A homeobox gene essential for zebrafish notochord development

Talbot, William S.; Trevarrow, Bill; Halpern, Marnie E.; Melby, Anna E.; Farr, Gist H.; Postlethwait, John H.; Jowett, Trevor; Kimmel, Charles B.; Kimelman, David

doi:10.1038/378150a0

Cited by 434 publications

(269 citation statements)

References 48 publications

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“…In agreement herewith, in floating head (flh) and no tail (ntl) mutants, which lack a notochord and at least in the flh mutant also a hypochord (Rissi et al, 1995;Talbot et al, 1995), defects in the formation of the axial vessels, and in particular the DA, are found at an early stage (Fouquet et al, 1997;Sumoy et al, 1997). Also at 24 hpf and later stages, a functional relationship between hypochord and DA still exists.…”

Section: Discussionsupporting

confidence: 80%

Egfl7 knockdown causes defects in the extension and junctional arrangements of endothelial cells during zebrafish vasculogenesis

Mazière

Parker²,

Dijk

et al. 2008

Developmental Dynamics

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The endothelial cell (EC) -specific secreted protein EGFL7 is important for tubulogenesis in newly forming blood vessels. We studied its role in vascular tube formation by a quantitative ultrastructural analysis of Egfl7-knockdown zebrafish embryos. At 24 hours postfertilization, the endothelia of dorsal aorta (DA) and posterior cardinal vein (PCV) were correctly anchored to the hypochord and endoderm, respectively, but failed to expand into the vascular area. This resulted in vessels with reduced or split lumen and open sheets of ECs. Concomitantly, the organization of hematopoietic cells-identified by the presence of previously undescribed membrane tubules-between DA and PCV, and within the vessels, was severely disturbed. Strikingly, ectopic cell junctions occurred across the obstructed vessel lumen, on the luminal EC surfaces, which in control conditions never display junctions of any kind. These data suggest that Egfl7 provides ECs with a cue for their extension into the vascular area and in establishing EC cell polarity. Developmental Dynamics 237:580 -591, 2008.

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Section: Discussionsupporting

confidence: 80%

Egfl7 knockdown causes defects in the extension and junctional arrangements of endothelial cells during zebrafish vasculogenesis

Mazière

Parker²,

Dijk

et al. 2008

Developmental Dynamics

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“…This combination of phenotypes resembles known mutants with defects in notochord formation such as floating head and no tail (ntl). 25,26 The notochord is a rod-like structure found in all chordate embryos that functions as a major skeletal element and an essential signaling center for tissue patterning. Injection of zDL3, zFasL, zTNF1, or zTNF2 did not cause discernible defects (Figure 3b).…”

Section: Extrinsic Apoptosis Pathway Homologs In Zebrafishmentioning

confidence: 99%

Delineation of the cell-extrinsic apoptosis pathway in the zebrafish

et al. 2006

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The mammalian extrinsic apoptosis pathway is triggered by Fas ligand (FasL) and Apo2 ligand/tumor necrosis factor (TNF)-related apoptosis-inducing ligand (Apo2L/TRAIL). Ligand binding to cognate receptors activates initiator caspases directly in a death-inducing signaling complex. In Drosophila, TNF ligand binding activates initiator caspases indirectly, through JNK. We characterized the extrinsic pathway in zebrafish to determine how it operates in a nonmammalian vertebrate. We identified homologs of FasL and Apo2L/TRAIL, their receptors, and other components of the cell death machinery. Studies with three Apo2L/TRAIL homologs demonstrated that they bind the receptors zHDR (previously linked to hematopoiesis) and ovarian TNFR (zOTR). Ectopic expression of these ligands during embryogenesis induced apoptosis in erythroblasts and notochord cells. Inhibition of zHDR, zOTR, the adaptor zFADD, or caspase-8-like proteases blocked ligand-induced apoptosis, as did antiapoptotic Bcl-2 family members. Thus, the extrinsic apoptosis pathway in zebrafish closely resembles its mammalian counterpart and cooperates with the intrinsic pathway to trigger tissue-specific apoptosis during embryogenesis in response to ectopic Apo2L/TRAIL expression.

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“…In the zebrafish (Danio rerio), systematic mutational analysis of early development has identified several notochord-expressed genes, such as no tail (ntl) and floating head (flh) (Halpern et al, 1993;SchulteMerker et al, 1994;Talbot et al, 1995;Odenthal et al, 1996;Stemple et al, 1996;Currie and Ingham, 1996;Fouquet et al, 1997;Blagden et al, 1997;Amacher and Kimmel, 1998), in which loss-of-function mutations cause defects in the formation and/or maintenance of the notochord and within other tissues. Nevertheless, the notochord also serves as the major skeletal element of the embryo, and shows important mechanical processes, such as elongation, straightening and stiffening, during neurogenesis and somitogenesis stages.…”

Section: Introductionmentioning

confidence: 99%

Molecular characterization of Calymmin, a novel notochord sheath‐associated extracellular matrix protein in the zebrafish embryo

Cerdà

Gründ

Franke

et al. 2002

Developmental Dynamics

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During the screening of a zebrafish postsomitogenesis embryo cDNA library, we have identified a cDNA corresponding to a novel type of protein localized to the notochordal sheath-associated extracellular matrix (ECM) of the embryo. The 4.049-kb mRNA encodes a predicted polypeptide of 1,207 amino acids (122 kDa, pI 10.50) with a potential signal peptide of 20 amino acids. After the signal peptide, the mature protein consists of 1,187 amino acids (119 kDa, pI 10.46), for which the name "Calymmin" (from Greek ␣ ␣, to envelop, to cover) is proposed. The Calymmin mRNA is highly and transiently expressed by the notochord cells of the embryo from the 10-to 12-somite stage to the pharyngula period (13 and 24 hours postfertilization, respectively), and light and electron microscopical immunolocalization analysis revealed that the protein was specifically localized within a granular and filamentous layer of the ECM compartment surrounding the notochord. In zebrafish no tail mutants (ntl tc41 ), in which the notochord precursor cells are present but fail to differentiate, the Calymmin protein was not detected, confirming the notochord origin of Calymmin. These results indicate that Calymmin is a novel constitutive protein of the ECM compartment associated to the perinotochordal sheath in the zebrafish embryo, which is specifically expressed by the differentiating notochord cells.

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A homeobox gene essential for zebrafish notochord development

Cited by 434 publications

References 48 publications

Egfl7 knockdown causes defects in the extension and junctional arrangements of endothelial cells during zebrafish vasculogenesis

Egfl7 knockdown causes defects in the extension and junctional arrangements of endothelial cells during zebrafish vasculogenesis

Delineation of the cell-extrinsic apoptosis pathway in the zebrafish

Molecular characterization of Calymmin, a novel notochord sheath‐associated extracellular matrix protein in the zebrafish embryo

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