Nav: Home

Mycobacteria use protein to create diverse populations, avoid drugs

May 31, 2017

WHAT:

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.
-end-
This research was funded by NIAID grants F32AI104287 and U19 AI107774.

ARTICLE:

EH Rego et al. Deletion of a mycobacterial divisome factor collapses single-cell phenotypic heterogeneity. Nature DOI: 10.1038/nature22361 (2017).

WHO:

NIAID Director Anthony S. Fauci, M.D., is available to comment on this research. Karen Lacourciere, Ph.D., Alison Yao, Ph.D., of NIAID's Division of Microbiology and Infectious Diseases, are also available.

CONTACT:

To schedule interviews, please contact Anne A. Oplinger, aoplinger@niaid.nih.gov, (301) 402-1663.


NIAID conducts and supports research--at NIH, throughout the United States, and worldwide--to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov/.

NIH/National Institute of Allergy and Infectious Diseases

Related Bacteria Articles:

Conducting shell for bacteria
Under anaerobic conditions, certain bacteria can produce electricity. This behavior can be exploited in microbial fuel cells, with a special focus on wastewater treatment schemes.
Controlling bacteria's necessary evil
Until now, scientists have only had a murky understanding of how these relationships arise.
Bacteria take a deadly risk to survive
Bacteria need mutations -- changes in their DNA code -- to survive under difficult circumstances.
How bacteria hunt other bacteria
A bacterial species that hunts other bacteria has attracted interest as a potential antibiotic, but exactly how this predator tracks down its prey has not been clear.
Chlamydia: How bacteria take over control
To survive in human cells, chlamydiae have a lot of tricks in store.
Stress may protect -- at least in bacteria
Antibiotics harm bacteria and stress them. Trimethoprim, an antibiotic, inhibits the growth of the bacterium Escherichia coli and induces a stress response.
'Pulling' bacteria out of blood
Magnets instead of antibiotics could provide a possible new treatment method for blood infection.
New findings detail how beneficial bacteria in the nose suppress pathogenic bacteria
Staphylococcus aureus is a common colonizer of the human body.
Understanding your bacteria
New insight into bacterial cell division could lead to advancements in the fight against harmful bacteria.
Bacteria are individualists
Cells respond differently to lack of nutrients.

Related Bacteria Reading:

Best Science Podcasts 2019

We have hand picked the best science podcasts for 2019. Sit back and enjoy new science podcasts updated daily from your favorite science news services and scientists.
Now Playing: TED Radio Hour

Jumpstarting Creativity
Our greatest breakthroughs and triumphs have one thing in common: creativity. But how do you ignite it? And how do you rekindle it? This hour, TED speakers explore ideas on jumpstarting creativity. Guests include economist Tim Harford, producer Helen Marriage, artificial intelligence researcher Steve Engels, and behavioral scientist Marily Oppezzo.
Now Playing: Science for the People

#524 The Human Network
What does a network of humans look like and how does it work? How does information spread? How do decisions and opinions spread? What gets distorted as it moves through the network and why? This week we dig into the ins and outs of human networks with Matthew Jackson, Professor of Economics at Stanford University and author of the book "The Human Network: How Your Social Position Determines Your Power, Beliefs, and Behaviours".