The tighter funding gets, the more likely it is that young investigators pursuing big ideas will get passed over and science grant money will stay with safer, more established projects. Fortunately there are exceptions to that general rule, including a new program established by the Paul G. Allen Family Foundation specifically to support select pioneering research projects that aim to unlock fundamental questions in biology. They recently awarded investigators from 5 prestigious US universities a total of $7.5M to pursue basic questions about the origins and mechanisms of cellular behavior. One of those 5 Distinguished Investigator awards, for $1.6M, is going to quantitative biologist and recent hire Suckjoon Jun, who works in physics and molecular biology at the University of California San Diego. His project title is "Cell-size control and its evolution at the single-cell level," and includes developing methods to perform long-term directed single-cell evolution experiments, as well as single-cell on-chip manipulation, sequencing, and mathematical modeling.
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Lab scientists at the University of Pittsburgh Cancer Institute and UP's Center for Biologic Imaging have recently published an important paper in the Journal of Cell Science that sheds light on a novel method of interrupting mitosis in a cell by effectively depriving its mitochondria of a key protein. The resulting replication stress means cancer cells are stopped from successfully multiplying. Colorful images of the targeted cells actually show them stuck in anaphase trying to divide and subsequently tearing themselves apart. By identifying a compound that carries out this protein interference and disrupts normal mitochondrial fission, researchers have identified a promising therapeutic avenue for halting cancer growth.
If Dr. Seuss were still writing his wonderous books and turned his attention to biotechnology today, we might see a title like Ah, the Things You Can Do With Algae! At the University of California San Diego a number of research institutions have joined together to form the San Diego Center for Algae Biotechnology (SD-CAB) where scientists are pursuing all sorts of innovative projects using the ubiquitous green matter that also happens to be a genetic model organism. Which means it is not only easy to grow, but it can do things that bacteria and even mammalian cells can't, like host a genetically engineered protein that targets cancer.
Dr. J. Lee Nelson (right) has been studying the fascinating phenomenon of microchimerism in the context of autoimmune disorders ever since she joined the Fred Hutchinson Cancer Research Center faculty in 1986. Microchimerism refers to the presence of two distinct sets of cells in one individual and is surprisingly common as a result of cell exchange between mother and child during pregnancy. The numbers of these outside cells is typically small, but Dr. Nelson's research has implicated them in various autoimmune responses, both positive and negative.
The word antibacterial is popping up on more and more household items as merchandisers find that consumers generally believe that chemicals designed to kill bacteria are a useful additive to a product and boost its appeal. Very often the chemical that's added is one called triclosan, and according to recently published research by a team of University of California Davis biomedical scientists, the common polychloro phenoxy phenol causes muscle impairment in animal and lab tissue models. Specifically, it limits the ability of the muscle to expand and contract. A beating heart is one example.
It's getting to the point where there's less and less relevant distinction to be made between life science and physical science research. It was clearer when one lab had petri dishes and the other had circuitboards, but what happens when you have both? That's the case in the Harvard University labs of chemist Charles Lieber and his medical school colleague Daniel Kohane, where the bio research team has successfully created living tissue embedded with tiny nanowires capable of running an electrical current so subtle that it does not harm the tissue cells. These 3D bioelectronic structures could potentially both relay complex information about what's going on inside the tissue and receive signals from an outside source such as instructions for repairs. Several news outlets are calling it cyborg tissue and envision its future use in implants, prosthetics, or even some kind of therapeutic microbot. More immediately it will most likely be used for drug testing in labs, as a precursor to animal or human trials.
Oregon State researchers recently discovered DNA in a nematode, a type of roundworm, that may provide an insight into the mechanisms of human aging. The researchers found a specific portion of DNA within the mitochondria of the nematode which displayed the characteristics of "selfish" DNA, in other words, DNA which actually hurts the animal's chances of survival. Scientists have previously found instances of selfish DNA occurring in plants, but this is the first example found in an animal. “We weren’t even looking for this when we found it, and at first we thought it must be a laboratory error,” said Dee Denver, Oregon State associate professor of zoology (photo left courtesy of OSU). "Selfish DNA is not supposed to be found in animals."
Given that the ubiquity of sweat glands over the surface of the body is such a defining aspect of human physiology (and evolution), it's a wonder how little basic research has been done to understand how they work at the cellular level. Until Rockefeller University cell biologists published their recent findings in Cell, we didn't even know if sweat glands had unique stem cells. It turns out they do. The study also demonstrated that, while sweat glands are close cousins to mammary glands, adult stem cell activity is markedly different in the two systems (though they have a common progenitor), and in fact that there are four separate stem cell types that regulate maintenance and repair of glands and their epidermal-level counterparts throughout our lives.
The smooth and efficient functioning of any system necessarily requires a mechanism for recognizing and removing components that have served their purpose and are no longer needed, in order to make way for ones that are. It's waste disposal, and at the cellular level it's the important activity of proteasomes that maintain cellular health by identifying and degrading proteins that have been targeted as obsolete or damaged. (To put this in perspective, consider that at any given moment a human cell typically contains about 100,000 different proteins.) This housekeeping function of proteasomes is critical to a broad range of vital biochemical processes, including transcription, DNA repair, and the immune defense system. Since the proteasome process was only first described in 2004 (by Nobel Prize-winning chemists), our understanding of its mechanics has been limited.