Humans are capable of great charity, taking hits to their bank accounts and bodies to benefit their peers. But such acts of altruism aren’t limited to us; they can be found in the simple colonies of bacteria too.
Bacteria are famed for their ability to adapt to our toughest antibiotics. But resistance doesn’t spring up evenly across an entire colony. A new study suggests that a small cadre of hero bacteria are responsible for saving their peers. By shouldering the burden of resistance at a personal cost, these charitable cells ensure that the entire colony survives.
In the film Slumdog Millionaire, Jamal Malik, a teenager from Mumbai’s slums, wins India’s version of Who Wants to be a Millionaire? As the film continues, flashbacks reveal how events in Jamal’s life inadvertently furnished him with the knowledge to answer all fifteen questions and net the top prize. The film illustrates how some of life’s most useful events have no apparent value at first; their true worth lies in allowing us to exploit future opportunities. It’s a lesson that evolution also teaches, time and time again.
One such lesson has just been narrated by Jesse Bloom from the California Institute of Technology and stars the H1N1 flu virus. One of our main defences against this dangerous infection is the drug oseltamivir, better known as Tamiflu. The drug was generally effective against the H1N1 swine flu from last year’s pandemic, but it doesn’t work against seasonal strains of H1N1 that naturally circulate among humans. In 2007, the first signs of resistance emerged and within a year, virtually all strains of seasonal H1N1 were shrugging off Tamiflu. And we’ve only just worked out why this happened.
If you search for decent definitions of evolution, the chances are that you’ll see genes mentioned somewhere. The American Heritage Dictionary talks about natural selection acting on “genetic variation”, Wikipedia discusses “change in the genetic material of a population… through successive generations”, and TalkOrigins talks about changes that are inherited “via the genetic material”. But, as the Year of Darwin draws to a close, a new study suggests that all of these definitions are too narrow.
Jiali Li from the Scripps Institute in Florida has found that prions – the infectious proteins behind mad cow disease, CJD and kuru – are capable of Darwinian evolution, all without a single strand of DNA or its sister molecule RNA.
Prions are rogue version of a protein called PrP. Like all proteins, they are made up of chains of amino acids that fold into a complex three-dimensional structure. Prions are versions of PrP that have folded incorrectly and this misfolded form, called PrPSc, is social, evangelical and murderous. It converts normal prion proteins into a likeness of its abnormal self, and it rapidly gathers together in large clumps that damage and kill surrounding tissues.
Li has found that variation can creep into populations of initially identical prions. Their amino acid sequence stays the same but their already abnormal structures become increasingly twisted. These “mutant” forms have varying degrees of success in different environments. Some do well in brain tissue; others thrive in other types of cell. In each case, natural selection culls the least successful ones. The survivors pass on their structure to the “next generation”, by altering the folds of normal prion proteins.
This process follows the principles of Darwinian evolution, the same principles that shape the genetic material of viruses, bacteria and other living things. In DNA, mutations manifest as changes in the bases that line the famous double helix. In prions, mutations are essentially different styles of molecular origami. In both cases, they are selectively inherited and they can lead to adaptations such as drug resistance. In prions, it happens in the absence of any genetic material.
Immunity to viral infections sounds like a good thing, but it can come at a price. Millions of years ago, we evolved resistance to a virus that plagued other primates. Today, that virus is extinct, but our resistance to it may be making us more vulnerable to the present threat of HIV.
Many extinct viruses are not completely gone. Some members of a group called retroviruses insinuated themselves into our DNA and became a part of our genetic code. Indeed, a large proportion of the genomes of all primates consists of the embedded remnants of ancient viruses. Looking at these remnants is like genetic archaeology, and it can tell us about infections both past and present.
When retroviruses (such as HIV, right) infect a cell, they insert their own DNA into their host’s genome, using it as a base of operations. From there, the virus can pop out again and make new copies of itself, re-infect its host or move on to new cells.
If it manages to infect an egg or sperm cell, the virus could pass onto the next generation. Hidden inside the embryo’s DNA, it becomes replicated trillions of times over and ends up in every single one of the new individual’s cells.
These hitchhikers are called ‘endogenous retroviruses‘. While they could pop out at any time, they quickly gain mutations in their DNA that knocks out their ability to infect. Unable to move on, they become as much a part of the host’s DNA as its own genes.
In 2005, a group of scientists led by Evan Eichler compared endogenous retroviruses in different primates and found startling differences. In particular, chimps and gorillas have over a hundred copies of the virus PtERV1 (or Pan troglodytes endogenous retrovirus in full). Our DNA has none at all, and this is one of the largest differences between our genome and that of chimps.