WT vs Klf5 KO ES

Homozygous disruption of Bteb2/Klf5, a homolog of Drosophila gap gene Krüppel, led to increased expression of various differentiation marker genes, such as Fgf5, Cdx2, and Brachyury in mouse ES cells without compromising their ability to differentiate into all three germ layers. Upon removal of LIF, Klf5-deficient ES cells showed faster differentiation kinetics than wild-type ES cells. In contrast, overexpression of Klf5 in ES cells suppressed the transcription of differentiation marker genes, and maintained pluripotency in the absence of LIF. In order to search downstream genes of Klf5, we surveyed genes implicated in ES cell proliferation by microarray analysis Keywords: cell type comparison WT (clone 1 and 2) and Klf5 KO (clone 1 and 2) ES cells were maintained in ES medium + 15%FBS + LIF. Total RNAs from those ES cells were prepared using RNeasy Kit. Genes down-regulated in Klf5 KO ES cells were searched by GeneSpring software.