IN THIS ISSUE .
March 17, 2010
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Like a major city, our cells use a complex transportation network to deliver molecular goods to different destinations. This snapshot shows the cargo-carrying motor protein kinesin (blue) stopped along a special cellular track called a microtubule (gray). Kinesin is powered by a fuel molecule called ATP (bright yellow). When ATP attaches, the motor protein rocks up and down like a seesaw, scooting across the microtubule. Researchers only recently sequenced these steps by creating a blend of atomic models (ribbons) and 3-D maps (transparent surface). Since kinesin's movement helps support cell division, blocking its action could potentially derail cancer. Courtesy of biochemist Charles Sindelar, Brandeis University.
Look closely for an inscription honoring the late Warren DeLano, a pioneer in molecular visualization software.
For decades, scientists have wondered what drives seasonal influenza outbreaks in the wintertime. Now, a study led by Oregon State University climatologist Jeffrey Shaman and Harvard School of Public Health epidemiologist Marc Lipsitch suggests that the a key culprit is absolute humidity—the amount of water vapor in the air. By analyzing 31 years of U.S. flu and weather data and then building a computer model that reproduces historical patterns of seasonal flu spread, Shaman's team found that seasonal changes in absolute humidity predicted when and how easily people caught the flu and infected others. The results could improve flu research, help manage contagion and even forecast seasonal outbreaks.
This work also was supported by NIH's Fogarty International Center.
Researcher profiles (Lipsitch, Shaman)
Article abstract (from the February 23 issue of PLoS Biology)
Proteins play a well-known role in controlling gene activation, the process that governs much of a cell's identity and function. In a typical scenario, proteins fastened to a stretch of DNA can activate a distant gene by looping out the DNA in between. A team of physicists led by Jens-Christian Meiners of the University of Michigan has revealed that DNA looping is exquisitely sensitive to tension—even a tiny bit of mechanical force cuts loop formation tenfold. The finding suggests that tension caused by the regular shifting and buffeting of DNA in cells may have a larger impact on gene activity than previously recognized.
The biological clock helps govern the timing of key cellular processes in all organisms, but little is known about exactly how the clock exerts its control. Now, a team of molecular biologists led by Susan Golden of the University of California, San Diego, has discovered a set of clock proteins that helps regulate cell division in bacteria. Her team found that the proteins block the formation of a ring that pinches the cell in two until the bacterium is ready to divide. The findings may lead to a better understanding of how the clock controls our sleep cycle, weight and response to certain medicines.
This work also was supported by NIH's National Institute of Neurological Disorders and Stroke and the American Recovery and Reinvestment Act.
Our genes not only determine our hair color, eye color and height, but they also can determine whether or not we are susceptible to certain diseases and how well we respond to medications. Jackson Lab biostatistician Gary Churchill uses computer programs to link gene combinations to traits in mice—including disease susceptibility. Meanwhile, University of Florida clinical pharmacist Julie Johnson tries to figure out how different genes work together to influence how people respond to high blood pressure drugs. Read about these two scientists and more in the March 2010 issue of Findings.