ZFIN Image: Zhou et al., 2016, Fig. 5

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Figure Caption

Fig. 5

Mog1 regulates cardiac morphogenesis and development during zebrafish embryogenesis.

(A,B) Whole-mount in situ hybridization with embryos injected with 16 ng of control Std-MO (A) or 16 ng of mog1 MO1 (B) with a cardiac marker, cmlc2, at 48 hpf. (C,D) Whole-mount in situ hybridization with embryos injected with 16 ng of mog1 MO1 together with 200 pg of zebrafish mog1 mRNA (C) or with 200 pg of human MOG1 mRNA (D) with a cardiac marker, cmlc2, at 48 hpf. Note that overexpression of mog1 rescued the defects in mog1 morphants. The construct for making zebrafish mog1 mRNA was mutated at 5 positions (from ATG TCA CGG CCT CTG TTT to ATG TCT CGT CCG CTA TTC) so that mog1 MO1 can knock endogenous zebrafish mog1 mRNA down, but not the in vitro synthesized mog1 mRNA used for injection. The mog1 MO1 cannot bind to human MOG1 mRNA so that it cannot knock the in vitro synthesized human MOG1 mRNA down. (E,F) Whole-mount in situ hybridization with embryos injected with 16 ng of control Std-MO (E) or 16 ng of mog1 MO2 (F) with a cardiac marker, cmlc2, at 48 hpf. (G,H) Overexpression of mog1 did not cause changes of cardiac phenotype compared with embryos injected with EGFP mRNA (negative controls). The numbers in the upper right corner (e.g. 38/42 in A) describe the ratio of the number of embryos with the phenotype (e.g. 38) in the image over the number of total embryos analyzed (e.g. 42). Scale bar = 100 μM.

Figure Data

Phenotype details

Acknowledgments

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