Jackson researchers identify a gene implicated in oxidative stress and neurodegeneration. Researchers at The Jackson Laboratory announced that they have located a gene that protects certain brain and retinal neurons from oxidative stress, and prevents neurodegeneration. National Institutes of Health [EurekAlert - Medicine & Health]

Oxidative stress is a real problem following strokes also. A molecule I worked on, CD39, appeared to be upregulated (i.e. its expression was increased) in neurons for the first few hours following a stroke (actually, it was a murine model of stroke that could more accurately be described as a restriction of blood flow to the brain). CD39 seemed to have a pallitive effect in these murine models and may be part of the body's own defense against the damage from oxidative stress. Remember, oxygen is a 'bad' element and way too reactive for life. We can survive this reactive molecule because of the processes that cells have evolved to deal with it. They can carry out a tremendous amount of high energy chemitry by using oxygen. This makes life as we know it possible. Otherwise we might only be very primitive anaerobic bacteria. But oxygen, in the form of superoxide radicals, is always looking for an opening to cause real damage. We have good protection mechanisms but not always.  11:37:44 PM    

Rare disorder provides new insight into fighting infection. NIAID scientists and collegues found that an enzyme called caspase-8, known to help trigger apoptosis, is also involved in activating many immune system cells to fight off infections. This information, to be published in the September 26 issue of Nature, is the result of a study of an ALPS-like genetic condition known to exist in only two individuals. NIH/National Institute of Allergy and Infectious Diseases [EurekAlert - Medicine & Health]

Another valuable lesson about life in general and humans in particular. Just because we 'know' what a protein's function is, does not mean we know what a protein does. That is, the same protein in different cellular settings can have different purposes. This is one way that we can get by with only 50,000 genes or so. Some proteins do several different things. It may be a mistake to assume that a particular protein is only good for one thing. Especially a protein, such as caspase-8, which is an enzyme, usually responsible for clipping parts off of other proteins. Depending what other proteins are around, it can have drastically different effects.  11:31:43 PM    

Newly revealed viral structure suggests a continuum in the evolution of viruses. Scientists have uncovered the molecular-level framework of a common bacteriophage, a virus that infects bacteria. The results suggest that viruses developed a continuum of progressively more complex architectural strategies to cope with their increasing size as they evolved. The findings also may open a novel approach to developing therapies for certain difficult-to-treat bacterial infections. Human Frontiers Science Program, Natonal Science Foundation, National Institutes of Health, Fannie E. Rippel Foundation, Academy of Finland [EurekAlert - Medicine & Health]

I wrote about these techniques in some columns. The combination of X-ray crystallography and electron microscopy, coupled with novel software, is providing us with some incredible new views of microscopic life. Viruses have to solve some very simple problems. One is how to pack its genome into a protein shell. The larger its geneome is, the better it can cope with anti-viral mechanisms cells devise. The size of the protein shell limits the size of the viral genome (e.g. only so much volume for the viral DNA). So, if the virus needs a larger genome, it must come up with a larger protein shell to house the genome. This is not really an easy problem, so it is not surprising that different viruses have solved it in similar fashions. What is nifty are the details that are emerging regarding how they do it.  11:26:22 PM    

Tough Earth bug may be from Mars [New Scientist]

Okay, this is a report that overlooks so much as to make itself as sensational as possible. I wrote about this bug in one of my columns. Deinococcus has an amazing resistance to ionizing radiation. But this is because it has an amazing ability to heal DNA breaks. Radiation kills cells by destroying the DNA, breaking it into little pieces. Deinococcus can bring these small pieces back together with an amazing system. But it most likely did not evolve to resist radiation. There are lots of other environmental hazards that result in broken DNA, dehydration being one of them. It may very well be that Deinococcus evolved to survive habitats that had cycles of very dry conditions. Overcoming the resultant DNA breaks would have given it a selective advantage. This same process also gives it an advantage to ionizing radiation, but the radiation is NOT what selected for the survival trait. It is a common error for scientists to feel that if a trait is successful= it MUST have evolved FOR that purpose. But, life is adaptable and uses what it can to survive, to move around problems imposed by the environment. The trait we see may very well have come about for a reason totally different that the reasons we suppose. But, if for some reason the environment changed and ionizing radiation became a strong selective force, Deinococcus would have a selective advantage. But the trait was there before the particular selective pressure. Post hoc ergo propter hoc problems often abound when the media tries to explain science.  11:16:30 PM