Figure 6.

HAC1 mediates sugar responses by facilitating the acetylation of H3K27. A, Immunoblot analysis showing changes in the levels of H3K27ac, H3K9ac, H3K14ac, and H3ac in response to treatment with 15 mm Glc or Mtl in the 7-d-old wild-type seedlings. H3 proteins were used as loading controls. B, ChIP-qPCR assays of histone acetylation levels in the promoter regions of GPT2, DFR, and CHS in response to treatment with 15 mm Glc or Mtl for the indicated times. C, Immunoblot analysis showing the accumulation of H3K27ac in wild-type and hac1-4 mutant plants. Bands were quantified with ImageJ in (A) and (C). D, ChIP-qPCR assays for enrichment of H3K27ac in the promoter regions of GPT2, DFR, and CHS in hac1-4 and w18 w53 (w w) mutants in response to Glc treatment. The fragments used for ChIP-qPCR assays in (B) and (D) are shown in Figure 3D. The ACT12 promoter was used as a negative control. *P < 0.05; **P < 0.01 in (B) and (D). E, A working model for the involvement of WRKYs and HAC1 in the response to Glc. After the plant perceives the increased Glc signal, WRKY18 and WRKY53 bind to the W-Box cis-elements and then recruit HAC1 into the promoter regions of sugar-responsive genes through physical interactions. The subsequent acetylation of H3K27 further promotes the transcription of downstream targets.