This rainbow-hued image shows the isolated feeding tube, or pharynx, of a tiny freshwater flatworm called a planarian, with the hairlike cilia in red and muscle fibers in green. Scientists use these wondrous worms, which have an almost infinite capacity to regrow all organs, as a simple model system for studying regeneration. A research team led by Alejandro Sánchez Alvarado of the Stowers Institute for Medical Research exploited a method known as selective chemical amputation to remove the pharynx easily and reliably. This allowed the team to conduct a large-scale genetic analysis of how stem cells in a planaria fragment realize what’s missing and then restore it. The researchers initially identified about 350 genes that were activated as a result of amputation. They then suppressed those genes one by one and observed the worms until they pinpointed one gene in particular—a master regulator called FoxA—whose absence completely blocked pharynx regeneration. Scientists believe that researching regeneration in flatworms first is a good way to gain knowledge that could one day be applied to promoting regeneration in mammals.
The nerve cells, or neurons, lit up in blue and red in this image of mouse brain tissue are expressing algae-derived, light-sensitive proteins called opsins. To control neurons with light, scientists engineer the cells to produce particular opsins, most of which respond to light in the blue-green range. Then they shine light on the cell to activate it. Now, a team of researchers led by Ed Boyden of the Massachusetts Institute of Technology and Gane Ka-Shu Wong of the University of Alberta has discovered an opsin that responds to red light preferentially, enabling them to manipulate two groups of neurons simultaneously with different colors of light and get a more comprehensive look at how those two sets of brain cells interact. Other opsins have shown potential for vision restoration in animal studies, and, because red light causes less damage to tissue than blue-green light, this new opsin might eventually be used for such treatments in humans.
MIT News Release
What looks like an abstract oil painting is actually an image of several cholera-causing V. cholerae bacterial communities. These communities, called biofilms, include productive and exploitive microbial members. The industrious bacteria (yellow) tend to thrive in denser biofilms (top) while moochers (red) thrive in weaker biofilms (bottom). In an effort to understand this phenomenon, Princeton University researchers led by Bonnie Bassler discovered two ways the freeloaders are denied food. They found that some V. cholerae cover themselves with a thick coating to prevent nutritious carbon- and nitrogen-containing molecules from drifting over to the scroungers. In addition, the natural flow of fluids over biofilms can wash away any leftovers. Encouraging such bacterial fairness could boost the efficient breakdown of organic materials into useful products, such as biofuels. On the other hand, counteracting it could lead to better treatment of illnesses, like cholera, by starving the most productive bacteria and thereby weakening the infection.
Princeton University News Release
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
Like plants and animals, different types of E. coli thrive in different environments. Now, scientists can even predict which environments—such as the bladder, stomach or blood—are most amenable to the growth of various strains, including pathogenic ones. A research team led by Bernhard Palsson of the University of California, San Diego, accomplished this by using genome data to reconstruct the metabolic networks of 55 E. coli strains. The metabolic models, which identify differences in the ability to manufacture certain compounds and break down various nutrients, shed light on how certain E. coli strains become pathogenic and how to potentially control them. One approach could be depriving the deadly strains of the nutrients they need to survive in their niches. The researchers plan to use their new method to study other bacteria, such as those that cause staph infections.
This work also was funded by NIH’s National Cancer Institute.
University of California, San Diego News Release
Inflammation is part of the body’s natural response to trauma, playing a vital role in wound healing and prevention of infection. However, when inflammation becomes widespread, or systemic, it can lead to sepsis, a condition that can damage organs and cause death. Scientists led by Ping Wang of the Feinstein Institute for Medical Research have found a way to potentially target harmful systemic inflammation. They identified a protein–cold-inducible RNA-binding protein (CIRP)–that triggers inflammatory responses during hemorrhagic shock and sepsis. Wang then hypothesized that blocking CIRP activity might mitigate the body’s overall inflammatory response and improve patient survival. In a preclinical study using mice, an antibody against CIRP decreased mortality after hemorrhage and sepsis. The molecule could lead to the development of an anti-CIRP drug.
This work also was funded by the NIH Office of the Director and NIH’s National Heart, Lung, and Blood Institute.