Abstract
Proper control of cell division in the intracellular pathogen Mycobacterium tuberculosis is central to its growth, survival, pathogenesis, and resistance to antibiotics. Nevertheless, the divisome components and mechanisms by which mycobacteria regulate their cell cycle are not entirely understood. Here we demonstrate that the previously uncharacterized Rv0954 protein localizes to the mid-cell during cell division and interacts with the division-related proteins LamA, PbpA, and PknH. Deletion of rv0954 did not result in alterations in cell morphology or sensitivity to cell wall-targeting antibiotics but transposon mutagenesis demonstrated genetic interactions with genes related to cell division. This work suggests that Rv0954 participates in cell division and reveals potential components of the mycobacterial divisome for future investigation.
Highlights
Our knowledge on how one bacterium becomes two has advanced significantly since Y
There are several possible roles that Rv0954 could play during cell division
With four predicted transmembrane helixes (TMHs) and a stretched C-terminal domain, Rv0954 could serve as a structural scaffold to recruit additional division proteins
Summary
Our knowledge on how one bacterium becomes two has advanced significantly since Y. Jacob first characterized a collection of thermosensitive Escherichia coli (E. coli) cell division mutants about half a century ago (Hirota et al, 1968). In the pathogenic mycobacterial species, Mycobacterium tuberculosis (Mtb) and Mycobacterium leprae, cell division control is an integral part of host-pathogen interactions and may contribute to disease outcomes (Kieser and Rubin, 2014). There are many remaining questions to answer and new components to discover in mycobacterial cell division
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