The murine homolog of SALL4, a causative gene in Okihiro syndrome, is essential for embryonic stem cell proliferation, and cooperates with Sall1 in anorectal, heart, brain and kidney development
Development Sakaki-Yumoto et al.
133: 3005
DEV02457 Supplementary Material
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Supplemental Figure 1
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Fig. S1. Additional Sall4 targeting constructs. (A) Promoterless targeting construct in which exons 2 and 3 and intron 2 are replaced with IRES-βgeo. (B) Exons 2 and 3 and intron 2 are replaced with IRES-Hyg. (C) Exons 2 and 3, introns 2 and 3, and the entire coding region of exon 4 are deleted and replaced with Hyg driven by the pGK promoter by following the same strategy as shown in Fig. 1A. (D) Floxed allele of Sall4. Exons 2 and 3 and intron 2 are flanked by loxP sites. Neor is flanked by Frt sequences and inserted into the intron 2.
