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. 2018 Dec;28(12):1882–1893. doi: 10.1101/gr.239582.118

Figure 5.

Figure 5.

Absence of Set2 H3K36 methyltransferase partially rescues replication defects due to noncoding transcription readthrough. (A) Experimental scheme as described in Figure 1C. (B) Metagene analysis of the BrdU-seq for the 142 nonaffected ARSs (<35%) and the 17 most affected ARSs (>50%) for the Nrd1-AA and Nrd1-AA set2Δ strains. Plots for the Nrd1-AA strain were already presented in Figure 1F, with the exception of the normalized coverage, for which calculation is detailed in Methods. Profiles represent the mean coverage smoothed by a 200-bp moving window. ARSs were oriented according to their ACS T-rich sequence. (C) Scatter dot-plot presenting the normalized BrdU ratio for the different classes of ARS affected in BrdU incorporation in an Nrd1-AA strain and for the same classes of ARSs in the Nrd1-AA set2Δ strain. (D) Snapshot depicting the BrdU-seq reads for a part of Chromosome XIII. ARSs that are rescued in BrdU incorporation in the Nrd1-AA set2Δ +Rap condition are depicted in red, while nonaffected ARSs are in green. (E) Metagene analysis of BrdU incorporation 5 kb around nonreplicating ACSs (nr-ACS) in the indicated strains grown in −/+Rap. The representation is smoothed over a 200-bp moving window. (F) Snapshot illustrating the activation of a dormant nr-ACS in the Nrd1-AA set2Δ +Rap condition. (*) P-value < 0.05; (**) P-value < 0.01; (***) P-value < 0.001.