XB-IMG-172690
Xenbase Image ID: 172690
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Fig. 5. AKT signaling mediates the effect of PFKFB4 on premigratory NC
maturation. (A) In embryos, PFKFB4 regulates AKT signaling in addition to
glycolysis. Dissected morphant st.14 NB or st.17 NC displayed decreased AKT
signaling. (B) AKT regulates many aspects of cell homeostasis including cell
proliferation, cell survival, and cell metabolism. However, EdU incorporation
showed that cell proliferation rate was normal after PFKFB4MO injections.
Error bars represent s.e.m. n.s., not significant. (C,D) PFKFB4MO affected late
NC specifier twist1 expression, whereas the NC stem cell marker cmyc was
normally activated. (E-H) Pharmacological treatment during neural fold stage
(st.14-18) showed that blocking MAPK signaling (E,G) did not affect NC
development, but blocking PI3K-AKT signaling (F,H) affected twist1 but not
cmyc, thus phenocopying the PFKFB4MO effect. (I,J) Co-injection of
PFKFB4MO with a constitutively AKT (caAkt; blue arrows) rescued the
morphant twist1 phenotype (red arrowheads): two sibling embryos for each
injection are shown. St.18 pfkfb4 morphants presented diminished twist1. In
contrast, siblings co-injected with PFKFB4MO and caAkt mRNA had normal
twist1 expression in the majority of cases. Scale bars: 500 μm. Phenotype
scores are shown in Tables S8, S13. Image published in: Figueiredo AL et al. (2017) Copyright © 2017. Image reproduced with permission of the publisher and the copyright holder. This is an Open Access article distributed under the terms of the Creative Commons Attribution License.
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