FIGURE

Fig. 1

ID
ZDB-FIG-220526-3
Publication
Jiang et al., 2020 - Tek/Tie2 is not required for cardiovascular development in zebrafish
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Fig. 1

No gross vascular morphology defects in RNA-less or in-frame deletion zebrafish tek mutants. (A) Schematic representation of the Tek protein domains and the lesion in each allele. Blue star represents ENU-induced lesion; red stars and scissors represent CRISPR target sites. Lesions in tekhu1667 and tekbns278 result in a premature termination codon in the TK domain- and TM domain-encoding exons, respectively. The lesion in tekbns347 is an in-frame deletion that is predicted to severely impair Tek function (Fig. S1). tekbns399 and tekbns400 are full-locus deletion alleles. tekbns401 contains a 261 bp deletion around the translational start site. (B) tek expression levels in different tek mutant alleles when compared with their corresponding +/+ siblings at 24 hpf. (C-H′) Lateral views of 48 hpf trunk vessels. No obvious vascular phenotype is observed in any of these alleles (C′-H′) when compared with their corresponding +/+ siblings (C-H). PTC, premature termination codon; Ig, immunoglobulin domain; EGF, epidermal growth factor repeat; FNIII, fibronectin type 3 domain; TM, transmembrane domain; TK, tyrosine kinase domain. In B, data are mean±s.d. Scale bar: 200 μm.

Expression Data
Gene:
Fish:
Anatomical Term:
Stage: Long-pec

Expression Detail
Antibody Labeling
Phenotype Data

Phenotype Detail
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