No abstract

The Polycomb repressive complex 2 (PRC2) catalyzes histone H3 Lys27 trimethylation (H3K27me3) to repress gene transcription in multicellular eukaryotes. Despite its importance in gene silencing and cellular differentiation, how PRC2 is recruited to target loci is still not fully understood. Here, we report genome-wide evidence for the recruitment of PRC2 by the transcriptional repressors VIVIPAROUS1/ABI3-LIKE1 (VAL1) and VAL2 in Arabidopsis thaliana. We show that the val1 val2 double mutant possesses somatic embryonic phenotypes and a transcriptome strikingly similar to those of the swn clf double mutant, which lacks the PRC2 catalytic subunits SWINGER (SWN) and CURLY LEAF (CLF). We further show that VAL1 and VAL2 physically interact with SWN and CLF in vivo. Genome-wide binding profiling demonstrated that they colocalize with SWN and CLF at PRC2 target loci. Loss of VAL1/2 significantly reduces SWN and CLF enrichment at PRC2 target loci and leads to a genome-wide redistribution of H3K27me3 that strongly affects transcription. Finally, we provide evidence that the VAL1/VAL2–RY regulatory system is largely independent of previously identified modules for Polycomb silencing in plants. Together, our work demonstrates an extensive genome-wide interaction between VAL1/2 and PRC2 and provides mechanistic insights into the establishment of Polycomb silencing in plants.

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In contrast to typical radially symmetrical flowers, zygomorphic flowers, such as those produced by pea (Pisum sativum L.), have bilateral symmetry, manifesting dorsoventral (DV) and organ internal (IN) asymmetry. However, the molecular mechanism controlling IN asymmetry remains largely unclear. Here, we used a comparative mapping approach to clone SYMMETRIC PETALS 1 (SYP1), which encodes a key regulator of floral organ internal asymmetry. Phylogenetic analysis showed that SYP1 is an ortholog of Arabidopsis thaliana LIGHT-DEPENDENT SHORT HYPOCOTYL 3 (LSH3), an ALOG (Arabidopsis LSH1 and Oryza G1) family transcription factor. Genetic analysis and physical interaction assays showed that COCHLEATA (COCH, Arabidopsis BLADE-ON-PETIOLE ortholog), a known regulator of compound leaf and nodule identity in pea, is involved in organ internal asymmetry and interacts with SYP1. COCH and SYP1 had similar expression patterns and COCH and SYP1 target to the nucleus. Furthermore, our results suggested that COCH represses the 26S proteasome-mediated degradation of SYP1 and regulates its abundance. Our study suggested that the COCH-SYP1 module plays a pivotal role in floral organ internal asymmetry development in legumes.

In flowering plants, repression of the seed maturation program is essential for the transition from the seed to the vegetative phase, but the underlying mechanisms remain poorly understood. The B3-domain protein VIVIPAROUS1/ABSCISIC ACID INSENSITIVE3-LIKE 1 (VAL1) is involved in repressing the seed maturation program. Here we uncovered a molecular network triggered by the plant hormone brassinosteroid (BR) that inhibits the seed maturation program during the seed-to-seedling transition in Arabidopsis (Arabidopsis thaliana). val1-2 mutant seedlings treated with a BR biosynthesis inhibitor form embryonic structures, whereas BR signaling gain-of-function mutations rescue the embryonic structure trait. Furthermore, the BR-activated transcription factors BRI1-EMS-SUPPRESSOR 1 (BES1) and BRASSINAZOLE-RESISTANT 1 (BZR1) bind directly to the promoter of AGAMOUS-LIKE15 (AGL15), which encodes a transcription factor involved in activating the seed maturation program, and suppress its expression. Genetic analysis indicated that BR signaling is epistatic to AGL15 and represses the seed maturation program by downregulating AGL15. Finally, we showed that the BR-mediated pathway functions synergistically with the VAL1/2-mediated pathway to ensure the full repression of the seed maturation program. Together, our work uncovered a mechanism underlying the suppression of the seed maturation program, shedding light on how BR promotes seedling growth.