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Mycobacteria use protein to create diverse populations, avoid drugs

Date:
May 31, 2017
Source:
NIH/National Institute of Allergy and Infectious Diseases
Summary:
Subgroups of tuberculosis-causing bacteria can persist even when antibiotics wipe out most of the population. The need to eliminate these persistent subpopulations is one reason why TB treatment regimens are so lengthy. Now, NIAID-supported researchers have shown that a single protein allows mycobacteria to generate diverse populations that can avoid TB drugs. The protein may be a target for intervention; blocking it might result in less mycobacterial diversity and shorten TB treatment courses.
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Subgroups of tuberculosis (TB)-causing bacteria can persist even when antibiotics wipe out most of the overall population. The need to eliminate these persistent subpopulations is one reason why TB treatment regimens are so lengthy. Now, researchers have shown that a single protein allows mycobacteria to generate diverse populations that can avoid TB drugs. The protein may be a target for intervention; blocking it might result in less mycobacterial diversity and shorten TB treatment courses. The research was supported by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.

Eric J. Rubin, M.D., Ph.D., of Harvard T.H. Chan School of Public Health, and E. Hesper Rego, Ph.D., of Yale University School of Medicine, and their coworkers first studied Mycobacterium smegmatis, a close relative of Mycobacterium tuberculosis (Mtb), the microbe that causes TB. Using fluorescent reporter molecules and time-lapse microscopy, they examined individual cells as they grew and divided. Mycobacteria can generate daughter cells through asymmetric growth, resulting in genetically identical, but physiologically diverse, populations. The mechanisms underlying this ability and the extent to which the cells' size, growth rate and other physiological properties relate to survival in mycobacterial populations were not well understood.

Dr. Rubin and colleagues determined that the protein product of a single gene, lamA, is a member of the protein machinery that is active when mycobacteria divide. The protein -- which is not known to exist in other rod-shaped bacteria or other organisms -- seems to allow for asymmetrical growth in new mycobacterial cells made during cell division. The asymmetrical growth leads to bacteria with wide variations in physiological properties and susceptibility to antibiotics.

In experiments using Mtb, the scientists found that mycobacteria without lamA formed far less diverse bacteria with more uniform susceptibility to antibiotics. When exposed to the front-line TB drug rifampicin, for example, Mtb cells lacking lamA were less able to survive than wildtype bacteria. In the future, it may be possible to devise ways to inhibit lamA or its protein. This could lead to reduced variation in Mtb populations and, potentially, to more uniform vulnerability to drugs, according to the scientists.


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Materials provided by NIH/National Institute of Allergy and Infectious Diseases. Note: Content may be edited for style and length.


Journal Reference:

  1. E. Hesper Rego, Rebecca E. Audette, Eric J. Rubin. Deletion of a mycobacterial divisome factor collapses single-cell phenotypic heterogeneity. Nature, 2017; 546 (7656): 153 DOI: 10.1038/nature22361

Cite This Page:

NIH/National Institute of Allergy and Infectious Diseases. "Mycobacteria use protein to create diverse populations, avoid drugs." ScienceDaily. ScienceDaily, 31 May 2017. <www.sciencedaily.com/releases/2017/05/170531133258.htm>.
NIH/National Institute of Allergy and Infectious Diseases. (2017, May 31). Mycobacteria use protein to create diverse populations, avoid drugs. ScienceDaily. Retrieved December 5, 2024 from www.sciencedaily.com/releases/2017/05/170531133258.htm
NIH/National Institute of Allergy and Infectious Diseases. "Mycobacteria use protein to create diverse populations, avoid drugs." ScienceDaily. www.sciencedaily.com/releases/2017/05/170531133258.htm (accessed December 5, 2024).

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