Kyle J. Minch

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Mycobacterium tuberculosis (MTB) is a highly successful pathogen that infects over a billion people. As with most organisms, MTB adapts to stress by modifying its transcriptional profile. Remodeling of the transcriptome requires both altering the transcription rate and clearing away the existing mRNA through degradation, a process that can be directly(More)
Mycobacterium tuberculosis senses and responds to the shifting and hostile landscape of the host. To characterize the underlying intertwined gene regulatory network governed by approximately 200 transcription factors of M. tuberculosis, we have assayed the global transcriptional consequences of overexpressing each transcription factor from an inducible(More)
The resilience of Mycobacterium tuberculosis (MTB) is largely due to its ability to effectively counteract and even take advantage of the hostile environments of a host. In order to accelerate the discovery and characterization of these adaptive mechanisms, we have mined a compendium of 2325 publicly available transcriptome profiles of MTB to decipher a(More)
Mycobacterium tuberculosis (MTB) infects 30% of all humans and kills someone every 20-30 s. Here we report genome-wide binding for ~80% of all predicted MTB transcription factors (TFs), and assayed global expression following induction of each TF. The MTB DNA-binding network consists of ~16,000 binding events from 154 TFs. We identify >50 TF-DNA consensus(More)
Mycobacterium tuberculosis (MTB) is a pathogenic bacterium responsible for 12 million active cases of tuberculosis (TB) worldwide. The complexity and critical regulatory components of MTB pathogenicity are still poorly understood despite extensive research efforts. In this study, we constructed the first systems-scale map of transcription factor (TF)(More)
Mycobacterium tuberculosis (MTB) is the causative bacterium of tuberculosis, a disease responsible for over a million deaths worldwide annually with a growing number of strains resistant to antibiotics. The development of better therapeutics would greatly benefit from improved understanding of the mechanisms associated with MTB responses to different(More)
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