Fig. S6 Klf6a represses cdkn1a in two different manners: p53-dependent and p53-independent.
(A, B) The WISH and qPCR assay showed that the be1-globin expression (arrowheads) was reduced when overexpression of cdkn1a or knockdown of klf6a and the defect was rescued by co-injection of cdkn1a MO into klf6a morphants (mean ± SD, t-test, ***P<0.001, **P<0.01, n = 3). (C) O-dianisidine staining positive cells were decreased dramatically in klf6a morphants and modestly decreased in p53 mutants embryos injected with klf6aMO. The arrowheads mark o-dianisidine staining positive cells. (D) qPCR analysis showed that be1-globin expression was reduced and cdkn1a was still up-regulated in embryos co-injected with klf6aMO and p53MO, compared to klf6a morphants (mean ± SD, t-test, **P<0.01, *P<0.05, n = 3).
Reprinted from Developmental Biology, 403(2), Xue, Y., Gao, S., Liu, F., Genome-wide Analysis of the Zebrafish Klf Family Identifies Two Genes important for Erythroid Maturation, 115-27, Copyright (2015) with permission from Elsevier. Full text @ Dev. Biol.