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. 2014 Dec 1;34(2):236–250. doi: 10.15252/embj.201488544

Figure 8. Replication–transcription relationship.

Figure 8

  1. Analysis of Rrm3 recruitment in WT and rpb1-1. Rrm3 IP histogram bars in the y-axis show the average signal log2 ratio of loci enriched in the immunoprecipitated fraction along the indicated regions in the x-axis. When the ratio fulfills the P-value criteria (P < 0.01) it is shown in red.
  2. Composite profile of Rrm3 occupancy across the average ORF plotted as Rrm3 percentage of significant ChIP hits per segment. Each gene was divided into 10 equivalent segments from the start and end coordinates (segments 2–10). Two additional segments of the same size were considered upstream (5′) and downstream (3′) of each ORF (segments 1 and 12, respectively). The average signal log2 ratio for Rrm3 significant hits that map on each segment was plotted.
  3. Composite profile of Rrm3 occupancy across the average ARS plotted as Rrm3 percentage of significant ChIP hits per segment. Each ARS was divided into 11 equivalent segments from the start and end coordinates. The average signal log2 ratio for Rrm3 significant hits that map on each segment was plotted.
  4. Model for a role of RNAPII as a source of genetic instability. Conflicts between transcription and replication machineries affect replication progression causing DSBs at high levels under exogenous replicative stress, which demands the HR machinery for the repair and restart of RFs. RNAPII would have a function facilitating RF progression upon a transcription–replication encounter. This function would be affected in the rpb1 and rpb9 mutants analyzed here, causing RF progression impairment and genome instability.