Our work defines mechanisms by which β-catenin signals remodel chromatin and control induction and maintenance of tumour propagating cells.

During the last decade, a number of nuclear protein complexes with the ability to remodel chromatin and regulate gene transcription have been reported.

MLE is related to the ATPases present in complexes that remodel chromatin by altering the positioning or the architectural relationship between nucleosomes and DNA.

It hydrolyses ATP to remodel chromatin structure by sliding and evicting histone octamers3-8, creating DNA regions that become accessible to other essential factors.

We propose that Ttk69 represses some target genes by remodelling chromatin structure through the recruitment of the dNuRD complex.