(T.J.S.)Arabidopsis thaliana SWP73A and SWP73B are homologs of mammalian BRAHMA-associated factors (BAF60s) that tether SWITCH/SUCROSE NONFERMENTING chromatin remodeling complexes to transcription factors of genes regulating various cell differentiation pathways. Here, we show that Arabidopsis thaliana SWP73s modulate several important developmental pathways. While undergoing normal vegetative development, swp73a mutants display reduced expression of FLOWERING LOCUS C and early flowering in short days. By contrast, swp73b mutants are characterized by retarded growth, severe defects in leaf and flower development, delayed flowering, and male sterility. MNase-Seq, transcript profiling, and ChIP-Seq studies demonstrate that SWP73B binds the promoters of ASYMMETRIC LEAVES1 and 2, KANADI1 and 3, and YABBY2, 3, and 5 genes, which regulate leaf development and show coordinately altered transcription in swp73b plants. Lack of SWP73B alters the expression patterns of APETALA1, APETALA3, and the MADS box gene AGL24, whereas other floral organ identity genes show reduced expression correlating with defects in flower development. Consistently, SWP73B binds to the promoter regions of APETALA1 and 3, SEPALLATA3, LEAFY, UNUSUAL FLORAL ORGANS, TERMINAL FLOWER1, AGAMOUS-LIKE24, and SUPPRESSOR OF CONSTANS OVEREXPRESSION1 genes, and the swp73b mutation alters nucleosome occupancy on most of these loci. In conclusion, SWP73B acts as important modulator of major developmental pathways, while SWP73A functions in flowering time control.

Seed dormancy is adopted by plants to optimize their reproductive strategy. The DOG1 (DELAY OF GERMINATION 1) gene is the main QTL controlling this trait in Arabidopsis (Bentsink et al., 2006) and therefore is extensively regulated. This includes the alternative polyadenylation (APA) of DOG1 mRNA (Cyrek et al., 2016) and an antisense transcript, asDOG1, which in cis suppresses DOG1 expression during seed maturation (Fedak et al., 2016). As with many antisense transcripts (Mellor et al., 2016; Rosa et al., 2016), asDOG1 originates from close to the transcription termination site of the sense gene. This raises the question of how this proximity affects antisense promoter activity.