Viral RNA (red) in an RSV-infected cell. Credit: Eric Alonas and Philip Santangelo, Georgia Institute of Technology and Emory University.
What looks like a colorful pattern produced as light enters a kaleidoscope is an image of a cell infected with respiratory syncytial virus (RSV) illuminated by a new imaging technology. Although relatively harmless in most children, RSV can lead to bronchitis and pneumonia in others. Philip Santangelo of the Georgia Institute of Technology and Emory University, along with colleagues nationwide, used multiply-labeled tetravalent RNA imaging probes (MTRIPS) to observe the entry, assembly and replication of RSV inside a living cell. Once introduced into RSV-plagued cells, the MTRIPS latched onto the viral RNA (in the image, red) without altering the level of infectivity. This led to fluorescent RSV viral particles that let the researchers track the viral RNA in host cells and better understand what the virus was doing. The knowledge gained from this new technique might aid in the development of RSV antiviral drugs and possibly a vaccine. Scientists could also one day use the imaging approach to study other RNA viruses, such as the flu and Ebola.
Georgia Tech News Release
Yeast cells deficient in zinc and the Tsa1 protein have protein tangles. Credit: Colin MacDiarmid and David Eide, University of Wisconsin-Madison.
Just in time for the holidays, we’ve wrapped up a few red and green cellular images from basic research studies. In this snapshot, we see a group of yeast cells that are deficient in zinc, a metal that plays a key role in creating and maintaining protein shape. The cells also lack a protein called Tsa1, which normally keeps proteins from sticking together. Green areas highlight protein tangles caused by the double deficiency. Red outlines the cells. Protein clumping plays a role in many human diseases, including Parkinson’s and Alzheimer’s, so knowledge of why it happens—and what prevents it in healthy cells—could aid the development of treatments.
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Master clock in mouse brain with the nuclei of the clock cells shown in blue and the VIP molecule shown in green. Credit: Cristina Mazuski in the lab of Erik Herzog, Washington University in St. Louis.
Our biological clocks play a large part in influencing our sleep patterns, hormone levels, body temperature and appetite. A small molecule called VIP, shown in green, enables time-keeping neurons in the brain’s central clock to coordinate daily rhythms. New research shows that, at least in mice, higher doses of the molecule can cause neurons to get out of synch. By desynchronizing mouse neurons with an extra burst of VIP, Erik Herzog of Washington University in St. Louis found that the cells could better adapt to abrupt changes in light (day)-dark (night) cycles. The finding could one day lead to a method to reduce jet lag recovery times and help shift workers better adjust to schedule changes.
Washington University in St. Louis News Release
Circadian Rhythms Fact Sheet
Tick Tock: New Clues About Biological Clocks and Health Article from Inside Life Science
A Light on Life’s Rhythms Article from Findings Magazine
Credit: Yaron Fuchs and Samara Brown in the lab of Hermann Steller, Rockefeller University.
Whether injured by a scrape, minor burn or knife wound, skin goes through the same steps to heal itself. Regrowing hair over new skin is one of the final steps. All the hair you can see on your body is non-living, made up of “dead” cells and protein. It sprouts from living cells in the skin called hair follicle stem cells, shown here in red and orange. For more pictures of hair follicle stem cells—and many other stunning scientific images and videos—go to the NIGMS Image and Video Gallery.
Rockefeller University News Release
This image shows a cell in two stages of division: prometaphase (top) and metaphase (bottom). To form identical daughter cells, chromosome pairs (blue) separate via the attachment of microtubules made up of tubulin proteins (pink) to specialized structures on centromeres (green). Credit: Lilian Kabeche, Dartmouth.
Chromosome segregation during cell division is like speed dating, according to Geisel School of Medicine at Dartmouth researcher Duane Compton. He and postdoctoral fellow Lilian Kabeche learned that protein cyclin A plays moderator, helping to properly separate chromosomes via the attachment of microtubule fibers to kinetochore structures. Here’s how Compton described the process:
“The chromosomes are testing the microtubules for compatibility—that is, looking for the right match—to make sure there are correct attachments and no errors. The old view of this process held that chromosomes and microtubules pair up individually to find the correct attachment, like conventional dating. However, our results show that the system is more like speed dating. All the chromosomes have to try many connections with microtubules in a short amount of time. Then they all make their final choices at the same time. Cyclin A acts like a timekeeper or referee to make sure no one makes bad connections prematurely.”
Such bad connections can cause chromosome segregation errors that lead to cells with an abnormal number of chromosomes, a hallmark of cancer cells. So in addition to aiding our understanding of a fundamental biological process, the new insights may point to potential ways to correct such errors.
Dartmouth News Release
Credit: Phillip Klebba, Kansas State University.
It looks like a fluorescent pill, but this image of an E. coli cell actually shows a new potential target in the fight against infectious diseases. The green highlights a protein called TonB, which is produced by many gram-negative bacteria, including those that cause typhoid fever, meningitis and dysentery. TonB lets bacteria take up iron from the host’s body, which they need to survive. New research from Phillip Klebba of Kansas State University and his colleagues shows how TonB powers iron uptake. When TonB spins within the cell envelope (the bacteria’s “skin”) like a tiny motor, it produces energy that lets another protein pull iron into the cell. This knowledge may lead to the development of antibiotics that block the motion of TonB, potentially stopping an infection in its tracks.
Kansas State University News Release
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