ATP-dependent chromatin remodeling is essential for development, cancer, and stem cell biology. These complexes, encoded by 27 human genes, regulate chromatin structure through ATP hydrolysis. The SWI/SNF family, in particular, has evolved to regulate chromatin during multicellularity. Recent studies show that BAF complexes are involved in cancer progression and development. The mechanisms of these complexes are not fully understood, and their roles in development and cancer require further investigation. The SWI/SNF complex is a multi-subunit complex that regulates transcription by sequence-specific transcription factors. It is evolutionarily conserved and found in flies, plants, and mammals. The Drosophila homologue of SWI2/SNF2, Brahma (BRM), is involved in homeotic gene regulation. The SWI/SNF complex is required for transcription by sequence-specific transcription factors, including yeast GAL4 and the glucocorticoid receptor. LexA fusions of SNF2, SNF5, and SNF6 can activate transcription when bound to DNA. The SWI/SNF family is evolutionarily conserved, and homologous proteins were identified in flies, plants, and mammals. The Drosophila homologue of SWI2/SNF2, Brahma (BRM), was identified in a screen for genes that suppress the body segment defects caused by mutations in Polycomb. BRM mutants cause homeotic transformations consistent with the reduced transcription of homeotic genes. The demonstration of antagonism between BRM and Polycomb, a known chromatin regulator, provided complementary support in flies for the role of SWI/SNF as a regulator of chromatin structure. The SWI/SNF complex is required for transcription by sequence-specific transcription factors, including yeast GAL4 and the glucocorticoid receptor. LexA fusions of SNF2, SNF5, and SNF6 can activate transcription when bound to DNA. The SWI/SNF complex was thus proposed to be a general activator of transcription, working in coordination with sequence-specific transactivators and the histone acetylase GCN5. The SWI/SNF family is evolutionarily conserved, and homologous proteins were identified in flies, plants, and mammals. The Drosophila homologue of SWI2/SNF2, Brahma (BRM), was identified in a screen for genes that suppress the body segment defects caused by mutations in Polycomb. BRM mutants cause homeotic transformations consistent with the reduced transcription of homeotic genes. The demonstration of antagonism between BRM and Polycomb, a known chromatin regulator, provided complementary support in flies for the role of SWI/SNF as a regulator of chromatin structure. It was subsequently found that BRM localizes to a fraction of actively transcribed genes on polytene chromosomes and is required for Pol II localization to these loci. However, in contrast to the genetic studiesATP-dependent chromatin remodeling is essential for development, cancer, and stem cell biology. These complexes, encoded by 27 human genes, regulate chromatin structure through ATP hydrolysis. The SWI/SNF family, in particular, has evolved to regulate chromatin during multicellularity. Recent studies show that BAF complexes are involved in cancer progression and development. The mechanisms of these complexes are not fully understood, and their roles in development and cancer require further investigation. The SWI/SNF complex is a multi-subunit complex that regulates transcription by sequence-specific transcription factors. It is evolutionarily conserved and found in flies, plants, and mammals. The Drosophila homologue of SWI2/SNF2, Brahma (BRM), is involved in homeotic gene regulation. The SWI/SNF complex is required for transcription by sequence-specific transcription factors, including yeast GAL4 and the glucocorticoid receptor. LexA fusions of SNF2, SNF5, and SNF6 can activate transcription when bound to DNA. The SWI/SNF family is evolutionarily conserved, and homologous proteins were identified in flies, plants, and mammals. The Drosophila homologue of SWI2/SNF2, Brahma (BRM), was identified in a screen for genes that suppress the body segment defects caused by mutations in Polycomb. BRM mutants cause homeotic transformations consistent with the reduced transcription of homeotic genes. The demonstration of antagonism between BRM and Polycomb, a known chromatin regulator, provided complementary support in flies for the role of SWI/SNF as a regulator of chromatin structure. The SWI/SNF complex is required for transcription by sequence-specific transcription factors, including yeast GAL4 and the glucocorticoid receptor. LexA fusions of SNF2, SNF5, and SNF6 can activate transcription when bound to DNA. The SWI/SNF complex was thus proposed to be a general activator of transcription, working in coordination with sequence-specific transactivators and the histone acetylase GCN5. The SWI/SNF family is evolutionarily conserved, and homologous proteins were identified in flies, plants, and mammals. The Drosophila homologue of SWI2/SNF2, Brahma (BRM), was identified in a screen for genes that suppress the body segment defects caused by mutations in Polycomb. BRM mutants cause homeotic transformations consistent with the reduced transcription of homeotic genes. The demonstration of antagonism between BRM and Polycomb, a known chromatin regulator, provided complementary support in flies for the role of SWI/SNF as a regulator of chromatin structure. It was subsequently found that BRM localizes to a fraction of actively transcribed genes on polytene chromosomes and is required for Pol II localization to these loci. However, in contrast to the genetic studies