title: Mutations affecting the cardiovascular system and other internal organs in zebrafish.
abstract: In a screen for early developmental mutants of the zebrafish, we have identified mutations specifically affecting the internal organs. We identified 53 mutations affecting the cardiovascular system. Nine of them affect specific landmarks of heart morphogenesis. Mutations in four genes cause a failure in the fusion of the bilateral heart primordia, resulting in cardia bifida. In lonely atrium, no heart venticle is visible and the atrium is directly fused to the outflow tract. In the overlooped mutant, the relative position of the two heart chambers is distorted. The heart is enormously enlarged in the santa mutant. In two mutants, scotch tape and superglue, the cardiac jelly between the two layers of the heart is significantly reduced. We also identified a number of mutations affecting the function of the heart. The mutations affecting heart function can be subdivided into two groups, one affecting heart contraction and another affecting the rhythm of the heart beat. Among the contractility group of mutants are 5 with no heart beat at all and 15 with a reduced heart beat of one or both chambers. 6 mutations are in the rhythmicity group and specifically affect the beating pattern of the heart. Mutations in two genes, bypass and kurzschluss, cause specific defects in the circulatory system. In addition to the heart mutants, we identified 23 mutations affecting the integrity of the liver, the intestine or the kidney. In this report, we demonstrate that it is feasible to screen for genes specific for the patterning or function of certain internal organs in the zebrafish. The mutations presented here could serve as an entry point to the establishment of a genetic hierarchy underlying organogenesis.
authors.affiliation: Max-Planck-Institut für Entwicklungsbiologie, Tübingen, Germany. chenj@helix.mgh.harvard.edu
authors.forename: J N
authors.initials: JN
authors.lastname: Chen
authors.forename: P
authors.initials: P
authors.lastname: Haffter
authors.forename: J
authors.initials: J
authors.lastname: Odenthal
authors.forename: E
authors.initials: E
authors.lastname: Vogelsang
authors.forename: M
authors.initials: M
authors.lastname: Brand
authors.forename: F J
authors.initials: FJ
authors.lastname: van Eeden
authors.forename: M
authors.initials: M
authors.lastname: Furutani-Seiki
authors.forename: M
authors.initials: M
authors.lastname: Granato
authors.forename: M
authors.initials: M
authors.lastname: Hammerschmidt
authors.forename: C P
authors.initials: CP
authors.lastname: Heisenberg
authors.forename: Y J
authors.initials: YJ
authors.lastname: Jiang
authors.forename: D A
authors.initials: DA
authors.lastname: Kane
authors.forename: R N
authors.initials: RN
authors.lastname: Kelsh
authors.forename: M C
authors.initials: MC
authors.lastname: Mullins
authors.forename: C
authors.initials: C
authors.lastname: Nüsslein-Volhard
mesh_terms: D000818:Animals; D019521:Body Patterning / Q000235:genetics; D006332:Cardiomegaly / Q000196:embryology / Q000235:genetics; D002319:Cardiovascular System / Q000196:embryology*; D047108:Embryonic Development; D006325:Heart Atria / Q000002:abnormalities / Q000196:embryology; D006330:Heart Defects, Congenital / Q000196:embryology / Q000235:genetics; D006339:Heart Rate / Q000235:genetics; D006352:Heart Ventricles / Q000002:abnormalities / Q000196:embryology; D007422:Intestines / Q000002:abnormalities / Q000196:embryology; D007668:Kidney / Q000002:abnormalities / Q000196:embryology; D008099:Liver / Q000002:abnormalities / Q000196:embryology; D009154:Mutation; D009200:Myocardial Contraction / Q000235:genetics; D010641:Phenotype; D015027:Zebrafish / Q000196:embryology* / Q000235:genetics*