MtrA Response Regulator Controls Cell Division and Cell Wall Metabolism and Affects Susceptibility of Mycobacteria to the First Line Antituberculosis Drugs
| Autor: | Jarosław Dziadek, Akash T. Satsangi, Malini Rajagopalan, Robert J. Donnelly, Purushotham Gorla, Renata Plocinska, Murty V. V. S. Madiraju, Emmanuel Vijay Paul Pandeeti, Krishna Sarva |
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| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Microbiology (medical) MtrA-cell division biology Cell division Kinase 030106 microbiology Mutant lcsh:QR1-502 MtrA-response regulator biology.organism_classification Microbiology lcsh:Microbiology 3. Good health Cell biology Mycobacterium 03 medical and health sciences Response regulator MtrA-CHIPSeq Regulon two component regulatory system Gene Intracellular Original Research |
| Zdroj: | Frontiers in Microbiology Frontiers in Microbiology, Vol 9 (2018) |
| ISSN: | 1664-302X |
| Popis: | The biological processes regulated by the essential response regulator MtrA and the growth conditions promoting its activation in Mycobacterium tuberculosis, a slow grower and pathogen, are largely unknown. Here, using a gain-of-function mutant, MtrAY 102C, which functions in the absence of the cognate MtrB sensor kinase, we show that the MtrA regulon includes several genes involved in the processes of cell division and cell wall metabolism. The expression of selected MtrA targets and intracellular MtrA levels were compromised under replication arrest induced by genetic manipulation and under stress conditions caused by toxic radicals. The loss of the mtrA gene in M. smegmatis, a rapid grower and non-pathogen, produced filamentous cells with branches and bulges, indicating defects in cell division and cell shape. The ΔmtrA mutant was sensitized to rifampicin and vancomycin and became more resistant to isoniazid, the first line antituberculosis drug. Our data are consistent with the proposal that MtrA controls the optimal cell division, cell wall integrity, and susceptibility to some antimycobacterial drugs. |
| Databáze: | OpenAIRE |
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