aldh7a1 regulates eye and limb development in zebrafish
Uveal coloboma is a potentially blinding congenital ocular malformation caused by failure of the optic fissure to close during development. Although mutations in numerous genes have been described, these account for a minority of cases, complicating molecular diagnosis and genetic counseling. Here w...
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| Veröffentlicht in: | PloS one 2014-07, Vol.9 (7), p.e101782 |
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| creator | Babcock, Holly E Dutta, Sunit Alur, Ramakrishna P Brocker, Chad Vasiliou, Vasilis Vitale, Susan Abu-Asab, Mones Brooks, Brian P |
| description | Uveal coloboma is a potentially blinding congenital ocular malformation caused by failure of the optic fissure to close during development. Although mutations in numerous genes have been described, these account for a minority of cases, complicating molecular diagnosis and genetic counseling. Here we describe a key role of aldh7a1 as a gene necessary for normal eye development. We show that morpholino knockdown of aldh7a1 in zebrafish causes uveal coloboma and misregulation of nlz1, another known contributor to the coloboma phenotype, as well as skeletal abnormalities. Knockdown of aldh7a1 leads to reduced cell proliferation in the optic cup of zebrafish, delaying the approximation of the edges of the optic fissure. The aldh7a1 morphant phenotype is partially rescued by co-injection of nlz1 mRNA suggesting that nlz1 is functionally downstream of aldh7a1 in regulating cell proliferation in the optic cup. These results support a role of aldh7a1 in ocular development and skeletal abnormalities in zebrafish. |
| doi_str_mv | 10.1371/journal.pone.0101782 |
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Although mutations in numerous genes have been described, these account for a minority of cases, complicating molecular diagnosis and genetic counseling. Here we describe a key role of aldh7a1 as a gene necessary for normal eye development. We show that morpholino knockdown of aldh7a1 in zebrafish causes uveal coloboma and misregulation of nlz1, another known contributor to the coloboma phenotype, as well as skeletal abnormalities. Knockdown of aldh7a1 leads to reduced cell proliferation in the optic cup of zebrafish, delaying the approximation of the edges of the optic fissure. The aldh7a1 morphant phenotype is partially rescued by co-injection of nlz1 mRNA suggesting that nlz1 is functionally downstream of aldh7a1 in regulating cell proliferation in the optic cup. These results support a role of aldh7a1 in ocular development and skeletal abnormalities in zebrafish.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0101782</identifier><identifier>PMID: 25004007</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Abnormalities ; Acids ; Aldehyde Dehydrogenase - genetics ; Animals ; Biology and Life Sciences ; Cell Proliferation ; Coinjection ; Danio rerio ; Dehydrogenases ; Developmental biology ; DNA-Binding Proteins - genetics ; Embryo, Nonmammalian ; Embryonic Development - genetics ; Embryos ; Environmental health ; Extremities - embryology ; Eye - embryology ; Eye - metabolism ; Gene Expression ; Gene Expression Regulation, Developmental ; Gene Knockdown Techniques ; Genes ; Genetic counseling ; Genetic screening ; Genetics ; Genotype & phenotype ; Health sciences ; Hybridization ; Localization ; Metastasis ; mRNA ; Mutation ; Pediatrics ; Pharmaceutical sciences ; Phenotype ; Phenotypes ; Retina ; RNA ; Toxicology ; Tretinoin - pharmacology ; Xenopus ; Zebrafish ; Zebrafish - embryology ; Zebrafish - genetics ; Zebrafish Proteins - genetics</subject><ispartof>PloS one, 2014-07, Vol.9 (7), p.e101782</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014. This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-fc6f95687a0ff160fd3badeec50066d34c00f7479a78d8f923d04c2612e856313</citedby><cites>FETCH-LOGICAL-c692t-fc6f95687a0ff160fd3badeec50066d34c00f7479a78d8f923d04c2612e856313</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4086958/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4086958/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23847,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25004007$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Riley, Bruce</contributor><creatorcontrib>Babcock, Holly E</creatorcontrib><creatorcontrib>Dutta, Sunit</creatorcontrib><creatorcontrib>Alur, Ramakrishna P</creatorcontrib><creatorcontrib>Brocker, Chad</creatorcontrib><creatorcontrib>Vasiliou, Vasilis</creatorcontrib><creatorcontrib>Vitale, Susan</creatorcontrib><creatorcontrib>Abu-Asab, Mones</creatorcontrib><creatorcontrib>Brooks, Brian P</creatorcontrib><title>aldh7a1 regulates eye and limb development in zebrafish</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Uveal coloboma is a potentially blinding congenital ocular malformation caused by failure of the optic fissure to close during development. Although mutations in numerous genes have been described, these account for a minority of cases, complicating molecular diagnosis and genetic counseling. Here we describe a key role of aldh7a1 as a gene necessary for normal eye development. We show that morpholino knockdown of aldh7a1 in zebrafish causes uveal coloboma and misregulation of nlz1, another known contributor to the coloboma phenotype, as well as skeletal abnormalities. Knockdown of aldh7a1 leads to reduced cell proliferation in the optic cup of zebrafish, delaying the approximation of the edges of the optic fissure. The aldh7a1 morphant phenotype is partially rescued by co-injection of nlz1 mRNA suggesting that nlz1 is functionally downstream of aldh7a1 in regulating cell proliferation in the optic cup. These results support a role of aldh7a1 in ocular development and skeletal abnormalities in zebrafish.