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Powering off TB: New electron transport gene is a potential drug target

Date:
August 12, 2015
Source:
American Chemical Society
Summary:
The US Food and Drug Administration recently approved the first new drug to fight tuberculosis in more than 40 years, but treatment still takes six months, 200 pills and leaves 40 percent of patients uncured. Thus, new targets are needed. Today researchers report they have identified one such target -- a gene that allows the disease to camp out in human immune cells, and is thus essential for the organism's proliferation.
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The U.S. Food and Drug Administration recently approved the first new drug to fight tuberculosis (TB) in more than 40 years, but treatment still takes six months, 200 pills and leaves 40 percent of patients uncured. Thus, new targets are needed. Today in ACS Central Science, researchers report they have identified one such target -- a gene that allows the disease to camp out in human immune cells, and is thus essential for the organism's proliferation.

TB kills about 1.3 million people around the world every year. The microorganism that causes the disease, Mycobacterium tuberculosis, can hide from the immune system in the macrophage cells of the lungs and go undetected for years. Drugs that target M. tuberculosis generally target cell-wall and protein synthesis, like most antibiotics. However, since TB remains in a latent phase for many patients, and these treatments target growth processes, they are often ineffective at eliminating the bacteria. Other universal processes may provide better targets for rapid treatment of the disease. One such essential process is electron transport, which powers all life forms by shuttling electrons between key protein complexes. In bacteria, the only electron chauffeur is a molecule called menaquinone (MK) that has species-specific variations in its structure. Dean Crick and coworkers at Colorado State University set out to determine how MK might be involved in TB virulence.

First, the researchers compared genes in TB with those known to modify the electron shuttles for other organisms, leading them to a gene they called MenJ. This gene was shown to produce the specific form of MK unique to TB. To test MenJ's function, Crick and coworkers created a mutant strain of M. tuberculosis without the MenJ gene and found that while this deletion did not kill the bacteria outright, it lost its ability to infect human macrophage cells in less than four days. Crick says they have identified a novel virulence factor that could be ripe for drug development.


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Materials provided by American Chemical Society. Note: Content may be edited for style and length.


Journal Reference:

  1. Ashutosh Upadhyay, Fabio L. Fontes, Mercedes Gonzalez-Juarrero, Michael R. McNeil, Debbie C. Crans, Mary Jackson, Dean C. Crick. Partial Saturation of Menaquinone inMycobacterium tuberculosis: Function and Essentiality of a Novel Reductase, MenJ. ACS Central Science, 2015; 150812073024006 DOI: 10.1021/acscentsci.5b00212

Cite This Page:

American Chemical Society. "Powering off TB: New electron transport gene is a potential drug target." ScienceDaily. ScienceDaily, 12 August 2015. <www.sciencedaily.com/releases/2015/08/150812103650.htm>.
American Chemical Society. (2015, August 12). Powering off TB: New electron transport gene is a potential drug target. ScienceDaily. Retrieved May 23, 2017 from www.sciencedaily.com/releases/2015/08/150812103650.htm
American Chemical Society. "Powering off TB: New electron transport gene is a potential drug target." ScienceDaily. www.sciencedaily.com/releases/2015/08/150812103650.htm (accessed May 23, 2017).

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