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The left-right body axis is defined relative to the dorsal-ventral and anterior-posterior body axes. Since left-right asymmetries are not randomly oriented with respect to dorsal-ventral and anterior-posterior spatial patterns, it is possible that a common mechanism determines all three axes in a coordinate manner. Two approaches were undertaken to determine whether alteration in dorsal-anterior development perturbs the left-right orientation of heart looping. Treatments known to decrease dorsal-anterior development in Xenopus laevis, UV irradiation during the first cell cycle or Xwnt-8 DNA injections into dorsal blastomeres, caused an increase in cardiac left-right reversals. The frequency of left-right reversal was correlated with the severity of dorsal-anterior perturbation and with the extent of anterior notochord regression. Injection of Xwnt-8 DNA into dorsal midline cells resulted in decreased dorsal-anterior development and a correlated increase in cardiac left-right reversals. In contrast, injection of Xwnt-8 DNA into cardiac progenitor blastomeres did not result in left-right reversals, and dorsal-anterior development and notochord formation were normal. Disrupting development of dorsal-anterior cells, including cells that give rise to the Organizer region and the notochord, results in the randomization of cardiac left-right asymmetry. These results suggest dorsal-anterior development and the regulation of left-right orientation are linked.
Fig. 1. Embryos derived from UV treatment, shown at stage 45. (A) Ventral view of a normal heart in a DAI 5 embryo. (B) Ventral view of a
left-right reversed heart in a DAI 4 embryo. Ventricle (v), atrium (a) and conus or outflow tract (c) are indicated; hearts were stained with
MF20 antibody and epidermis was removed. (C,D) Lateral view of a DAI 5 embryo and a DAI 4 embryo for comparison of dorsal-anterior
development. Scale bars, 0.1 mm (A and B); 1.0 mm (C and D).
Fig. 2. The frequency of cardiac left-right reversal is correlated to the
extent of dorsal-anterior deficiencies. The percentage of cardiac
reversals was scored for each DAI from UV-treated embryos (white
bars) and embryos in which Xwnt-8 was injected into dorsal cells
(grey bars). The number of embryos scored in each category are
shown beneath its abscissa.
Fig. 3. Drawing of 32-cell stage embryo to show injection locations,
labelled using the nomenclature of Nakamura and Kishiyama (1971).
The C2 blastomeres are fate mapped to give rise to precursor heart
cells. The stippling shows the region that will give rise to the
notochord (Keller, 1975, 1976; Bauer et al., 1994). Injections done at
this stage were either into C1 blastomeres to target the notochord and
other axial structures (see text), or into C2 blastomeres to target the
heart.
Fig. 4. Notochord deficiencies in dorsal-anterior deficient embryos
(stages 33-38) were detected by in situ hybridizations with the
collagen II probe. Embryos treated with UV during the first cell
cycle, scored as DAI 5 (A), DAI 4 (C), and DAI 3 (E), stained with
the antisense probe. Embryos dorsally injected with Xwnt-8, scored
as DAI 5 (B), DAI 4 (D), or DAI 3 (F), stained with the antisense
probe. Arrows mark the anterior extent of the notochords. As
hybridization controls, DAI 5 (G) and DAI 3 (H) embryos (obtained
from Xwnt-8 injections) were stained with the sense probe. Scale bar,
1.0 mm.
Fig. 5. Decrease in anterior notochord development is correlated
with dorsal-anterior deficiencies. The amount of notochord for each
DAI from UV-treated embryos (white bars) and embryos in which
Xwnt-8 was injected into dorsal cells (grey bars) was measured. The
ratio of notochord length to body length was calculated for each
embryo (10-14 embryos in each category) and normalized by
dividing this ratio by the mean ratio in untreated embryos (83±1,
from measurements of 10 untreated embryos).
