Fig. 1. SESAME phosphorylates H3T11 at gene promoters and telomere regions.

a The composite binding profile of H3pT11 at 5065 genes which were divided into five groups according to their transcription rates. The log₂ ratio of normalized enrichment (H3pT11/H3, H3K4me3/H3) for each gene region, including 500 bp upstream and downstream regions from the gene, were used for average gene analysis. The transcription start site (TSS) and termination site (TES) are indicated. b ChIP-seq tracks showing the occupancy of H3K4me3/H3, H3pT11/H3, Pyk1, and Ser33 at representative genes. c Venn diagram of genes that overlap among the Pyk1-peak, Ser33-peak, and H3pT11-peak gene sets as determined by ChIP-seq. The numbers of binding sites are represented. d, e ChIP-seq tracks showing the occupancy of H3pT11/H3, Pyk1, and Ser33 at the left and right telomere regions of chromosome VIII (TEL VIII) (d) and chromosome XII (TEL XII) (e). The control tracks were generated using untagged BY4741 strain with anti-FLAG antibody. f ChIP-qPCR analysis of Pyk1, Ser33, and Sam1 at telomeres of chromosome VI (TEL VIL and TEL VIR), chromosome VIII (TEL VIIIL and TEL VIIIR), and chromosome XII (TEL XIIL and TEL XIIR). The YJR011C was used as a non-target region. g ChIP-qPCR analysis of H3pT11 at telomeres in WT, pyk1-ts, ser33Δ, and sam1Δ mutants. Pyk1 was inactivated by growing pyk1-ts mutant at non-permissive temperature (37 °C) for 2 h. H3pT11 was normalized to histone H3 level. For Fig. 1f, g, the quantitative data represent the mean ± SE; n = 3 biological independent experiments. Statistical significance was tested using two-sided Student’s t test. *p < 0.05; **p < 0.01; ***p < 0.001.