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Fig. S1
Lateral views of 4 dpf wild-type (top panels) and fscn1a MZ (bottom panels) embryos injected with coMO or fscn1aMO as indicated.
The fscn1aMO causes severe morphological defects in both wild-type and fscn1a MZ embryos, indicating that compensatory genetic pathways are not activated in fscn1a null mutants. All experiments in this figure were performed independently at least two times with similar results (n = 50 embryos/condition).
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