Fig. 2: Genomic instability and induced mutagenesis caused by gentamicin.

a Activation of SOS response by gentamicin treatment. Shown are the fold changes of transcripts per million (TPM) of representative genes in SOS regulon measured by RNA-seq. b DNA damage induced by gentamicin. DNA damage levels at 0 min, 30 min, 60 min, and 90 min post gentamicin addition were measured by the TUNEL assay and flow cytometry. Damage-positive cell ratio: 0 min, 31.3%; 30 min, 36.6%; 60 min, 48.2%; 90 min, 50.9%. Representative of 2 biological replicates. c, d Mutations isolated after gentamicin treatment (c) and spontaneous mutations (d). The positions of the mutations on the genome were indicated, along with the positions of oriC (3,925,744–3,925,975) and terC (1,609,157–1,609,179) for reference. Different rings represent different types of mutations: base pair substitutions (cyan), mobile element insertions (red), deletions and insertions (yellow). e Spectrums of spontaneous mutations and of mutations isolated after gentamicin treatment. Shown are the percentages of different mutation categories. f Spectrums of the base pair substitutions category shown in (e). g Transcript coverage of exampled operons cpxRA and hemL measured by RNA-seq at 0 min (black outline) and 60 min (red outline) after gentamicin treatment. h Distributions of fold changes of 5′ coverage bias at 0 min and 60 min after gentamicin treatment. Shown are histograms of the fold changes of 5′ coverage bias from 3126 protein-coding genes (see “Methods” section), and the fold changes at 0 min were calculated from two replicates without gentamicin (P = 9.07 × 10⁻⁸⁸, one-sided MWU test). The values of 20 protein-coding genes with detected mutations in (c) were marked by dashed lines. Source data are provided as a Source Data file.