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Of the 37 mutant rpoB genotypes, 36 were correctly detected; the single mutant not detected contained a 9 base insertion.
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We examined 14 diploid mutants not detected in the initial DOX screen that interconnect to DOX resistance gene nodes defined within the proteomic network (Fig 4A).
In a similar manner we utilized the proteomic interaction map within Fig. 4A to identify potential DOX sensitive diploid deletion mutants not detected in the initial screen.
Interestingly, three of these CALR mutations were low-allele-burden mutants not detected using Sanger sequencing.
Overall, each method detected two or three mutants not detected by the other method, but the majority of the mutations were detected by both.
Although the hmg2 mutant was not detected as a candidate, the mutant of the lovastatin target hmg1 was identified (R = 0.520; Figure 4B and C).
Because this fell outside the detection area of the probes, the mutant was not detected by the deletion assay (SampleID 1012 in Supplementary Table S3).
As expected, revertants of the lysA deletion mutant were not detected after plating up to 108 particles on a control strain.
Moreover, the ST462,474AA mutant was not detected from either G1- or G2/M-arrested cell extracts with these antibodies.
Finally, we cannot exclude the coexistence of minor mutant strains, not detected by UDPS in serum, that could have been found in the liver or leukocytes.
However, the presence of broad shoulders like those of the Fe(III) forms of both ALKBH4 and the C15A/C17A mutant were not detected.
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