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. 2009 Jan 30;106(6):1832–1837. doi: 10.1073/pnas.0809632106

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© 2009 by The National Academy of Sciences of the USA

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Fig. 6. — Rescue of the early lethality of compound mutant Ppp1r15a^ΔC/ΔC; Ppp1r15b^−/− embryos by the S51A mutation that eliminates the phosphorylation site on eIF2α. (A) Table of genotypes observed in e17.5 embryos isolated from intercrosses of Ppp1r15a^ΔC/ΔC; eIF2a^+/S51A; Ppp1r15b^+/− parents with the number and percent of expected (#Ex, %Ex) and observed (#Ob, %Ob) indicated. (*Probability of all 7 Ppp1r15a^ΔC/ΔC; Ppp1r15b^−/− embryos inheriting an eIF2a^A/A genotype by chance; P = 6.1 × 10⁻⁰⁵.) (B) Photomicrograph of e17.5 embryos isolated from intercrosses of Ppp1r15a^ΔC/ΔC; eIF2a^+/S51A; Ppp1r15b^+/− parents (abbreviated 15a^ΔC/ΔC; e^+/A; 15b^+/−). Genotypes are indicated below each embryo. (C) Photograph of crystal violet-stained mouse embryonic fibroblasts of the indicated genotype 10 days after transduction with a Puro^r-marked retrovirus expressing either a wild-type or a S51A mutant allele of human eIF2α and selection with puromycin.