“…For instance, mutants affected in ATRX7 (H3K4 methyltransferase), EFS/SDG8 (H3K36 di-and trimethylation), EBS (an H3K4me2/3 "reader" interacting with HDA6) or HUB1 and HUB2 (H2B monoubiquitination) display lower ABI3 expression and dormancy, whereas those affected in H3K9 methylation (kyp/suvh4) or H3K4 demethylation (ldl1 and ldl2) display the opposite phenotype (Liu et al, 2007b;Bassel et al, 2011;Zheng et al, 2012;Zhao et al, 2015;Narro-Diego et al, 2017). Moreover, although PRC1/2 are not required for proper embryo development, mutations affecting PRC1 or PRC2 lead to a failure in both, the repression of LAFL expression and directly switch from embryo to seedling development (Chanvivattana et al, 2004;Makarevich et al, 2006;Aichinger et al, 2009;Bratzel et al, 2010;Chen et al, 2010;Berger et al, 2011;Bouyer et al, 2011;Muller et al, 2012;Tang et al, 2012a;Zhang et al, 2012;Deng et al, 2013;Yang et al, 2013;Molitor et al, 2014;Ikeuchi et al, 2015;Xiao and Wagner, 2015;Feng et al, 2016;Trindade et al, 2017;Xiao et al, 2017;Lee and Seo, 2018). Similar accumulation of seed proteins in vegetative tissues is also observed when the RETINOBLASTOMA-RELATED1 (RBR1) that is required to maintain the PRC2-dependent repression of LEC2 and ABI3 is affected (Gutzat et al, 2011;Kuwabara and Gruissem, 2014) and in mutant of the SWI2/SNF2 chromatin remodelling ATPase BRAHMA (BRM) (Tang et al, 2008), although BRM has been shown to controls the transition from juvenile to adult vegetative phase antagonistically to PRC2 (Xu et al, 2016).…”