Loss of RMI2 Increases Genome Instability and Causes a Bloom-Like Syndrome
Bloom syndrome is a recessive human genetic disorder with features of genome instability, growth deficiency and predisposition to cancer. The only known causative gene is the BLM helicase that is a member of a protein complex along with topoisomerase III alpha, RMI1 and 2, which maintains replicatio...
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| creator | Hudson, Damien F Amor, David J Boys, Amber Butler, Kathy Williams, Lorna Zhang, Tao Kalitsis, Paul |
| description | Bloom syndrome is a recessive human genetic disorder with features of genome instability, growth deficiency and predisposition to cancer. The only known causative gene is the BLM helicase that is a member of a protein complex along with topoisomerase III alpha, RMI1 and 2, which maintains replication fork stability and dissolves double Holliday junctions to prevent genome instability. Here we report the identification of a second gene, RMI2, that is deleted in affected siblings with Bloom-like features. Cells from homozygous individuals exhibit elevated rates of sister chromatid exchange, anaphase DNA bridges and micronuclei. Similar genome and chromosome instability phenotypes are observed in independently derived RMI2 knockout cells. In both patient and knockout cell lines reduced localisation of BLM to ultra fine DNA bridges and FANCD2 at foci linking bridges are observed. Overall, loss of RMI2 produces a partially active BLM complex with mild features of Bloom syndrome. |
| doi_str_mv | 10.1371/journal.pgen.1006483 |
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The only known causative gene is the BLM helicase that is a member of a protein complex along with topoisomerase III alpha, RMI1 and 2, which maintains replication fork stability and dissolves double Holliday junctions to prevent genome instability. Here we report the identification of a second gene, RMI2, that is deleted in affected siblings with Bloom-like features. Cells from homozygous individuals exhibit elevated rates of sister chromatid exchange, anaphase DNA bridges and micronuclei. Similar genome and chromosome instability phenotypes are observed in independently derived RMI2 knockout cells. In both patient and knockout cell lines reduced localisation of BLM to ultra fine DNA bridges and FANCD2 at foci linking bridges are observed. Overall, loss of RMI2 produces a partially active BLM complex with mild features of Bloom syndrome.</description><identifier>ISSN: 1553-7404</identifier><identifier>ISSN: 1553-7390</identifier><identifier>EISSN: 1553-7404</identifier><identifier>DOI: 10.1371/journal.pgen.1006483</identifier><identifier>PMID: 27977684</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Biology and Life Sciences ; Bloom Syndrome - complications ; Bloom Syndrome - genetics ; Bloom Syndrome - pathology ; Cancer ; Cell division ; Children & youth ; Chromosomal Instability - genetics ; Chromosomes ; Cloning ; Colleges & universities ; Colonies & territories ; Cytogenetics ; Deoxyribonucleic acid ; DNA ; DNA Helicases - genetics ; DNA, Cruciform - genetics ; DNA-Binding Proteins - genetics ; Families & family life ; Fanconi Anemia Complementation Group D2 Protein - genetics ; Fibroblasts ; Funding ; Genetic disorders ; Genetic Predisposition to Disease ; Genetics ; Genomes ; Genomic Instability ; Humans ; Laboratories ; Localization ; Medicine and Health Sciences ; Multiprotein Complexes - genetics ; Mutation ; Neoplasms - complications ; Neoplasms - genetics ; Neoplasms - pathology ; Nuclear Proteins - genetics ; Proteins ; Research and Analysis Methods ; Siblings ; Sister Chromatid Exchange - genetics</subject><ispartof>PLoS genetics, 2016-12, Vol.12 (12), p.e1006483-e1006483</ispartof><rights>2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Hudson DF, Amor DJ, Boys A, Butler K, Williams L, Zhang T, et al. (2016) Loss of RMI2 Increases Genome Instability and Causes a Bloom-Like Syndrome. PLoS Genet 12(12): e1006483. doi:10.1371/journal.pgen.1006483</rights><rights>2016 Hudson et al 2016 Hudson et al</rights><rights>2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Hudson DF, Amor DJ, Boys A, Butler K, Williams L, Zhang T, et al. (2016) Loss of RMI2 Increases Genome Instability and Causes a Bloom-Like Syndrome. 