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A mutation in the zebrafish\n                      <jats:italic>out of sight<\/jats:italic>\n                      (\n                      <jats:italic>out<\/jats:italic>\n                      ) locus results in a particularly severe reduction of eye size. The goal of this study is to characterize the\n                      <jats:italic>out<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>m233<\/jats:italic>\n                      <\/jats:sup>\n                      mutant, and to determine whether mutations in the\n                      <jats:italic>out<\/jats:italic>\n                      gene cause microphthalmia in humans.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In this study, we show that the severe reduction of eye size in the\n                      <jats:italic>out<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>m233<\/jats:italic>\n                      <\/jats:sup>\n                      mutant is caused by a mutation in the zebrafish\n                      <jats:italic>gdf6a<\/jats:italic>\n                      gene. Despite the small eye size, the overall retinal architecture appears largely intact, and immunohistochemical studies confirm that all major cell types are present in\n                      <jats:italic>out<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>m233<\/jats:italic>\n                      <\/jats:sup>\n                      retinae. Subtle cell fate and patterning changes are present predominantly in amacrine interneurons. Acridine orange and TUNEL staining reveal that the levels of apoptosis are abnormally high in\n                      <jats:italic>out<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>m233<\/jats:italic>\n                      <\/jats:sup>\n                      mutant eyes during early neurogenesis. Mutation analysis of the\n                      <jats:italic>GDF6<\/jats:italic>\n                      gene in 200 patients with microphthalmia revealed amino acid substitutions in four of them. In two patients additional skeletal defects were observed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      This study confirms the essential role of GDF6 in the regulation of vertebrate eye size. The reduced eye size in the zebrafish\n                      <jats:italic>out<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>m233<\/jats:italic>\n                      <\/jats:sup>\n                      mutant is likely to be caused by a transient wave of apoptosis at the onset of neurogenesis. Amino acid substitutions in\n                      <jats:italic>GDF6<\/jats:italic>\n                      were detected in 4 (2%) of 200 patients with microphthalmia. In two patients different skeletal defects were also observed, suggesting pleitrophic effects of\n                      <jats:italic>GDF6<\/jats:italic>\n                      variants. Parents carrying these variants are asymptomatic, suggesting that\n                      <jats:italic>GDF6<\/jats:italic>\n                      sequence alterations are likely to contribute to the phenotype, but are not the sole cause of the disease. Variable expressivity and penetrance suggest a complex non-Mendelian inheritance pattern where other genetic factors may influence the outcome of the phenotype.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/1471-2156-11-102","type":"journal-article","created":{"date-parts":[[2010,11,11]],"date-time":"2010-11-11T14:15:39Z","timestamp":1289484939000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":46,"title":["Genetic defects of GDF6 in the zebrafish out of sight mutant and in human eye developmental anomalies"],"prefix":"10.1186","volume":"11","author":[{"given":"Anneke I","family":"den Hollander","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janisha","family":"Biyanwila","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Kovach","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanya","family":"Bardakjian","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elias I","family":"Traboulsi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicola K","family":"Ragge","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adele","family":"Schneider","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jarema","family":"Malicki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2010,11,11]]},"reference":[{"key":"849_CR1","doi-asserted-by":"publisher","first-page":"38","DOI":"10.1016\/S0008-4182(05)80115-2","volume":"40","author":"RB Lowry","year":"2005","unstructured":"Lowry RB, Kohut R, Sibbald B, Rouleau J: Anophthalmia and microphthalmia in the Alberta Congenital Anomalies Surveillance System. 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