The yeast SWI/SNF complex is required for expression of many genes and for the full functioning of several transcriptional activators. Genetic and biochemical studies indicate that SWI/SNF uses the energy of ATP hydrolysis to antagonize chromatin-mediated transcriptional repression. We have tested the possibility that SWI/SNF might also play a role in DNA replication. A mitotic minichromosome stability assay was used to investigate the replication efficiency of a variety of autonomous replication sequences (ARSs) in the presence and absence of SWI/SNF. The stability of minichromosomes that contain ARS1, ARS309 or ARS307 is not altered by lack of SWI/SNF, whereas the functioning of ARS121 is crippled when SWI/SNF is inactivated. The SWI/SNF dependence of ARS121 does not require the replication enhancer factor, ABF1, and thus, it appears to be a property of a minimal ARS121 origin. Likewise, a minimal derivative of ARS1 that lacks the ABF1 replication enhancer acquires SWI/SNF dependence. Replacing the ABF1 binding site at ARS1 with a binding site for the LexA-GAL4 chimeric activator also creates a SWI/SNF-dependent ARS. Our studies suggest that the SWI/SNF chromatin remodeling complex can play a role in both replication and transcription and, furthermore, that SWI/SNF dependence of ARS elements is a property of both an ARS-specific replication enhancer and the overall organization of ARS sequence elements.