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Figure S7. Combined Loss of T-box TFs Causes Embryos to Produce Excess Neural Tissue at the Expense of Axial and Paraxial Mesoderm and in the Absence of Apoptosis, Related to Figure 6(A) WMISH on control, Xbra/Xbra3, Xbra/Xbra3/Eomes, Xbra/Xbra3/zVegT and Xbra/Xbra3/Eomes/zVegT KD embryos for neural differentiation marker N-tubulin at early tailbud stage (stage 20-21, lateral view). 1, 2 and 3 mark the position of cross-sections through control, Xbra/Xbra3 KD and Xbra/Xbra3/zVegT KD embryos. Abbreviations: no, notochord; nt, neural tube (d, dorsal; v, ventral); pm, paraxial mesoderm.(B) WMISH for actc1, hoxd8 and tal1 at late tailbud stage illustrates the loss of mesodermal derivatives such as skeletal muscle (sm), heart (he), pronephros (pn) and ventral blood island (vbi) upon Xbra/Xbra3/Eomes/zVegT KD. Statistics in bottom right corner indicates the number of embryos observed with the depicted WMISH pattern versus the number of embryos analyzed in total.(C) TUNEL staining on control, Xbra/Xbra3 and Xbra/Xbra3/Eomes/zVegT KD embryos (cleared with Murray’s clear) at early tailbud stage (stage 20). Positive controls, embryos treated for 4 hr in 35 μM cycloheximide (chx) and fixed embryos incubated with DNase I. Arrowheads mark apoptotic cells in the brain region (where apoptosis can occasionally be observed in embryos even under normal conditions) and the posterior nervous system induced by cycloheximide.Scale bar, 0.2 mm.

Image published in: Gentsch GE et al. (2013)

Image downloaded from an Open Access article in PubMed Central. © 2013 The Authors

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