Fig. 1
- ID
- ZDB-FIG-160714-11
- Publication
- Kawauchi et al., 2016 - Using mouse and zebrafish models to understand the etiology of developmental defects in Cornelia de Lange Syndrome
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Nipbl-deficient mutant animals show growth abnormalities. (A) Nipbl+/- mouse is markedly smaller than wildtype (+/+) sibling at 4 weeks of age. (B) Nipbl a+b morpholino (MO) co-injected zebrafish larvae (nipbl a/b morphants) resemble uninjected and mixed MO controls at 18.5 hr post-fertilization (hpf), but show marked circulatory defects, pericardial edema (asterisk) and tail defects (arrowheads) by 34 hpf. Scale bar = 100 µm. (C) Structural comparison of NIPBL orthologues among different species. H.s., Homo sapiens, 2,804 amino acids (aa).; M.m., Mus musculus, 2,798 aa; D.r. (a), Danio rerio, form a, 2,876 aa; D.r. (b), form b, 2,381 aa; D.m., Drosophila melanogaster, 2,077 aa; S.c., Saccharomyces cerevisiae, 1,493 aa. Numbers indicate percent amino acid sequence identity compared to human NIPBL. Adapted from [Kawauchi et al., 2009; Muto et al., 2011]. |