Patterning of the floral organs is exquisitely controlled and executed by four classes of homeotic regulators. Among these, the class B and class C floral homeotic regulators are of central importance as they specify the male and female reproductive organs. Inappropriate induction of the class B gene APETALA3 (AP3) and the class C gene AGAMOUS (AG) causes reduced reproductive fitness and is prevented by polycomb repression. At the onset of flower patterning, polycomb repression needs to be overcome to allow induction of AP3 and AG and formation of the reproductive organs. We show that the SWI2/SNF2 chromatin-remodeling ATPases SPLAYED (SYD) and BRAHMA (BRM) are redundantly required for flower patterning and for the activation of AP3 and AG. The SWI2/SNF2 ATPases are recruited to the regulatory regions of AP3 and AG during flower development and physically interact with two direct transcriptional activators of class B and class C gene expression, LEAFY (LFY) and SEPALLATA3 (SEP3). SYD and LFY association with the AP3 and AG regulatory loci peaks at the same time during flower patterning, and SYD binding to these loci is compromised in lfy and lfy sep3 mutants. This suggests a mechanism for SWI2/SNF2 ATPase recruitment to these loci at the right stage and in the correct cells. SYD and BRM act as trithorax proteins, and the requirement for SYD and BRM in flower patterning can be overcome by partial loss of polycomb activity in curly leaf (clf) mutants, implicating the SWI2/SNF2 chromatin remodelers in reversal of polycomb repression. P lant development occurs largely postembryonically (1), and, as a consequence, many cell-fate choices do not take place until long after embryogenesis. One example is flower development; in the rapid-flowering winter annual Arabidopsis the first flowers are formed 1 mo to 1 y after germination (2). Precocious activation of the floral homeotic genes required for flower patterning results in pleiotropic defects including poor seed set and is prevented by chromatin repression, which is faithfully inherited throughout cell divisions until the first flowers are formed (3-7). The repressive chromatin needs to be erased for flower patterning to be initiated in flower primordia. For class B genes, such as APETALA3 (AP3), which are required for correct patterning of the showy petals and the male reproductive organs, activation of gene expression occurs in late stage 2 flower primordia in the cells that will give rise to whorls 2 and 3 of the flower (6). For class C gene AGAMOUS (AG), which is required for patterning both the male and the female reproductive organs, induction is observed in early stage 3 flowers in the cells that will give rise to whorls 3 and 4 (6).The mitotically heritable chromatin repression of AP3 and AG before flower formation is achieved by two polycomb complexes: polycomb repressive complex 1 (PRC1) and PRC2. PRC2 is responsible for trimethylation of lysine 27 of histone H3 (H3K27me3) (7,8). Two putative H3K27 methyltransferases and PRC2 complex components, SWINGER and ...