Fig. 1
- ID
- ZDB-FIG-151110-1
- Publication
- Kimmel et al., 2015 - Diabetic pdx1-mutant zebrafish show conserved responses to nutrient overload and anti-glycemic treatment
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Pdx1sa280 encodes the nonsense mutation Y37X. (a) Schematic of the zebrafish Pdx1 protein and sequence alignment showing the location of amino acid change Y37X resulting from mutant allele pdx1sa280. The mutated tyrosine at position 37, located within the highly conserved N-terminal transactivation domain of pdx1, causes a premature stop codon. (b) Sequencing of genomic DNA from 6-month-old adult offspring of a heterozygous incross revealed surviving homozygotes. (c) Genotype frequency at 6 months of incrossed heterozygotes. Surviving homozygous mutant pdx1/ fish were present at a lower than expected frequency. (Combined data from 4 independent crosses) (d) At 3 months of age, adult mutants (right) had normal morphology but reduced size compared to wild type controls (left). Scale bars, 0.5cm. (e) Homozygous mutants had decreased length, weight and BMI as compared to wild types. n(pdx1+/+) = 18, n(pdx1/) = 19, ***p < 0.0001 (t-test). |
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Stage: | Adult |