FIGURE

Fig. 1

ID

ZDB-FIG-170912-4

Publication

Xie et al., 2016 - S1pr2/Gα13 signaling regulates the migration of endocardial precursors by controlling endoderm convergence

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Fig. 1

S1pr2/Gα₁₃ signaling is required for the migration, but not differentiation, of endocardial precursors. (A-D) Projections of four single XY confocal Z-planes of 26 hpf-Tg(myl7: memGFP/kdrl: mCherry) embryos raised at 28.5 °C, showing the myocardium (green) and endothelial cells (magenta). Arrows indicate the presumptive endocardium among the endothelial cells, which formed inside of cardiac population in control embryos (A), but outside of cardiac population in the mutant (B, C). (E) Frequencies of heart defects in 26-hpf embryos injected with gna13a/b MO, s1pr2 MO, or s1pr2 MO and a human Gα₁₃ RNA (GNA13) raised at 28.5 °C, as assessed by epifluorescence imaging. *, P<0.01. Bars indicate the mean±s.e.m. (F-K) Expression of nfatc1 and cdh5, as detected by whole-mount in situ hybridization (ISH), in control, mil mutant, and gna13a/b MO-injected embryos. White arrowheads: endocardial populations. All images are dorsoanterior views with anterior up. Scale bars: 100 µm.

Expression Data

Genes:	cdh5 GFP mCherry nfatc1
Fish:	WT s1pr2^m93/m93 is5Tg; ui6Tg is5Tg; ui6Tg + MO1-s1pr2 WT + MO1-gna13a + MO1-gna13b is5Tg; ui6Tg + MO1-gna13a + MO1-gna13b
Knockdown Reagents:	MO1-gna13a MO1-gna13b MO1-s1pr2
Anatomical Terms:	endocardium endothelial cell myocardium vascular endothelium
Stage:	Prim-5

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	s1pr2^m93/m93 is5Tg; ui6Tg + MO1-s1pr2 WT + MO1-gna13a + MO1-gna13b is5Tg; ui6Tg + MO1-gna13a + MO1-gna13b
Knockdown Reagents:	MO1-gna13a MO1-gna13b MO1-s1pr2
Observed In:	endocardium
Stage:	Prim-5

Phenotype Detail

Acknowledgments

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Reprinted from Developmental Biology, 414, Xie, H., Ye, D., Sepich, D., Lin, F., S1pr2/Gα13 signaling regulates the migration of endocardial precursors by controlling endoderm convergence, 228-43, Copyright (2016) with permission from Elsevier. Full text @ Dev. Biol.