ZFIN Image: Selland et al., 2018, Fig. 8

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Fig. 8

RA signaling is altered in pbx depleted embryos.

To determine if the loss of hindbrain identity is due to defects in RA signaling, aldh1a2 expression was examined. Pbx4^−/− mutants that are treated with pbx2/4 morpholinos have a near complete knockdown of both maternal and zygotic Pbx. At early stages of hindbrain specification there is a decrease in aldh1a2 expression in wildtype embryos treated with pbx2/4 morpholinos (C) as compared to uninjected wildtype (A) or pbx4^−/− mutants (B). There is a decrease in both aldh1a2 expression level and domain in pbx4^−/− mutants injected with pbx2/4 morpholinos (22/22 embryos)(D). The area of aldh1a2 expression was measured using Image J, and the average was calculated (E). Zygotic pbx4^−/− mutants treated with pbx2/4 morpholinos have a 21% decrease in the area of aldh1a2 expression compared to uninjected wildtype embryos. Error bars indicate standard deviation. Uninjected wildtype: 135890.431 μm², Uninjected pbx4^−/−: 130628.408 μm², pbx2/4MO injected wildtype: 110737.578 μm², pbx2/4MO injected pbx4^−/−: 107364.171 μm². (ANOVA, post-hoc Tukey's: Uninjected wildtype vs pbx2/4MO injected wildtype, p-value 0.003; Uninjected wildtype vs pbx2/4MO injected pbx4^−/−, p-value 0.001) All embryos have been genotyped for pbx4^b557. All images are dorsal views, anterior to the top, 90% epiboly.

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Acknowledgments

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Reprinted from Mechanisms of Development, 150, Selland, L.G., Koch, S., Laraque, M., Waskiewicz, A.J., Coordinate regulation of retinoic acid synthesis by pbx genes and fibroblast growth factor signaling by hoxb1b is required for hindbrain patterning and development, 28-41, Copyright (2018) with permission from Elsevier. Full text @ Mech. Dev.