Extended Data Fig. 7: CNV analysis reveals a partial duplication of chromosome III in 12 of 30 unstable (UR) caffeine-resistant isolates.
From: Epigenetic gene silencing by heterochromatin primes fungal resistance
a, Chromosome III coverage plots with overlaid segments in UR isolates showing partial duplication of chromosome III. Location of cds1+ is highlighted. Wild-type ChIP-seq input data were used as the reference. b–d, Epigenetic changes preceded genetic changes (CNV) in unstable caffeine-resistant isolate UR-2. b, H3K9me2 ChIP-seq enrichment at the ncRNA.394/cup1 locus (left) and chromosome III coverage plots with overlaid segments (right) in UR-2 (4day/+CAF) cells and following their prolonged growth on +CAF for an additional 3 d (7day/+CAF). Wild-type ChIP-seq input data were used as the reference for CNV analysis. c, clr4+ (clr4Δ) or an unlinked intergenic region (controlΔ) were deleted in UR-2 cells (4day/+CAF) and UR-2 (7day/+CAF). All (6/6) UR-2 (4day/+CAF) clr4Δ transformants lost resistance to caffeine, whereas only 50% (3/6, transformants 1, 4 and 5) UR-2 (7day/+CAF) lost resistance to caffeine. Experiments were independently repeated at least twice with similar results. cds1+ DNA levels in extracted genomic DNA were assessed by qPCR. Data are mean ± s.d. from three biological replicates. d, H3K9me2 ChIP-seq enrichment at the ncRNA.394/cup1 locus (left) and chromosome III coverage plots with overlaid segments (right) in UR-2 (7day/+CAF) cells and following their prolonged growth on non-selective medium for 14 days (7day/+CAF→14day/–CAF). Wild-type ChIP-seq input data were used as the reference for CNV analysis.
