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Fig. 3 | Genome Biology

Fig. 3

From: Replication stress generates distinctive landscapes of DNA copy number alterations and chromosome scale losses

Fig. 3

Transcription of giant genes can underlie cell type-dependent susceptibility to large aCNAs. A Diagram summarizing all BJ aCNAs taken from 168 cells, after removing clonal events (see “Methods”). Yellow lines show centromeres, purple lines indicate positions of BJ-specific CFS. B Frequency of CNAs occurring in BJ cells after DMSO or aphidicolin as indicated (n = 92 and 168 cells respectively). C Range of sizes of CNAs divided into loss and gain in BJ cells (32 CNAs identified in DMSO, 85 in aphidicolin). D Frequency of small or large CNAs for each chromosome in BJ cells after aphidicolin treatment. E Map of large CNAs in RPE1 and BJ cells after aphidicolin. F Upper panel; schematic indicating S-phase fractions isolated using FACS for single-cell replication timing. Lower panel: single-cell replication timing analyses for RPE1 and BJ cells as indicated from each S-phase fraction. Dark blue indicates replicated genomic regions. G Replication timing factor (see “Methods”) was plotted for each aCNA in RPE1 and BJ cells, and compared to random control regions (470 in silico randomly generated 2 Mb windows, see “Methods”). Statistical tests compare all aCNA classes to in silico control CNAs using a one-way ANOVA Kruskal-Wallis test with post hoc Dunn’s correction

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