Stringent Response in Mycobacteria: From Biology to Therapeutic Potential
<i>Mycobacterium tuberculosis</i> is a human pathogen that can thrive inside the host immune cells for several years and cause tuberculosis. This is due to the propensity of <i>M. tuberculosis</i> to synthesize a sturdy cell wall, shift metabolism and growth, secrete virulenc...
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| Autores principales: | , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
MDPI AG
2021
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/c24af16e37ce403b9805adda7a545ecb |
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| Sumario: | <i>Mycobacterium tuberculosis</i> is a human pathogen that can thrive inside the host immune cells for several years and cause tuberculosis. This is due to the propensity of <i>M. tuberculosis</i> to synthesize a sturdy cell wall, shift metabolism and growth, secrete virulence factors to manipulate host immunity, and exhibit stringent response. These attributes help <i>M. tuberculosis</i> to manage the host response, and successfully establish and maintain an infection even under nutrient-deprived stress conditions for years. In this review, we will discuss the importance of mycobacterial stringent response under different stress conditions. The stringent response is mediated through small signaling molecules called alarmones “(pp)pGpp”. The synthesis and degradation of these alarmones in mycobacteria are mediated by Rel protein, which is both (p)ppGpp synthetase and hydrolase. Rel is important for all central dogma processes—DNA replication, transcription, and translation—in addition to regulating virulence, drug resistance, and biofilm formation. Rel also plays an important role in the latent infection of <i>M. tuberculosis</i>. Here, we have discussed the literature on alarmones and Rel proteins in mycobacteria and highlight that (p)ppGpp-analogs and Rel inhibitors could be designed and used as antimycobacterial compounds against <i>M. tuberculosis</i> and non-tuberculous mycobacterial infections. |
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