lesions from bubble or single-stranded structures, suggesting its involvement in transcription-coupled DNA repair. Perturbation in NEIL2 expression may, therefore, significantly impact BER capacity and promote genomic instability. To characterize the genetic and environmental factors regulating NEIL2 gene expression, we mapped the human NEIL2 transcriptional start site and partially characterized the promoter region of the gene using a luciferase reporter assay. We identified a strong positive regulatory region from nucleotide −206 to +90 and found that expression from this region was contingent on its being isolated from an adjacent strong negative regulatory region located downstream (+49 to +710 bp), suggesting that NEIL2 transcription is influenced by both these regions. We also found that oxidative stress, induced by glucose oxidase treatment, reduced the positive regulatory region expression levels, suggesting that ROS may play a significant role in regulating NEIL2 transcription. In an initial attempt to characterize the underlying mechanisms, we used in silico analysis to identify putative cis-acting binding sites for ROS-responsive transcription factors within this region and then used site-directed mutagenesis to investigate their role. A single-base change in the region encompassing nucleotides −206 to +90 abolished the effect of oxidative stress that was observed in the absence of the mutation. Our study is the first to provide an initial partial characterization of the NEIL2 promoter and opens the door for future research aimed at understanding the role of genetic and environmental factors in regulating NEIL2 expression.
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If not repaired, these lesions could lead to genomic instability and, potentially, to cancer development. NEIL2 (EC 4.2.99.18), a mammalian base excision repair (BER) protein and ortholog of the bacterial Fpg/Nei, excises oxidized DNA lesions from bubble or single-stranded structures, suggesting its involvement in transcription-coupled DNA repair. Perturbation in NEIL2 expression may, therefore, significantly impact BER capacity and promote genomic instability. To characterize the genetic and environmental factors regulating NEIL2 gene expression, we mapped the human NEIL2 transcriptional start site and partially characterized the promoter region of the gene using a luciferase reporter assay. We identified a strong positive regulatory region from nucleotide −206 to +90 and found that expression from this region was contingent on its being isolated from an adjacent strong negative regulatory region located downstream (+49 to +710 bp), suggesting that NEIL2 transcription is influenced by both these regions. We also found that oxidative stress, induced by glucose oxidase treatment, reduced the positive regulatory region expression levels, suggesting that ROS may play a significant role in regulating NEIL2 transcription. In an initial attempt to characterize the underlying mechanisms, we used in silico analysis to identify putative cis-acting binding sites for ROS-responsive transcription factors within this region and then used site-directed mutagenesis to investigate their role. A single-base change in the region encompassing nucleotides −206 to +90 abolished the effect of oxidative stress that was observed in the absence of the mutation. 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If not repaired, these lesions could lead to genomic instability and, potentially, to cancer development. NEIL2 (EC 4.2.99.18), a mammalian base excision repair (BER) protein and ortholog of the bacterial Fpg/Nei, excises oxidized DNA lesions from bubble or single-stranded structures, suggesting its involvement in transcription-coupled DNA repair. Perturbation in NEIL2 expression may, therefore, significantly impact BER capacity and promote genomic instability. To characterize the genetic and environmental factors regulating NEIL2 gene expression, we mapped the human NEIL2 transcriptional start site and partially characterized the promoter region of the gene using a luciferase reporter assay. We identified a strong positive regulatory region from nucleotide −206 to +90 and found that expression from this region was contingent on its being isolated from an