focused on the microbe’s response to bedaquiline,
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, a drug used to treat multidrug-resistant TB. Baliga measured the microbe’s transcriptome in the presence of different doses of bedaquiline and at different times after introducing the drug.
From this giant data dump,
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, computer models helped narrow the focus to a smaller collection of genes,
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, proteins and other molecules that changed under certain conditions. Visualization programs turned these mathematical outputs into maps that scientists could analyze.
About 1,
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,100 genes behaved differently in the presence of bedaquiline,
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, Baliga’s team reported in August in Nature Microbiology. Measurements of the RNA indicated that most of those genes became less active,
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, but a few shifted into overdrive. The researchers suspected those hyperactive genes might be behind the resistance — playing off each other to create a smaller network within the larger tuberculosis response network.
But statistical analysis alone wasn’t enough to confirm the hunch. Correlation isn’t cause,
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, Fiehn points out. Scientists need to figure out which of those changes actually matter.

Drug fix


Researchers found two genes that were overactive in tuberculosis bacteria tolerant to the drug bedaquiline. The drug killed mutated strains with those genes knocked out faster than it killed the normal strain (solid lines),
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, even though the three strains grew similarly without the drug (dashed lines). That confirms the network

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