More snails

I love me some snail.

Biologists have tracked down genes that control the handedness of snail shells, and they turn out to be similar to the genes used by humans to set up the left and right sides of the body.

The finding, reported online in advance of publication in Nature by University of California, Berkeley, researchers, indicates that the same genes have been responsible for establishing the left-right asymmetry of animals for 500-650 million years, originating in the last common ancestor of all animals with bilateral body organization, creatures that include everything from worms to humans.

“Previous studies indicated that the methods for breaking left-right symmetry in animals seem to differ widely, so there was nothing suggesting that the common ancestor of humans, snails and other bilateral organisms had a common strategy for left-right asymmetry,” said Nipam H. Patel, UC Berkeley professor of integrative biology and of molecular and cell biology, and an investigator of the Howard Hughes Medical Institute.

“Indeed, scientists thought that one of the genes that is critical for setting up left-right asymmetry in vertebrates was only present in vertebrates and related groups and not in any other animals,” said UC Berkeley post-doctoral fellow Cristina Grande. “But we found that gene in snails, which has a lot of evolutionary implications. This cellular pathway was present already in the ancestors of most animals.”

There isn’t much I have to add to this right now. It’s just another good piece of evolutionary study. Pretty.

A theory in crisis!

A theory in crisis.

A team of Canadian and French scientists has shed new light on what’s being called the Earth’s “last universal common ancestor,” the 3.8-billion-year-old microscopic organism from which all living things – bacteria and humans and sunflowers alike – evolved.

The researchers, including Universite de Montreal evolutionary geneticist Nicolas Lartillot and colleagues from the Universite de Lyon, say they’ve discovered that “LUCA” was not the heat-craving entity scientists have traditionally believed it to be. Instead, the team argues in the journal Nature, the primitive speck of life that became mother and father to all plants and animals preferred relatively cool temperatures of less than 50 C – not the 90 C habitat generally assumed to be its ideal simmering temperature in life’s primordial soup.

“It is generally believed that LUCA was a heat-loving or ‘hyperthermophilic’ organism – a bit like one of those weird organisms living in the hot vents along the continental ridges deep in the oceans today,” said Nicolas Lartillot, a bio-informatics professor at the U de M. “However, our data suggests that LUCA was actually sensitive to warmer temperatures and lived in a climate below 50 degrees.”

The study states that the initial offspring lineages of the common ancestral life form must have adapted later to higher temperatures, “possibly in response to a climate change of the early Earth.”

The study provides a new look at the planet’s biological beginnings – even before the rudimentary chemical ingredients of life had assembled into DNA strands that would become fundamental to evolution.

“The group’s findings are an important step toward reconciling conflicting ideas about LUCA,” a research summary states. “In particular, they are much more compatible with the theory of an early RNA world, where early life on Earth was composed of ribonucleic acid (RNA), rather than deoxyribonucleic acid (DNA).”

The researchers note that heat-sensitive RNA was “unlikely to be stable in the hot temperatures of the early Earth” but that LUCA must have found “a cooler micro-climate” in which to develop.

“It is only in a subsequent step that LUCA’s descendants discovered the more thermostable DNA molecule, which they independently acquired (presumably from viruses), and used to replace the old and fragile RNA vehicle,” Lartillot said in the statement. “This invention allowed them to move away from the small, cool micro-climate, evolve and diversify into a variety of sophisticated organisms that could tolerate heat.”

Oh, hang on. It looks like scientists are just debating how evolution occurred, not whether it occurred. Business as usual.

HIV Evolution

Scientists have recently shown that the rate of evolution for HIV is not constant.

HIV is so deadly largely because it evolves so rapidly. With a single virus as the origin of an infection, most patients will quickly come to harbor thousands of different versions of HIV, all a little bit different and all competing with one another to most efficiently infect that person’s cells. Its rapid and unique evolution in every patient is what allows HIV to evade the body’s defenses and gives the virus great skill at developing resistance to a pantheon of antiviral drugs.

“A huge amount of HIV diversity accumulates in the body of a patient with HIV, and it’s a big reason why HIV is such a powerful virus,” said Ha Youn Lee, Ph.D., assistant professor of Biostatistics and Computational Biology at the University of Rochester and corresponding author of the study.

Lee and colleagues have settled a longstanding question about just how HIV morphs in the body. In a paper published Dec. 12 in PLoS Computational Biology , scientists show that HIV evolution in the body does not occur at a constant rate. Rather, the virus’s rate of change suddenly slows when the level of crucial immune cells known as CD4+ T-cells falls in a patient.

