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Published on: February 26, 2018
Persistent Mycobacterium tuberculosis infection in mice requires PerM for successful cell division
Ruojun Wang1,2, Kaj Kreutzfeldt1, Helene Botella1
1Department of Microbiology and Immunology, Weill Cornell Medical College, New York, United States.
Abstract:
The ability of Mycobacterium tuberculosis (Mtb) to persist in its host is central to the pathogenesis of tuberculosis, yet the underlying mechanisms remain incompletely defined. PerM, an integral membrane protein, is required for persistence of Mtb in mice. Here, we show that perM deletion caused a cell division defect specifically during the chronic phase of mouse infection, but did not affect Mtb's cell replication during acute infection. We further demonstrate that PerM is required for cell division in chronically infected mice and in vitro under host-relevant stresses because it is part of the mycobacterial divisome and stabilizes the essential divisome protein FtsB. These data highlight the importance of sustained cell division for Mtb persistence, define condition-specific requirements for cell division and reveal that survival of Mtb during chronic infection depends on a persistence divisome.
Insights
Mycobacterium tuberculosis persistence relies on the PerM protein, which is essential for cell division during chronic infection. This discovery reveals a specific survival mechanism for tuberculosis during prolonged host interaction.
Area of Science:
- Microbiology
- Infectious Diseases
- Molecular Biology
Background:
- Tuberculosis pathogenesis hinges on Mycobacterium tuberculosis (Mtb) persistence.
- Mechanisms of Mtb persistence are not fully understood.
- PerM, an integral membrane protein, is crucial for Mtb persistence in mice.
Purpose of the Study:
- To investigate the role of PerM in Mtb cell division during infection.
- To elucidate the function of PerM in Mtb survival under host-relevant conditions.
Main Methods:
- Analyzing Mtb cell division in acute and chronic mouse infections.
- Assessing Mtb replication in vitro under stress conditions.
- Investigating PerM's interaction with the mycobacterial divisome.
Main Results:
- PerM deletion caused cell division defects specifically in chronic mouse infections.
- PerM is required for Mtb cell division during chronic infection and under host-relevant stress.
- PerM is part of the mycobacterial divisome and stabilizes FtsB.
Conclusions:
- Sustained cell division is vital for Mtb persistence.
- Mtb exhibits condition-specific cell division requirements.
- Mtb survival during chronic infection depends on a specialized 'persistence divisome' involving PerM.
