FIGURE

Fig. S3

ID

ZDB-FIG-171110-11

Publication

Hirth et al., 2016 - Paxillin and Focal Adhesion Kinase (FAK) Regulate Cardiac Contractility in the Zebrafish Heart

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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.

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Phenotype Detail

Acknowledgments

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