Archive for the ‘Evolution’ Category
Or, to put it positively, why mundane routines are pleasurable. From a book review by Elizabeth Kolbert in the New Yorker:
. . . Consider the following scenario. One afternoon, you’re sitting in your office with wads of cotton stuck up your nose. (For the present purposes, it’s not important to know why.) Someone in your office has just baked a batch of chocolate-chip cookies. The aroma fills the air, but, since your nose is plugged, you don’t notice and continue working. Suddenly you sneeze, and the cotton gets dislodged. Now the smell hits, and you rush over to gobble up one cookie, then another.
According to Steinberg, adults spend their lives with wads of cotton in their metaphorical noses. Adolescents, by contrast, are designed to sniff out treats at a hundred paces. During childhood, the nucleus accumbens, which is sometimes called the “pleasure center,” grows. It reaches its maximum extent in the teen-age brain; then it starts to shrink. This enlargement of the pleasure center occurs in concert with other sensation-enhancing changes. As kids enter puberty, their brains sprout more dopamine receptors. Dopamine, a neurotransmitter, plays many roles in the human nervous system, the sexiest of which is signalling enjoyment.
“Nothing—whether it’s being with your friends, having sex, licking an ice-cream cone, zipping along in a convertible on a warm summer evening, hearing your favorite music—will ever feel as good as it did when you were a teenager,” Steinberg observes. And this, in turn, explains why adolescents do so many stupid things. It’s not that they are any worse than their elders at assessing danger. It’s just that the potential rewards seem—and, from a neurological standpoint, genuinely are—way, way greater. “The notion that adolescents take risks because they don’t know any better is ludicrous,” Steinberg writes.
Teen-agers are, as a rule, extremely healthy—healthier than younger children. But their death rate is much higher. The mortality rate for Americans between fifteen and nineteen years old is nearly twice what it is for those between the ages of one and four, and it’s more than three times as high as for those ages five to fourteen. The leading cause of death among adolescents today is accidents; this is known as the “accident hump.”
Steinberg explains the situation as the product of an evolutionary mismatch. . .
Evolution again: adolescents are exploratory and experimental-minded, with benefits to the group as a whole: finding new sources of food (plant, animal, or region), thinking up new ways to hunt, and undoubtedly a fair number dying from consuming toxic food—but the group thus learns and advances. Doesn’t this remind you of the viral swarm entity a few blog posts ago?
Steinberg explains why the risky behavior is done to get attention, and why attention is so important—i.e., such a reward.
Really worth reading in its entirety, and just the right level (at least for me) of technical detail: enough so you can understand how/why it works, but not so much that you get lost in the trees. Carrie Arnold writes in Quanta about how the virus isn’t the living, evolving entity; it’s the swarm, instead. Very science-fictiony, eh?
Sometime in late 2013, a mosquito-borne virus called chikungunya appeared for the first time in the Western Hemisphere. Chikungunya, or “chik,” as it’s called, rarely kills its human hosts. But it can cause fever, rash and debilitating joint pain. In the two years since it first arrived in the Caribbean, chik has spread wildly across the Americas. It is now suspected of having infected over 1 million people in 44 countries and territories, creating a hemisphere-wide horde of mosquito-borne suffering.
The same biological quirks that have contributed to chik’s success are showing researchers how to fight it — and other viruses like it. Chik is an RNA virus, just like influenza, West Nile virus, hepatitis and Ebola, among others. Unlike DNA viruses, which contain two copies of their genetic information, RNA viruses are single-stranded. When they replicate, any errors in the single strand get passed on. As a result, copying is sloppy, and so each new generation of RNA viruses tends to have lots of errors. In only a few generations, a single virus can become a mutant swarm of closely related viruses.
This viral genetic jumble has given Marco Vignuzzi, a virologist at the Pasteur Institute in Paris, a way to predict the future evolution of RNA viruses like chik. Vignuzzi has re-created a single mutation in chik that occurred early in the virus’s around-the-world adventure, work that illuminated how the virus was able to spread so widely in such a short amount of time. Now Vignuzzi is trying to predict chik’s future. This past June, at the annual meeting of the American Society for Microbiology in New Orleans, Vignuzzi showcased the two mutations in chik that are most likely to develop next.
Viruses are tricky and complex beasts; no one can predict exactly what they will do. But if researchers are ever to get a step ahead of the rapidly shifting world of viruses around us, they will need to deconstruct the viral swarm.
A Viral Potluck
For almost 40 years, scientists have worked to understand how RNA viruses can have so many mutations and still be so successful.
In the late 1970s, the virologist Esteban Domingo of the Autonomous University of Madrid was trying to measure the sloppiness of replication using an RNA virus that infects bacteria. He found that one mutation occurred every time the virus copied its genome, on average. As a result, a single virus produces an array of daughter viruses that are almost, but not quite, identical. Every generation spawns another array of viruses, leading to what Domingo called a “mutant cloud” of viruses.
However, most of the mutations in viral clouds create problems for the virus. Researchers assumed that any single mutated version of a healthy virus was likely destined for extinction. But then in 2006, scientists published an account of a thriving dengue virus in Myanmar with what should have been a catastrophic error in the middle of a vital gene. . .
