title: Genetic locus half baked is necessary for morphogenesis of the ectoderm.
abstract: The zebrafish epiboly mutants partially block epiboly, the vegetalward movement of the blastoderm around the giant yolk cell. Here, we show that the epiboly mutations are located near the centromere of Linkage Group 7 in a single locus, termed the half baked locus. Nevertheless, except for the similar mutants lawine and avalanche, we find the epiboly traits of each of the alleles to be distinguishable, forming an allelic series. Using in situ analysis, we show that the specification and the formation of the germ layers is unaffected. However, during early gastrulation, convergence movements are slowed in homozygous and zygotic maternal dominant (ZMD) heterozygous mutants, especially in the epiblast layer of the blastoderm. Using triple-mutant analysis with squint and cyclops, we show that ablating involution and hypoblast formation in hab has no effect on the epiboly phenotype on the ventral and lateral sides of the embryo, suggesting that the hypoblast has no role in epiboly. Moreover, the triple mutant enhances the depletion of cells on the dorsal side of the embryo, consistent with the idea that convergence movements are defective. Double-mutant analysis with one-eyed pinhead reveals that hab is necessary in the ectodermal portion of the hatching gland. In ZMD heterozygotes, in addition to the slowing of epiboly, morphogenesis of the neural tube is abnormal, with gaps forming in the midline during segmentation stages; later, ectopic rows of neurons form in the widened spinal cord and hindbrain. Cell transplantation reveals that half baked acts both autonomously and nonautonomously in interactions among cells of the forming neural tube. Together, these results suggest that half baked is necessary within the epiblast for morphogenesis during both epiboly and neurulation and suggest that the mechanisms that drive epiboly possess common elements with those that underlie convergence and extension.
authors.affiliation: University of Virginia Health Systems, Department of Pathology, Charlottesville, Virginia, USA.
authors.forename: Karen N
authors.initials: KN
authors.lastname: McFarland
authors.forename: Rachel M
authors.initials: RM
authors.lastname: Warga
authors.forename: Donald A
authors.initials: DA
authors.lastname: Kane
mesh_terms: D000483:Alleles; D000818:Animals; D030801:Animals, Genetically Modified; D002503:Centromere / Q000235:genetics; D004475:Ectoderm / Q000166:cytology / Q000378:metabolism*; D004625:Embryo, Nonmammalian / Q000166:cytology / Q000196:embryology / Q000378:metabolism; D006579:Heterozygote; D009024:Morphogenesis / Q000235:genetics*; D009154:Mutation / Q000235:genetics; D009436:Neural Tube Defects / Q000196:embryology / Q000378:metabolism; D010641:Phenotype; D010803:Physalaemin; D020161:Physical Chromosome Mapping; D015027:Zebrafish / Q000196:embryology* / Q000235:genetics*; D029961:Zebrafish Proteins / Q000235:genetics*
chemical_list: D029961:Zebrafish Proteins; D010803:Physalaemin