IN THIS ISSUE .
. .
November 19, 2008
- Cool Movie: Bacterial Crowd Control
- Cracking the Code of a Malarial Parasite
- Predicting the Fate of Cells
- Virtual Screening Advances Drug Design
- New Antibiotics Offer Hope for Tuberculosis
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Cool Movie: Bacterial Crowd Control
Note: You may need to download the free Quicktime player to view the movie.
Full-screen version (MOV, 8.0 MB)
Bacteria, unlike people, get more orderly when they're in large crowds. In this computer simulation, a few E. coli bacteria start out oriented perpendicular to the walls of a container (blue rods). As they multiply, the growing mass arranges into tidy columns parallel to the container walls (red rods). The study sheds light on how cells orient themselves in tight quarters and is especially relevant to understanding biofilms, the high-density bacterial communities associated with lung and ear infections, tooth decay, clogged medical implants, and other health issues. Courtesy of bioengineer Jeff Hasty and physicist Lev Tsimring, both at University of California, San Diego.
Full story
Systems Biodynamics Lab home page (directed by Drs. Tsimring and Hasty direct)
Article abstract (from the October 1 online issue of PNAS)
Cracking the Code of a Malarial Parasite
Parasite-infected mosquitoes transmit malaria when they ingest a blood meal from a human host. Courtesy of James Gathany, CDC.
The infectious disease malaria kills about 1 million people worldwide each year. In Latin America and Asia, it is transmitted by mosquitoes infected with P. vivax, one of four types of malaria-causing parasites. Although P. vivax is rarely lethal, it is a major health threat because it can remain in the body and reemerge months after infection. To date, the parasite has remained relatively understudied. Now, parasitologist Jane Carlton and an international research team have deciphered its genetic code, promising to accelerate research and the development of new ways to combat malaria.
Full story
Carlton lab home page
Article abstract (from the October 9 issue of Nature)
Predicting the Fate of Cells
A single cell colored with several fluorescent proteins. Courtesy of Seth J. Field and Michael B. Yaffe, MIT.
High res. image
(300 KB JPEG)
What would happen to an airplane if one of its parts failed? How about 50 parts? Analyzing such outcomes is now helping scientists understand something far more complex than airplanes—living cells. Take the work of researchers led by Michael Yaffe, a biochemist and biological engineer at Massachusetts Institute of Technology and Harvard Medical School. These scientists designed a computer model to predict the fate of cells bathed in various mixtures of molecules that tell cells to live or die. The sometimes surprising results revealed how myriad, interconnected molecular systems keep cells healthy, as well as how diseases like cancer arise and might be treated.
Full story
Yaffe lab home page
Article abstract (from the October 17 issue of Cell)
Virtual Screening Advances Drug Design
Trypanosoma brucei (bright pink, thread-like), the parasite that causes African sleeping sickness. Courtesy of the CDC/Mae Melvin.
High res. image
(44 KB JPEG)
About 150,000 people per year get the parasitic disease African sleeping sickness, but the only medicines to treat it are either difficult to administer, expensive, or toxic. A team led by computational biologist J. Andrew McCammon of the University of California, San Diego, may offer a solution. By computationally screening hundreds of compounds for their capacity to block an essential parasitic enzyme, the researchers identified five molecules that could serve as the basis for future drug development efforts. McCammon's computational approach could also be used to identify compounds for use against other illnesses for which we need better medications.
NIH's National Institute of Allergy and Infectious Diseases and National Institute of Neurological Disorders and Stroke also supported this work.
Full story
McCammon lab home page
Article abstract (from the November 3 online issue of the PNAS)
New Antibiotics Offer Hope for Tuberculosis
The RNA polymerase hinge region targeted by the antibiotics mediates the opening (red) and closing (green) of the enzyme's pincer-like extensions. The yellow indicates an intermediate state. Courtesy of Richard Ebright.
High res. image
(600 KB JPEG)
New antibiotic medicines are desperately needed due to the global spread of drug resistance among disease causing organisms. Now, a team led by molecular biologist Richard Ebright of Rutgers University has identified three antibiotics that could be developed into new medicines to combat a broad spectrum of bacterial species, including the one that causes tuberculosis. The researchers discovered that the antibiotics work by binding a hinge region of an essential bacterial enzyme, RNA polymerase, blocking its activity. This work reveals that the RNA polymerase hinge is an attractive drug target and offers the antibiotic structures as frameworks for future drug design efforts.
NIH's National Institute of Allergy and Infectious Diseases also supported this work.
Full story
Ebright lab home page
Article abstract (from the October 17 issue of Cell)