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Fig. 6 Klf17, Klf2a and Klf2b induce EVL-specific genes and regulate each other′s expression. The charts show fold change values for expression based on microarray probes for 9 selected EVL-specific genes (A–C), or klf2a, klf2b and klf17 probes (D–F) in Klf17 (A, D), Klf2a (B, E) and Klf2b (C, F) overexpression (OE) and knockdown (KD) assays compared to control injected embryos. Error bars – standard error of the mean, * – p-value <0.05 in Student′s T-test. Note, that while EVL-specific genes are induced by all Klfs, they are strongly repressed in Klf17 KD (A), but not in Klf2a or Klf2b KD (B, C). (D–F) Cross-regulatory interaction between klf17, klf2a and klf2b and their protein products. klf2a expression level is significantly higher in Klf17 KD, and klf2b expression levels are reduced by Klf17 OE (D). While Klf2a and Klf2b do not significantly affect expression of each other, they directly repress klf17 in MZspg, but not in WT background (E, F).

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Reprinted from Developmental Biology, 385(2), Kotkamp, K., Mössner, R., Allen, A., Onichtchouk, D., and Driever, W., A Pou5f1/Oct4 dependent Klf2a, Klf2b, and Klf17 regulatory sub-network contributes to EVL and ectoderm development during zebrafish embryogenesis, 433-47, Copyright (2014) with permission from Elsevier. Full text @ Dev. Biol.