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Fig. S3
Co-injection of MO2-fak1a and MO2-fak1b results in defective splicing and heart failure in vivo.
(A, B) Lateral view of (A) control MO (MO2-control) and (B) MO2-fak1a/fak1b-injected embryos at 72 hpf. The heart failure phenotype of fak1a/fak1b splice morphants was identical to that of embryos injected with the translation blocking FAK MOs (MO1-fak1a/fak1b). (C) RT-PCR of control-, MO2-fak1a- and MO2-fak1b-injected embryos. Injection of MO2-fak1a and MO2-fak1b caused intron integration (808 bp MO2-fak1a; 883 bp MO2-fak1b) leading to premature termination of FAK1a and FAK1b protein translation, respectively. Wild-type fak1a and fak1b RNA was severely reduced in the respective morphants (150 bp MO2-fak1a; 474 bp MO2-fak1b). (D) Western Blot analysis of control and fak1a/fak1b morphant embryos with an antibody against FAK. For each sample 50 embryos were pooled and 20 μg of protein lysate were loaded per lane.