Model of H3K36me3-H3K27me3 interplay in regulating secondary metabolism gene expression. In PH-1, SM genes are repressed by Ash1-catalyzed H3K36me3 (purple) and PRC2-medicated H3K27me3 (red) at promoters (left). ASH1 deletion causes loss of H3K36me3 and reduced H3K27me3, releasing repression and activating transcription (right). During elongation, kinase Ctk1 phosphorylates the Ser2 residue of the C-terminal domain (CTD) of RNA polymerase II (Pol II), facilitating Set2 recruitment. Set2 deposits H3K36me3 along gene bodies to sustain elongation of activated SM genes. Green arrow, activation; red arrow, repression. Figure created with BioRender (https://www.biorender.com).