Fig. 3: 3′-end-seq analysis revealed pervasive occurrence of 3′ termini induced by gentamicin. | Nature Communications

Fig. 3: 3′-end-seq analysis revealed pervasive occurrence of 3′ termini induced by gentamicin.

From: RNA polymerase stalling-derived genome instability underlies ribosomal antibiotic efficacy and resistance evolution

Fig. 3

a Schematic of the 3′-end-seq workflow. b, c. 3′-end-seq profiles across the cpxRA (b) and hemL (c) genes before (upper) and 60 min after gentamicin treatment (lower). The plotted spikes indicate counts per million (CPM) of 3′ end at each nucleotide analyzed from 3′-end-seq with strand specificity. The arrow-shaped boxes below the plots show the corresponding genes and their coordinates on the genome. d Dynamics of the dominant 3′ termini upon gentamicin treatment under five different thresholds. e Distributions of the fold changes of 3′ termini at 0 min and 60 min after gentamicin treatment (shown in black and red respectively, P = 2.68 × 10−159, one-sided Mann–Whitney U (MWU) test). Shown are histograms of the fold changes of 3′ termini from 3126 protein-coding genes, and the fold changes at 0 min were calculated from two replicates without gentamicin. Source data are provided as a Source Data file.

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