Fig. 4

Myo1G promotes Spaw signaling. a Time-course analysis of spaw expression indicates that initiation of spaw expression at the LRO and propagation to the Left LPM (black arrowhead) are delayed in MZ myo1g mutants. Vegetal views of the LRO region, anterior up. b, b′ qPCR analysis of spaw expression confirms that spaw levels are significantly reduced in MZ myo1g mutants (b). Conversely, spaw expression increases in Maternal Zygotic myo1cb (MZ myo1cb) mutants (b′, see also Supplementary Fig. 7b). c MZ myo1g mutants present a significantly reduced (p = 2E-05) rate of anterior-ward propagation of lft1 expression in the notochord (see also Supplementary Fig. 9a). d, e MZ myo1g mutants display a weaker induction of the nodal target gene lft1 in response to Spaw overexpression. d Animal pole views of germ ring stage embryos. While high amounts (20 pg) of Spaw RNA induce a similar lft1 induction in MZ myo1g mutants and wild-type controls, myo1g-deficient embryos present a reduced response to moderate amounts (10 pg) of Spaw RNA (arrow indicates ectopic expression, see Supplementary Fig. 9b for quantification). e qPCR analysis confirms that equal amounts of Spaw RNA induce a reduced lft1 induction response in MZ myo1g mutants compared to WT Control embryos from the same genetic background. f Conversely, the overexpression of Myo1G potentiates the capacity of low amounts (5 pg) of Spaw RNA to induce ectopic lft1. Scale bars: 100 µm. Box plots in b, b′, c, e, f indicate mean values ± SD. All p values were obtained using non-directional statistical tests. Complete numerical and statistical information for all experiments are provided in the Source Data files.