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The only known causative gene is the BLM helicase that is a member of a protein complex along with topoisomerase III alpha, RMI1 and 2, which maintains replication fork stability and dissolves double Holliday junctions to prevent genome instability. Here we report the identification of a second gene, RMI2, that is deleted in affected siblings with Bloom-like features. Cells from homozygous individuals exhibit elevated rates of sister chromatid exchange, anaphase DNA bridges and micronuclei. Similar genome and chromosome instability phenotypes are observed in independently derived RMI2 knockout cells. In both patient and knockout cell lines reduced localisation of BLM to ultra fine DNA bridges and FANCD2 at foci linking bridges are observed. Overall, loss of RMI2 produces a partially active BLM complex with mild features of Bloom syndrome.</description><subject>Biology and Life Sciences</subject><subject>Bloom Syndrome - complications</subject><subject>Bloom Syndrome - genetics</subject><subject>Bloom Syndrome - pathology</subject><subject>Cancer</subject><subject>Cell division</subject><subject>Children & youth</subject><subject>Chromosomal Instability - genetics</subject><subject>Chromosomes</subject><subject>Cloning</subject><subject>Colleges & universities</subject><subject>Colonies & territories</subject><subject>Cytogenetics</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Helicases - genetics</subject><subject>DNA, Cruciform - genetics</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Families & family life</subject><subject>Fanconi Anemia Complementation Group D2 Protein - genetics</subject><subject>Fibroblasts</subject><subject>Funding</subject><subject>Genetic disorders</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetics</subject><subject>Genomes</subject><subject>Genomic Instability</subject><subject>Humans</subject><subject>Laboratories</subject><subject>Localization</subject><subject>Medicine and Health Sciences</subject><subject>Multiprotein Complexes - genetics</subject><subject>Mutation</subject><subject>Neoplasms - complications</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - pathology</subject><subject>Nuclear Proteins - genetics</subject><subject>Proteins</subject><subject>Research and Analysis Methods</subject><subject>Siblings</subject><subject>Sister Chromatid Exchange - genetics</subject><issn>1553-7404</issn><issn>1553-7390</issn><issn>1553-7404</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkk2P0zAQhi0EYpfCP0AQicteUvwZ2xckqJalqAiJj7M1cSYlJYm7doLUf09Ks6tdxIGTrZlnXo9nXkKeM7pkQrPXuzDGHtrlfov9klFaSCMekHOmlMi1pPLhnfsZeZLSjlKhjNWPyRnXVuvCyHPycRNSykKdffm05tm69xEhYcqusA8dToE0QNm0zXDIoK-yFYzHLGTv2hC6fNP8xOzroa_iBD8lj2poEz6bzwX5_v7y2-pDvvl8tV693eS-4GrIUdkKy0pKZKwuC5C1xpIDKCpEUSsQWmBtlWRGMl9VFKTQvhLWCm-E9VwsyMuT7r4Nyc1jSI4ZZUyhZKEnYn0iqgA7t49NB_HgAjTuTyDErYM4NL5FxwTwihYWpQDJam6FRs6EksCpB6EmrTfza2PZYeWxHyK090TvZ_rmh9uGX04xpe20kwW5mAViuB4xDa5rkse2hR7DeOy7MIJKa_h_oIpxIzmTE_rqL_Tfg5AnysdpzRHr274ZdUcX3VS5o4vc7KKp7MXdP98W3dhG_AauRMNl</recordid><startdate>20161201</startdate><enddate>20161201</enddate><creator>Hudson, Damien F</creator><creator>Amor, David J</creator><creator>Boys, Amber</creator><creator>Butler, Kathy</creator><creator>Williams, Lorna</creator><creator>Zhang, Tao</creator><creator>Kalitsis, Paul</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-5569-0609</orcidid><orcidid>https://orcid.org/0000-0003-0802-1351</orcidid></search><sort><creationdate>20161201</creationdate><title>Loss of RMI2 Increases Genome Instability and Causes a Bloom-Like Syndrome</title><author>Hudson, Damien F ; Amor, David J ; Boys, Amber ; Butler, Kathy ; Williams, Lorna ; Zhang, Tao ; Kalitsis, Paul</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c625t-e59debd44e11fb6a4f7eb2aa50336f5a373ef9541841cdd0a437cd3993c839c23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Biology and Life Sciences</topic><topic>Bloom Syndrome - complications</topic><topic>Bloom Syndrome - genetics</topic><topic>Bloom Syndrome - pathology</topic><topic>Cancer</topic><topic>Cell division</topic><topic>Children & youth</topic><topic>Chromosomal Instability - genetics</topic><topic>Chromosomes</topic><topic>Cloning</topic><topic>Colleges & universities</topic><topic>Colonies & territories</topic><topic>Cytogenetics</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Helicases - genetics</topic><topic>DNA, Cruciform - genetics</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Families & family life</topic><topic>Fanconi Anemia Complementation Group D2 Protein - genetics</topic><topic>Fibroblasts</topic><topic>Funding</topic><topic>Genetic disorders</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetics</topic><topic>Genomes</topic><topic>Genomic Instability</topic><topic>Humans</topic><topic>Laboratories</topic><topic>Localization</topic><topic>Medicine and Health Sciences</topic><topic>Multiprotein Complexes - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hudson, Damien F</au><au>Amor, David J</au><au>Boys, Amber</au><au>Butler, Kathy</au><au>Williams, Lorna</au><au>Zhang, Tao</au><au>Kalitsis, Paul</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of RMI2 Increases Genome Instability and Causes a Bloom-Like Syndrome</atitle><jtitle>PLoS genetics</jtitle><addtitle>PLoS Genet</addtitle><date>2016-12-01</date><risdate>2016</risdate><volume>12</volume><issue>12</issue><spage>e1006483</spage><epage>e1006483</epage><pages>e1006483-e1006483</pages><issn>1553-7404</issn><issn>1553-7390</issn><eissn>1553-7404</eissn><abstract>Bloom syndrome is a recessive human genetic disorder with features of genome instability, growth deficiency and predisposition to cancer. The only known causative gene is the BLM helicase that is a member of a protein complex along with topoisomerase III alpha, RMI1 and 2, which maintains replication fork stability and dissolves double Holliday junctions to prevent genome instability. Here we report the identification of a second gene, RMI2, that is deleted in affected siblings with Bloom-like features. Cells from homozygous individuals exhibit elevated rates of sister chromatid exchange, anaphase DNA bridges and micronuclei. Similar genome and chromosome instability phenotypes are observed in independently derived RMI2 knockout cells. In both patient and knockout cell lines reduced localisation of BLM to ultra fine DNA bridges and FANCD2 at foci linking bridges are observed. Overall, loss of RMI2 produces a partially active BLM complex with mild features of Bloom syndrome.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27977684</pmid><doi>10.1371/journal.pgen.1006483</doi><orcidid>https://orcid.org/0000-0001-5569-0609</orcidid><orcidid>https://orcid.org/0000-0003-0802-1351</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Biology and Life Sciences Bloom Syndrome - complications Bloom Syndrome - genetics Bloom Syndrome - pathology Cancer Cell division Children & youth Chromosomal Instability - genetics Chromosomes Cloning Colleges & universities Colonies & territories Cytogenetics Deoxyribonucleic acid DNA DNA Helicases - genetics DNA, Cruciform - genetics DNA-Binding Proteins - genetics Families & family life Fanconi Anemia Complementation Group D2 Protein - genetics Fibroblasts Funding Genetic disorders Genetic Predisposition to Disease Genetics Genomes Genomic Instability Humans Laboratories Localization Medicine and Health Sciences Multiprotein Complexes - genetics Mutation Neoplasms - complications Neoplasms - genetics Neoplasms - pathology Nuclear Proteins - genetics Proteins Research and Analysis Methods Siblings Sister Chromatid Exchange - genetics |
| title | Loss of RMI2 Increases Genome Instability and Causes a Bloom-Like Syndrome |
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