DNA replication is initiated by the binding of initiation factors to the origin of replication. Nucleosomes inhibit access to the replication machinery at these origin sequences. Nucleosome remodeling factors increase the accessibility of nucleosomal DNA to transcriptional regulators (1). CHRAC15 and CHRAC17 are subunits of the nucleosomal remodeling factor CHRAC (chromatin accessibility complex),which increases the accessibility of nucleosomal DNA in an ATP-dependent manner (2). Unlike other known chromatin remodelling factors, CHRAC also functions during chromatin assembly by using ATP to convert irregular chromatin into a regular array of nucleosomes with even spacing (3). This conversion process occurs when CHRAC organizes randomly deposited histones into a regularly spaced array (4). In the presence of CHRAC, the nucleosomal ATPase ISWI catalyses several ATP-dependent transitions of chromatin structure (5).