Figure 1.
Generation of SLFN14 K208N mice using CRISPR-Cas9 gene editing and embryo development. (A) Schematic diagram of CRISPR-Cas9 gene-editing mechanism using human K219N donor oligonucleotide. (B) Wild-type, SLFN14K208N/+, and SLFN14K208N/K208N traces showing successful KI of G>T missense mutation (arrow). (C) Non-Mendelian inheritance pattern of SLFN14 K208N mice. χ2 square analysis shows significant deviation from Mendelian inheritance and prewean loss of homozygotes (P < .0001). Data are taken from 15 litters of heterozygote/heterozygote (cross 2) breeding pairs. (D) Representative images of backlit embryos taken at E12.5 and E14.5 (original magnification ×3). n = 3 to 9 embryos per genotype.

Generation of SLFN14 K208N mice using CRISPR-Cas9 gene editing and embryo development. (A) Schematic diagram of CRISPR-Cas9 gene-editing mechanism using human K219N donor oligonucleotide. (B) Wild-type, SLFN14K208N/+, and SLFN14K208N/K208N traces showing successful KI of G>T missense mutation (arrow). (C) Non-Mendelian inheritance pattern of SLFN14 K208N mice. χ2 square analysis shows significant deviation from Mendelian inheritance and prewean loss of homozygotes (P < .0001). Data are taken from 15 litters of heterozygote/heterozygote (cross 2) breeding pairs. (D) Representative images of backlit embryos taken at E12.5 and E14.5 (original magnification ×3). n = 3 to 9 embryos per genotype.

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