ATP-dependent chromatin remodeling is one of several mechanisms that permit the compaction and decompaction of DNA in the nucleus while retaining the capacity for replication, selective gene expression, and DNA repair and recombination. This mechanism was first discovered in yeast, ironically in screens for signal transduction molecules involved in responses to mating factor that lead to mating type switching (hence the name Switch or SWI) (5). Three of these genes were independently discovered in screens for signaling molecules leading to sucrose fermentation in response to nutrient switching in yeast (sucrose nonfermenting or SNF) (6). Genetic reversion of these signaling phenotypes was achieved by second mutations in histone genes, showing that specific SWI and SNF genes in yeast actually regulated chromatin remodeling rather than acting as participants in a signaling mechanism. Biochemical characterization then led to the discovery that these genes encoded proteins that associated with one another; hence, the term “SWI/SNF complex” was used to characterize this chromatin regulatory entity (7).