The team suggests several possible reasons for why HIV slows its evolution later in the disease process. One is that there are simply fewer immune cells left for the virus to infect. Another possibility is that since the immune system is no longer as effective targeting the virus, the virus no longer feels the “selective pressure” of the immune system, and the virus slows its evolution in response.

It’s no secret that HIV is a daunting virus. The fact that it has been shown now to have such a tremendous amount of variation should put no one at ease. There are literally thousands of different types of HIV in an infected individual’s body soon after the disease is contracted. Thousands.

Picture a criminal on the lam. When the police are out in force, the criminal must change his disguise more and more to survive, but when fewer police are present, the criminal can change his disguise less often. In the case of HIV, the virus actually eliminates the “police officers” – CD4+ T-cells patrolling the body. As time goes on and fewer immune cells are present to flag HIV, the virus no longer has the need to evolve as rapidly as it did when the cells were out in force.

This is a pretty apt analogy, if a bit 19th century/Sherlock Holmes-esq. As a secondary point, it’s nice to see such a blatant attempt at popularization within a science article.

As the virus mutates, giving birth to viral offspring called quasispecies, it presents an ever-changing face to the immune system, which is continually adapting itself to keep up with the onslaught. The immune system does a remarkable job fending off the assault, killing most of the viral particles every day. Even so, some of the virus is able to elude the body’s defenses and ultimately devastates the immune system in most patients.

Alas, not all evidence for evolution is pleasant. It’s roughly about as indifferent and pitiless as one might expect such a natural process to be.

Channel your inner fish

Shared errors

Over at Pharyngula, PZ Myers has a post which first destroys some creationist misconception, but then, far more interestingly, goes on to interpret a recent peer-reviewed paper on copy number variants, or CNVs. The whole piece is worth reading, but what I think is worth of a little extra attention is the brief point our shared errors.

An architecture does not imply intent or purpose, but they often imply a history. The pattern described — that chimps and humans share some common structural elements in their genomes — is better described as evidence of common ancestry than of well-designed function. An intron, for instance, is a piece of random, usually useless DNA inserted into the middle of the sequence of a gene that must be excised from RNA before it can be used to make a functional protein. It’s a little piece of garbage that must be cleaned up before the gene product can do its job. That a human and chimpanzee gene has identical introns is an example of an architecture, true enough, but it is of a shared error. Some all-knowing god—he seems to be consistently making the same mistake.

Okay, let’s take the recent hoo-hah with Coldplay and Joe Satriani. Basically, Satriani is claiming Coldplay ripped off one of his songs. There is some fairly compelling evidence to this claim, but it is far from airtight. What we have are four of the same chords repeating through parts of the songs, but only three consecutive notes are truly in common. We can potentially call this one a coincidence (especially since this song has been around forever and Satriani is only suing now that after Coldplay has won a slew of awards. Essentially, we see two instances of people creating similar things.

Now let’s consider someone learning the Satriani song. I don’t feel like finding the actual chord progressions, so let’s just say it goes A, B, C, D. The person begins to learn things, but is apparently a horrible musician and substitutes an F# for the C. Okay, fine. So we have a version of the song out there which is now A, B, F#, D. Now let’s say this person has a friend who wants to rip the song off. But instead of listening to the original Satriani version, he listens to the mutated version with the F#. Now we have some evidence of a copycat. It isn’t very strong evidence because there is just one error. In both instances, we have just four chords. But let’s say another error is made further along in the song. A chord in the bridge is misinterpreted by the original person learning the song. And, naturally, the copycat makes the same error. As we go deeper and deeper into errors, we begin to get better and better evidence of a common origin – the friend was learning from the interpreted version of the song, not the Satriani version, because it is unlikely he would make, say, 5 of the same errors as his friend. The chance for coincidence shrinks while the odds of identifying the correct source rise.

The way this is like CNVs is that we are seeing common errors being made again and again – and these errors are present in both human and chimp genomes. Of course, it should be noted that it isn’t entirely clear if these errors were directly inherited from a common ancestor or if it was the hotspot for ‘making’ errors is what was inherited, but at any rate, it is evidence for our common ancestory with the other apes. There are far too many common errors being made to simply file this under ‘God did it’. The evidence says that is – still and again – superfluous.