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Figure 3. (a–d) Overexpression of a dominant-negative XHMGA2 mutant in Xenopus embryos blocked XNkx2.5 expression. Ventral view of stage-23 (a, b) and lateral view of stage-34 (c, d) embryos. Expression of XNkx2.5 mRNA was decreased in XHMGA2–EnR mRNA-injected embryos (b, d, arrowheads), compared with that of control embryos (a, c, arrowheads). (e–p) MO-mediated XHMGA2 knockdown results in impaired cardiogenesis. Whole-mount in situ hybridization analysis was performed sequentially for Xenopus embryos at stage 15 (e–g), stage 23 (h–j) and stage 34 (k–m) for XNkx2.5, and at stage 41 for cardiac troponin I (cTnI) (n–p). Expression of XNkx2.5 mRNA was detected in uninjected control embryos (e, h, k, arrows), whereas it was attenuated in both XHMGA2–MO1 (f, i, l) and XHMGA2–MO2 (g, j, m)-injected embryos (arrowheads). In situ hybridization analysis for cardiac troponin I revealed that the heart size in MO-injected embryos (o, p, arrowheads) was smaller than that of control embryos (n, arrows). |