adjacent strong negative regulatory region located downstream (+49 to +710 bp), suggesting that NEIL2 transcription is influenced by both these regions. We also found that oxidative stress, induced by glucose oxidase treatment, reduced the positive regulatory region expression levels, suggesting that ROS may play a significant role in regulating NEIL2 transcription. In an initial attempt to characterize the underlying mechanisms, we used in silico analysis to identify putative cis-acting binding sites for ROS-responsive transcription factors within this region and then used site-directed mutagenesis to investigate their role. A single-base change in the region encompassing nucleotides −206 to +90 abolished the effect of oxidative stress that was observed in the absence of the mutation. 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Repair</subject><subject>Mutation</subject><subject>Nucleotides</subject><subject>Original</subject><subject>Oxidative Stress</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Promoters</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Regulatory sequences</subject><subject>Regulatory Sequences, Nucleic Acid - genetics</subject><subject>Site-directed mutagenesis</subject><subject>Transcription factors</subject><subject>Transcription Factors - metabolism</subject><subject>Transcription Initiation Site</subject><subject>Transcription, Genetic - genetics</subject><issn>0267-8357</issn><issn>1464-3804</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1v1DAQxS0EokvhyBX5guAS6o84ji9IVWlppW1RK5AQF2viOllDEqe2U3X_e7IkWuDU09Nofnpv7IfQa0o-UKL4UTcmaOxRYwciyidoRfMiz3hJ8qdoRVghs5ILeYBexPiTECpZQZ6jA6pULlQpVsjd2GZsIfmwxcE2zvdx0jhM6u4tTh77B3cLaTfENG0idj1OG4uH4DufbMC-_jNvxg56_OnqGDft1vi4bSFa3Nje4qvTizV7iZ7V0Eb7atFD9O3s9OvJebb-8vni5HidGUFVygBIxQoD1NRcCkNUzZUURFBeVAUoRmVlpidVpq5UbSpJaZVbJY2koqigVvwQfZx9h7Hq7K2xfQrQ6iG4DsJWe3D6_03vNrrx95qVTPCcTwbvFoPg70Ybk-5cNLZtobd-jFrmBeOc8V1UNpMm-BiDrfcplOhdO3puR8_tTPybf0_7Sy91TMDbBYBooK0D9MbFPceYoKLM84l7P3N-HB7NXG50MdmHPQzhly7k9MP6_PsPTRg7u-ZyrS_5b4oKuZ4</recordid><startdate>20100301</startdate><enddate>20100301</enddate><creator>Kinslow, Carla J.</creator><creator>El-Zein, Randa A.</creator><creator>Rondelli, Catherine M.</creator><creator>Hill, Courtney E.</creator><creator>Wickliffe, Jeffrey K.</creator><creator>Abdel-Rahman, Sherif Z.</creator><general>Oxford University Press</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7TM</scope><scope>C1K</scope><scope>5PM</scope></search><sort><creationdate>20100301</creationdate><title>Regulatory regions responsive to oxidative stress in the promoter of the human DNA glycosylase gene NEIL2</title><author>Kinslow, Carla J. ; El-Zein, Randa A. ; Rondelli, Catherine M. ; Hill, Courtney E. ; Wickliffe, Jeffrey K. ; Abdel-Rahman, Sherif Z.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c519t-aa0b26ca1cf375c09f397505136b6a9217bc835bcfb9fcb711b4e97c7156baf93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Base excision repair</topic><topic>Base Sequence</topic><topic>Binding Sites</topic><topic>Biological and medical sciences</topic><topic>Cancer</topic><topic>DNA glycosylase</topic><topic>DNA Glycosylases - genetics</topic><topic>DNA Glycosylases - metabolism</topic><topic>DNA repair</topic><topic>DNA-(Apurinic or Apyrimidinic Site) Lyase - genetics</topic><topic>DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism</topic><topic>Environmental factors</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - metabolism</topic><topic>Fundamental and applied biological sciences. 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Repair</topic><topic>Mutation</topic><topic>Nucleotides</topic><topic>Original</topic><topic>Oxidative Stress</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Promoters</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Regulatory sequences</topic><topic>Regulatory Sequences, Nucleic Acid - genetics</topic><topic>Site-directed mutagenesis</topic><topic>Transcription factors</topic><topic>Transcription Factors - metabolism</topic><topic>Transcription Initiation Site</topic><topic>Transcription, Genetic - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kinslow, Carla J.</creatorcontrib><creatorcontrib>El-Zein, Randa A.</creatorcontrib><creatorcontrib>Rondelli, Catherine M.