Nitish Malhotra

TL;DR: This work suggests the repurposing of chloroquine to potentiate and possibly shorten antibiotic treatment of tuberculosis and establishes a link between phagosomal pH, redox metabolism, and drug tolerance in replicating Mtb and suggest repositioning of CQ to shorten TB therapy and achieve a relapse-free cure.

TL;DR: In this article, a transcription factor SufR (Rv1460) senses NO via its 4Fe-4S cluster and promotes persistence of Mycobacterium tuberculosis (Mtb) by mobilizing the Fe-S cluster biogenesis system.

TL;DR: This work uses laboratory evolution experiments of ΔrnhA-ΔdnaA strains followed by deep sequencing to show that DNA replication preferentially initiates within a broad region located ∼0.4 to 0.7 Mb clockwise of oriC.

TL;DR: It is shown that Mtb utilizes the suf operon for Fe-S cluster biogenesis to persist under NO stress and data suggest that SufR is a sensor of NO that supports persistence by reprogramming Fe- S cluster metabolism and bioenergetics of Mtb.

TL;DR: It is shown that DNA replication preferentially initiates at a site ~0.6 Mb clockwise of oriC, which increases the possibility of conflicts at essential mRNA genes, which however would utilise only a miniscule fraction of RNA polymerase molecules most of which transcribe rRNA genes.