“…Bromodomains are capable of recognizing and specifically binding acetylated histones ( Chandrasekaran and Thompson, 2007 ; Shen et al., 2007 ; Awad and Hassan, 2008 ; Filippakopoulos et al., 2012 ; Morrison et al., 2017 ; Zhao et al., 2018 ) and are therefore considered major factors that enable the targeting of SWI/SNF complexes to nucleosomes enriched in epigenetic acetylation marks. Surprisingly, given this fact, mutations affecting bromodomains are in general considerably less severe than mutations in the ATPase or other major core subunits ( Elfring et al., 1998 ; Hohmann et al., 2016 ; Morrison et al., 2017 ; Ho et al., 2019 ). In accordance with this observation, Arabidopsis null mutants in BRM ATPase display a severe phenotype, including dwarfism, strong leaf curling, and sterility, whereas the brm-3 mutant, in which the BRM protein is deprived of its bromodomain, has only mild phenotypic defects ( Hurtado et al., 2006 ; Farrona et al., 2007 ).…”