Extended Data Fig. 10: phyB coordinates with PRC2 through VIL1 to regulate its target genes.

a, Hypocotyl length of seedlings of each genotypes grown for 7 days at four different temperatures (12 °C, 17 °C, 22 °C, and 27 °C) in SD. Scale bar: 5 mm. b, Quantification of hypocotyl length, n = 20 seedlings. c, Hypocotyl length of seedlings of Col-0, vil1-1, vrn2, phyB-9, vil1-1 phyB-9, and vrn2 phyB-9 grown for 7 days at 22 °C in SD, Scale bar: 5 mm, n = 20 seedlings. In b and c, the box plot boundaries reflect the interquartile range, the horizontal line is the median and the whiskers represent 1.5X the interquartile range from the lower and upper quartiles. The letters marked as same color above each box indicate statistical difference between the genotypes at each temperature determined by One-way ANOVA followed by Tukey HSD test for multiple comparisons (P < 0.05). d and e, Relative interaction frequency (RIF) in 3C assay between the Anchor primer and a series of F(forward) primers (d), or between the Anchor primer and a series of R(reverse) primers (e) in Col-0, and the vrn2 mutant at ZT6. The enrichment of each region was normalized to that of PP2A. These values were further normalized to the enrichment of each region in pATHB2:ATHB2-Flag plasmid DNAs. Error bars: ± s.d., n = 2, biological replicates (each biological replicate is an average value of four technical replicates). f and g, Model: A novel phyB regulatory module. f, phyB inhibits PIF4 by promoting its protein degradation and repression of DNA binding activity to repress the plant growth under the light. Our model shows a novel regulatory module in which the active form of phyB directly interacts with VIL1 to mediate chromatin remodeling at the growth-promoting genes by recruiting PRC2. Chromatin remodeling by the phyB-VIL1 module ensures the repression of growth-promoting genes, which otherwise can be activated by PIF4. g, On ATHB2 locus, active phyB forms a repressive chromatin loop with VIL1-PRC2. The presence of both phyB and VIL1 is important for the loop formation and for repressive H3K27me3 mark on this locus to fully inhibit ATHB2 expression. However, since neither phyB nor VIL1 can directly bind to DNA, it is possible that unknown DNA-binding protein (X) may be involved in phyB-VIL1 association with the target chromatin.