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. 2014 Aug 8;124(9):4028–4038. doi: 10.1172/JCI73264

Figure 5. Modeling of NSMCE2/MMS21 deficiency in zebrafish.

Figure 5

Injection of splice-site MOs targeted to Nsmce2 markedly reduce body size compared with that of control-injected or uninjected WT embryos. (A) Representative images of some arbitrarily defined length categories: normal, –1 to 1 SD; short, –1 to –2 SD; dwarf, –2 to –3 SD; severe, < –3 SD. (B) Quantification of length of MO-injected zebrafish (uninjected, n = 18; control, n = 28; MO, n = 37). (C–E) Coinjection of WT human NSMCE2/MMS21 mRNA (WT rescue) with nsmce2-targeting MOs attenuated the dwarf phenotype observed in the nsmce2 morphant alone (morph). In contrast, coinjection of either (C) human NSMCE2/MMS21 S116Lfs*18, (D) human NSMCE2/MMS21 A234Efs*4, or (E) SUMO LD human NSMCE2/MMS21 mRNAs together with nsmce2-targeting MOs did not affect the severity of the dwarf phenotype. Uninj, uninjected; con, control. Graphs show SD scores relative to those of uninjected WT zebrafish embryos from the same mating. n = 12–15 for each condition. P values were calculated by ANOVA with post-hoc Tukey test; **P < 0.01, ***P < 0.001.