</creatorcontrib><creatorcontrib>Hill, Courtney E.</creatorcontrib><creatorcontrib>Wickliffe, Jeffrey K.</creatorcontrib><creatorcontrib>Abdel-Rahman, Sherif Z.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nucleic Acids Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Mutagenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kinslow, Carla J.</au><au>El-Zein, Randa A.</au><au>Rondelli, Catherine M.</au><au>Hill, Courtney E.</au><au>Wickliffe, Jeffrey K.</au><au>Abdel-Rahman, Sherif Z.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulatory regions responsive to oxidative stress in the promoter of the human DNA glycosylase gene NEIL2</atitle><jtitle>Mutagenesis</jtitle><addtitle>Mutagenesis</addtitle><date>2010-03-01</date><risdate>2010</risdate><volume>25</volume><issue>2</issue><spage>171</spage><epage>177</epage><pages>171-177</pages><issn>0267-8357</issn><eissn>1464-3804</eissn><coden>MUTAEX</coden><abstract>Reactive oxygen species (ROS) generated endogenously or from exogenous sources produce mutagenic DNA lesions. If not repaired, these lesions could lead to genomic instability and, potentially, to cancer development. NEIL2 (EC 4.2.99.18), a mammalian base excision repair (BER) protein and ortholog of the bacterial Fpg/Nei, excises oxidized DNA lesions from bubble or single-stranded structures, suggesting its involvement in transcription-coupled DNA repair. Perturbation in NEIL2 expression may, therefore, significantly impact BER capacity and promote genomic instability. To characterize the genetic and environmental factors regulating NEIL2 gene expression, we mapped the human NEIL2 transcriptional start site and partially characterized the promoter region of the gene using a luciferase reporter assay. We identified a strong positive regulatory region from nucleotide −206 to +90 and found that expression from this region was contingent on its being isolated from an adjacent strong negative regulatory region located downstream (+49 to +710 bp), suggesting that NEIL2 transcription is influenced by both these regions. We also found that oxidative stress, induced by glucose oxidase treatment, reduced the positive regulatory region expression levels, suggesting that ROS may play a significant role in regulating NEIL2 transcription. In an initial attempt to characterize the underlying mechanisms, we used in silico analysis to identify putative cis-acting binding sites for ROS-responsive transcription factors within this region and then used site-directed mutagenesis to investigate their role. A single-base change in the region encompassing nucleotides −206 to +90 abolished the effect of oxidative stress that was observed in the absence of the mutation. Our study is the first to provide an initial partial characterization of the NEIL2 promoter and opens the door for future research aimed at understanding the role of genetic and environmental factors in regulating NEIL2 expression.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>19945985</pmid><doi>10.1093/mutage/gep058</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection
subjects Base excision repair
Base Sequence
Binding Sites
Biological and medical sciences
Cancer
DNA glycosylase
DNA Glycosylases - genetics
DNA Glycosylases - metabolism
DNA repair
DNA-(Apurinic or Apyrimidinic Site) Lyase - genetics
DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism
Environmental factors
Fibroblasts - cytology
Fibroblasts - metabolism
Fundamental and applied biological sciences. Psychology
Gene expression
Genomic instability
Glucose oxidase
Humans
Luciferases - metabolism
Lung - embryology
Lung - metabolism
Molecular and cellular biology
Molecular genetics
Molecular Sequence Data
Mutagenesis
Mutagenesis, Site-Directed
Mutagenesis. Repair
Mutation
Nucleotides
Original
Oxidative Stress
Promoter Regions, Genetic - genetics
Promoters
Reactive oxygen species
Reactive Oxygen Species - metabolism
Regulatory sequences
Regulatory Sequences, Nucleic Acid - genetics
Site-directed mutagenesis
Transcription factors
Transcription Factors - metabolism
Transcription Initiation Site
Transcription, Genetic - genetics
title Regulatory regions responsive to oxidative stress in the promoter of the human DNA glycosylase gene NEIL2
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