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tnni3xenopus   

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Experiment details for tnni3

Drysdale TA et al. (1994) Assay

Cardiac troponin I is a heart-specific marker in the Xenopus embryo: expression during abnormal heart morphogenesis.

Gene Clone Species Stages Anatomy
tnni3.L laevis NF stage 28 to NF stage 29 and 30 heart , cardiac mesoderm
tnni3.L laevis NF stage 37 and 38 heart

  F IG. 7. Expression of troponin 1c in lithium-treated embryos, (A) The heart in a stage 28/30 control embryo, Note that it has already formed a simple tube at the ventral midline. (B) A DAI 8 embryo that has an enlarged heart region. Cardiac tissue is absent on the dorsal side of the embryo and has not fused at the ventral midline. (C) A top view of a DAI 9 embryo showing the distribution of heart tissue (arrowheads). Although not visible in its entirety in this view, the heart forms a ring that could be detected around the entire circumference with the exception of a gap (g) on the dorsal side. The heart tissue is just beneath the surface, indicating that it has not involuted. (D) A stage 38 control embryo with the heart undergoing looping and deformations that result in the final morphology. (E) A DAI 9 embryo viewed from the side. The heart now appears radial and is moving to the final location at the center of the embryo. The timing of this movement corresponds to the normal looping and folding events, rather than migration to the ventral midline. (F) A stage 38 DAI 8 embryo with an almost radial heart. The heart has begun to move to the center of the embryo but the most dorsal side of the embryo (arrow) is still thin.

Gene Clone Species Stages Anatomy
tnni3.L laevis NF stage 37 and 38 heart

  FIG. 4. Heart morphology in embryos treated with retinoic acid. The heart morphology of control embryos at stage 38 is seen in (A), with an enlarged view of a control heart in (D). At the equivalent stage, embryos that were treated with 10 I-'M RA at stage 10.5 (B) have hearts which are extremely reduced in size or absent (bottom embryo). An enlarged view (E) shows the significant reduction in heart size in RA-treated embryos. Note that many other anterior structures are also absent. (C) Embryos at the equivalent of stage 38 that were treated with 10uM RA at stage 15. These show almost normal morphology of anterior structures but the hearts are smaller than those in control embryos. The enlarged view (F) shows a failure of the heart to separate into distinct chambers. In all RA treatments, the heart tissue migrated to the ventral midline.

Gene Clone Species Stages Anatomy
tnni3.L laevis NF stage 37 and 38 heart

  FIG. 5. Retinoic acid-treated embryos have abnormal hearts. The heart (h) of a normal stage 38 embryo in longitudinal section (A) is multichambered and is flattened against the gut (see Fig. 6). In (B), the heart (h) of the retinoic acid -treated embryo has a single large chamber that does not appear to have any of the normal constrictions or looping associated with normal cardiac morphogenesis. In both embryos anterior is to the left as indicated by tbe position of the cement gland (cg).