</description><subject>Abnormalities</subject><subject>Acids</subject><subject>Aldehyde Dehydrogenase - genetics</subject><subject>Animals</subject><subject>Biology and Life Sciences</subject><subject>Cell Proliferation</subject><subject>Coinjection</subject><subject>Danio rerio</subject><subject>Dehydrogenases</subject><subject>Developmental biology</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Embryo, Nonmammalian</subject><subject>Embryonic Development - genetics</subject><subject>Embryos</subject><subject>Environmental health</subject><subject>Extremities - embryology</subject><subject>Eye - embryology</subject><subject>Eye - metabolism</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Gene Knockdown Techniques</subject><subject>Genes</subject><subject>Genetic counseling</subject><subject>Genetic screening</subject><subject>Genetics</subject><subject>Genotype & phenotype</subject><subject>Health sciences</subject><subject>Hybridization</subject><subject>Localization</subject><subject>Metastasis</subject><subject>mRNA</subject><subject>Mutation</subject><subject>Pediatrics</subject><subject>Pharmaceutical sciences</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>Retina</subject><subject>RNA</subject><subject>Toxicology</subject><subject>Tretinoin - pharmacology</subject><subject>Xenopus</subject><subject>Zebrafish</subject><subject>Zebrafish - embryology</subject><subject>Zebrafish - genetics</subject><subject>Zebrafish Proteins - genetics</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl1rFDEUhgdRbK3-A9EBoeDFrsnkYzI3QilVFwoFv25DNjmZzZKZrMlMsf56s-607ICC5CLh5Dlvzjl5i-IlRktMavxuG8bYK7_chR6WCCNci-pRcYobUi14hcjjo_NJ8SylLUKMCM6fFicVQ4giVJ8WtfJmUytcRmhHrwZIJdxBqXpTetetSwO34MOug34oXV_-gnVU1qXN8-KJVT7Bi2k_K759uPp6-WlxffNxdXlxvdC8qYaF1dw2jItaIWsxR9aQtTIAOhfAuSFUI2RrWjeqFkbYpiIGUV1xXIFgnGByVrw-6O58SHLqOUnMKKkJpmxPrA6ECWord9F1Kt7JoJz8EwixlSoOTnuQIAhiFQNFsaWsoQ3HhJAKGLIYONCs9X56bVx3YHTuOio_E53f9G4j23ArKRK8YSILvJkEYvgxQhr-UfJEtSpX5XobspjuXNLygmLBCeWiydTyL1ReBjqn869bl-OzhLezhMwM8HNo1ZiSXH35_P_szfc5e37EbkD5YZOCHwcX-jQH6QHUMaQUwT5MDiO5N-39NOTetHIybU57dTz1h6R7l5LfP4_klg</recordid><startdate>20140708</startdate><enddate>20140708</enddate><creator>Babcock, Holly E</creator><creator>Dutta, Sunit</creator><creator>Alur, Ramakrishna P</creator><creator>Brocker, Chad</creator><creator>Vasiliou, Vasilis</creator><creator>Vitale, Susan</creator><creator>Abu-Asab, Mones</creator><creator>Brooks, Brian P</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140708</creationdate><title>aldh7a1 regulates eye and limb development in zebrafish</title><author>Babcock, Holly E ; Dutta, Sunit ; Alur, Ramakrishna P ; Brocker, Chad ; Vasiliou, Vasilis ; Vitale, Susan ; Abu-Asab, Mones ; Brooks, Brian P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-fc6f95687a0ff160fd3badeec50066d34c00f7479a78d8f923d04c2612e856313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Abnormalities</topic><topic>Acids</topic><topic>Aldehyde Dehydrogenase - 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Although mutations in numerous genes have been described, these account for a minority of cases, complicating molecular diagnosis and genetic counseling. Here we describe a key role of aldh7a1 as a gene necessary for normal eye development. We show that morpholino knockdown of aldh7a1 in zebrafish causes uveal coloboma and misregulation of nlz1, another known contributor to the coloboma phenotype, as well as skeletal abnormalities. Knockdown of aldh7a1 leads to reduced cell proliferation in the optic cup of zebrafish, delaying the approximation of the edges of the optic fissure. The aldh7a1 morphant phenotype is partially rescued by co-injection of nlz1 mRNA suggesting that nlz1 is functionally downstream of aldh7a1 in regulating cell proliferation in the optic cup. These results support a role of aldh7a1 in ocular development and skeletal abnormalities in zebrafish.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25004007</pmid><doi>10.1371/journal.pone.0101782</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Abnormalities Acids Aldehyde Dehydrogenase - genetics Animals Biology and Life Sciences Cell Proliferation Coinjection Danio rerio Dehydrogenases Developmental biology DNA-Binding Proteins - genetics Embryo, Nonmammalian Embryonic Development - genetics Embryos Environmental health Extremities - embryology Eye - embryology Eye - metabolism Gene Expression Gene Expression Regulation, Developmental Gene Knockdown Techniques Genes Genetic counseling Genetic screening Genetics Genotype & phenotype Health sciences Hybridization Localization Metastasis mRNA Mutation Pediatrics Pharmaceutical sciences Phenotype Phenotypes Retina RNA Toxicology Tretinoin - pharmacology Xenopus Zebrafish Zebrafish - embryology Zebrafish - genetics Zebrafish Proteins - genetics |
| title | aldh7a1 regulates eye and limb development in zebrafish |
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