Fig. 1: Disruption of Ace2 in zebrafish lead to growth retardation.

a Quantitative real‑time PCR analysis of ace2 mRNA expression in different zebrafish tissue (n = 3/each group), normalized to ef1a as the internal control. b Schematic representation of the genomic structure of zebrafish ace2 and the target site of CRISPR. Gross morphology (c), body length (d) and body weight (e) of zebrafish ace2 homozygous mutants (ace2−/−, n = 5) and sibling heterozygous controls (ace2+/−, n = 6) at 50 dpf. Gross morphology (f), body length (g) and body weight (h) of zebrafish ace2 homozygous mutants (ace2−/−, n = 21) and sibling heterozygous controls (ace2+/−, n = 14) at 110 dpf. i The relative body weight was normalized the aged-match controls at 50, 80, and 110 dpf (50 dpf: ace2+/−, n = 6; ace2−/−, n = 5; 80 dpf: ace2+/−, n = 19; ace2−/−, n = 13; 80 dpf: ace2+/−, n = 14; ace2−/−, n = 21). j The growth hormones (GH) encoded gene gh mRNA expression levels in zebrafish pituitary at 80 dpf assessed by quantitative real‑time PCR analysis (ace2+/−, n = 5; ace2−/−, n = 6). The significance was analyzed by Student’s t-test. (**P < 0.01; ***P < 0.001).