Charles Darwin recognized that natural selection can make eyes sharper, muscles stronger, and fur thicker. But evolution does more than just improve what’s already there. It also gives rise to entirely new things—like eyes and muscles and fur. To study how new things evolve, biologists usually have to rely on ancient clues left behind for hundreds of millions of years. But in a study published today, scientists at Michigan State University show that it’s possible to watch something new evolve in front of their eyes, in just a couple weeks.
The scientists were studying a virus, which evolved a new way of invading cells. As a result, their research not only sheds light on a fundamental question about evolution. It also suggests that it may worryingly easy for viruses such as influenza to turn into new epidemics. Check it out.
[Image of lambda virus: AJC1 on Flickr via Creative Commons]
January 27th, 2012 at 1:04 am
I thought viruses just feed, multiply and hibernate (when the condition is not condusive). It is interesting to learn that they can learn. Wish to know more if they display other characteristics like interact and play behaviour.
January 27th, 2012 at 5:02 am
I just finished reading Microcosm a few weeks ago and loved it. I’m sure my daughter is tired of me telling her amazing things from the book. When I read this article, it reminded me of the hypermutation e. coli will go through in times of stress. Do viruses do the same sort of thing?
January 29th, 2012 at 12:52 am
Evolving is not learning.
January 29th, 2012 at 6:19 pm
I wonder whether this portends a kind of coupling effect in natural systems we’ve missed- look at all the symmetry, antisymmetry and other mathematical phenomena in Nature, such as adherence to the Golden Mean, and so on. As I’ve found similar patterning at the atomic level, could it be that there is some way that the molecular genetic system’s parts can cooperate mutation-wise? We know that in eukaryotes very widely spread genes can literally come together in space and time even though they are far apart on the same chromosome, or even on different ones. In many enzymes string-separated parts come together in active sites. Lots to think about here. Do higher hierarchical levels affect the lower ones- a top-down situation, changing the probabilities of correlated alterations? Time to cogitate….
February 3rd, 2012 at 11:29 am
@ #3 David B. Benson
Yes, evolving is learning. It just is not the storage of knowledge in an electro-chemical feedback loop form. However, the new knowledge IS still encoded and stored, and will be repeated later. What rule says that learning something new means that you don’t forget something old?
@ #4 Jess Tauber
Huh? YOU’ve found these patterns of symmetry and asymmetry in the sub-atomic world? I don’t even know how to approach your comment, except with: No, the higher hierarchical levels are not in control, it all builds from the bottom up, complex interlocked feedback loops and cascade threshhold levels signalling different behaviors. I can’t even understand what you are trying to say for the most part. Our genetic systems actively try to repair mutations if possible, I’m not discounting the possibility of another mechanism that actively seeks out and encourages mutations, it might exist, but at first crack it seems to me that it would be severely evolutionarily disadvantageous unless the organism lived in wildly changing environs. And the enzyme stuff… are you just talking about the fact that proteins fold? Or are you talking about the fact that enzymes make chemical bonds with other proteins (their entire purpose)… where is the mystery here? That active sites bond? That is expected, it’s generally tough to get inactive sites to bond, usually because they are physically inaccessible because of the protein folding or just already electrically balanced and stable.
February 3rd, 2012 at 12:30 pm
Great paper and an excellent summary of it in the NYTs.
I’m not sure if you know about this but the same kind of thing happened with measles: when people were originally developing the vaccine they passaged clinical isolates on extremely unnatural cells like vero’s (monkey kidney fibroblasts). In doing so it turned out that the virus had adapted to using a molecule called CD46 on their surface. Only a number of years later (after lots of research done) did everyone realise that ‘wild’ clinical viruses used the receptor SLAM only found on immune cells. Although I don’t think anyone has done the kind of evolutionary work like these Michigan guys did, they have done extensive biochemical characterisation: http://www.ncbi.nlm.nih.gov/pubmed/17182683. Multiple mutations in the virus attachment gene allowed CD46 use.
February 5th, 2012 at 7:10 pm
I love how the article ends with a six orders of magnitude correction.