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. 2017 Mar 23;100(4):676–688. doi: 10.1016/j.ajhg.2017.03.001

Figure 3.

Figure 3

Phenotypic Effects of Otud6b Deficiency in Mice

(A) Schematic of the Otud6btm1b knockout allele. Exon 4 is deleted and β-galactosidase (lacZ) is expressed following splicing to exon 3 (SA = splice acceptor, pA = polyadenylation signal).

(B–E) LacZ expression, as determined by X-gal staining, from the Otud6btm1b allele is widespread in E12.5 Otud6btm1b/tm1b (B, C) and Otud6btm1b/+ (D, E) embryos.

(F and G) Representative μCT image of E14.5 wild-type (F) and Otud6btm1b/tm1b knockout (G) embryos. The ventricular septal defect in the Otud6btm1b/tm1b knockout embryo is indicated (arrow).

(H and I) Representative X-gal staining images of wild-type (H) and Otud6btm1b/+ (I) adult brains (>50 days of age).