Figure 2
From: Insulin-like factor regulates neural induction through an IGF1 receptor-independent mechanism
Insulin3-deficient embryos showed anterior defects in both X. laevis and X. tropicalis.
A translation-inhibiting MO was designed for X. laevis insulin3 and a splice-inhibiting MO for X. tropicalis insulin3. Forty ng and 12 ng of MOs were injected into the marginal zone of both blastomeres at the two-cell stage in (a) X. laevis and (b) X. tropicalis embryos, respectively. (a) Insulin3 MO induced anterior defects in X. laevis embryos. Insulin3 MO specifically inhibited the translation of 5′UTR-insulin3-HA, which has the targeted sequence of MO, but not mis-insulin3-HA, which has 7 mismatches in the targeted sequences. (b) Xt. insulin3 S MO induced anterior defects in X. tropicalis embryos. Xt. insulin3 S MO inhibited normal splicing of insulin3 mRNA. Full-length blots and gels are presented in Supplementary figure S7.
