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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Hum Genet. 2016 Jan 7;135(2):245–251. doi: 10.1007/s00439-015-1632-8

Figure 2. golga2 gene knockdown results in skeletal muscle defects in zebrafish.

Figure 2

(A) Embryos injected with 2.5 ng of golga2 translation- (T-MO) and splice-blocking (e13i13-MO) morpholinos both show dorsally curved phenotype at 3 dpf in comparison to WT-controls (left panel). Visualization of embryos underpolarized light showed an overall reduction in birefringence indicative of disorganized sarcomeric structure (B) Western blot demonstrates that T- and e13i13-MO-mediated knockdowns of golga2 result in significantly decreased levels of zebrafish golga2 protein by 3 dpf. (C) Overexpression of human GOLGA2 mRNA in morphants resulted in recue of skeletal muscle and brain phenotypes. Green indicates normal embryos, yellow indicates embryos displaying muscle and brain abnormalities, and red indicates dead embryos a 3 dpf. Two independent experiments were performed for all rescue studies, with at least 100 embryos injected for each group. Statistical significance relative to the MO-only experimental group was determined by a Student's t-test, P < 0.01.