Zebrafish taf1 knockout model revealed an essential function of taf1 during embryogenesis and neurodevelopment. (A) Sequencing results of taf1^{uu1941/uu1941} F2 zebrafish embryos confirmed a 10 bp deletion in exon 8, which results in a frameshift and a stop codon, p.Glu362Alafs*9. (B) Three days post fertilization (dpf) mutant taf1^{uu1941/uu1941} (right) zebrafish embryos showed heart and ventricle edema, blood filled cavities, bent body axis, and general underdevelopment (UD) including short pectoral fins, reduced length and underdeveloped cartilage, eyes, and ears. (C) Phenotype quantification demonstrated reduced length, underdevelopment of eyes, ears and tectum when comparing wild-type taf1^+/+ and heterozygous taf1^uu1941/+ (siblings; sib) with taf1^{uu1941/uu1941} mutants. Adjusted p-values were generated using Student’s t-test, adjusted with Bonferroni correction. (D) Gene set enrichment analysis of all differentially expressed genes revealed four major themes associated with loss of taf1. Chromatin and DNA assembly as well as muscle development pathways were upregulated (red) and pathways of ion transport as well as sensory and visual perception pathways were downregulated (blue) in taf1^{uu1941/uu1941} zebrafish embryos.

Comparison of two different taf1 knockout strains. (A) Schematic overview of deletions in two different strains, taf1^{uu1931/ uu1931} p.(Gly296Leufs*2) and taf1^{uu1941/ uu1941} p.Glu362Alafs*9. (B) Four zebrafish embryos of both taf1^{uu1931/ uu1931} and taf1^{uu1941/ uu1941} at 4 days post-fertilization show a similar abnormal phenotype compared to wild-type taf1 zebrafish (left). The malformations were lethal and included general developmental delay, reduced pigmentation, underdeveloped craniofacial cartilage, cerebral edema, underdeveloped and malformed ears, dorsally bent body axis, heart edema, blood-filled cavities, short pectoral fin, and underdeveloped eyes with coloboma.

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