Continue reading. He explains how it works and discovers the true entity, as alien as anything in a science-fiction story—and I think I’ve read a number of stories in which the alien was along these lines: the individual animals/plants/people were not the entity with which you had to deal, it was the total group: the swarm.
Read the whole thing. It’s fascinating.
Very interesting article in Quanta by Emily Singer:
Genes, like people, have families — lineages that stretch back through time, all the way to a founding member. That ancestor multiplied and spread, morphing a bit with each new iteration.
For most of the last 40 years, scientists thought that this was the primary way new genes were born — they simply arose from copies of existing genes. The old version went on doing its job, and the new copy became free to evolve novel functions.
Certain genes, however, seem to defy that origin story. They have no known relatives, and they bear no resemblance to any other gene. They’re the molecular equivalent of a mysterious beast discovered in the depths of a remote rainforest, a biological enigma seemingly unrelated to anything else on earth.
The mystery of where these orphan genes came from has puzzled scientists for decades. But in the past few years, a once-heretical explanation has quickly gained momentum — that many of these orphans arose out of so-called junk DNA, or non-coding DNA, the mysterious stretches of DNA between genes. “Genetic function somehow springs into existence,” said David Begun, a biologist at the University of California, Davis.
This metamorphosis was once considered to be impossible, but a growing number of examples in organisms ranging from yeast and flies to mice and humans has convinced most of the field that these de novo genes exist. Some scientists say they may even be common. Just last month, research presented at the Society for Molecular Biology and Evolution in Vienna identified 600 potentially new human genes. “The existence of de novo genes was supposed to be a rare thing,” said Mar Albà, an evolutionary biologist at the Hospital del Mar Research Institute in Barcelona, who presented the research. “But people have started seeing it more and more.”
Researchers are beginning to understand that de novo genes seem to make up a significant part of the genome, yet scientists have little idea of how many there are or what they do. What’s more, mutations in these genes can trigger catastrophic failures. “It seems like these novel genes are often the most important ones,” said Erich Bornberg-Bauer, a bioinformatician at the University of Münster in Germany.
The Orphan Chase
The standard gene duplication model explains many of the thousands of known gene families, but it has limitations. It implies that most gene innovation would have occurred very early in life’s history. According to this model, the earliest biological molecules 3.5 billion years ago would have created a set of genetic building blocks. Each new iteration of life would then be limited to tweaking those building blocks.
Yet if life’s toolkit is so limited, how could evolution generate the vast menagerie we see on Earth today? “If new parts only come from old parts, we would not be able to explain fundamental changes in development,” Bornberg-Bauer said.
The first evidence that a strict duplication model might not suffice came in the 1990s, when . . .
Very interesting article in Quanta by Roberta Kwok:
Is evolution predictable, or was it heavily shaped by random events? Biologists have argued over this question for decades. Some have suggested that if we replayed the history of life on our planet, the resulting species would be different. Opponents counter that life is largely deterministic.
Recently, researchers have begun to ask the same questions about rocks. About 5,000 minerals — crystalline substances such as quartz, zircon and diamond — have been found on Earth. But minerals didn’t just appear all at once when the Earth formed. They materialized over time, each crystal arising in response to the conditions of the particular epoch in which it formed. Minerals evolved — in some cases, in response to life. And so geologists are left to ask: Are today’s minerals a predictable consequence of the planet’s chemical makeup? Or are they the result of chance events? What if we were to look out at the cosmos and spot another Earth-like planet — would we expect its gemstones to match ours, or would they shine with a luster never seen before?
Robert Hazen, a mineral physicist at the Carnegie Institution of Washington’s Geophysical Laboratory, and his colleagues are publishing a series of four papers this year that reveal broad insights into whether geology is a matter of fate. Minerals on Earth may indeed have been guided by some deterministic rules that could apply to other worlds as well, they found. But our planet is rife with extremely rare minerals, which suggests that chance occurrences also play a significant part.
In addition, if we found an Earth-like twin elsewhere in the universe, many common minerals would likely be the same — but that planet would probably also hold many minerals unlike any that exist here.
The findings aren’t just a matter of curiosity. Some minerals may have helped early organisms emerge. And understanding which minerals could have formed on Earth-like planets may help scientists better predict which worlds are likeliest to harbor life. Conversely, some minerals arise only in the presence of organisms. So finding patterns in Earth’s mineral distribution could help scientists identify a mineralogical signature for life, which they could then search for on other planets.
Time and Chance
Traditionally, mineralogy has been dominated by analyzing the structures and formation of individual minerals. But in a 2008 study in American Mineralogist, Hazen and his colleagues took a more historical view. The researchers assessed Earth’s known minerals and tried to figure out when the conditions were right for their formation. The team concluded that about two-thirds of Earth’s minerals would not have emerged until life was present.
For example, early microorganisms seeded the atmosphere with oxygen, which interacted with existing minerals to yield new ones. The so-called Great Oxygenation Event “was a huge game changer,” said Hazen. “You open the door to literally thousands of new minerals.”
Hazen and collaborators then set out to investigate the role that chance played in mineral formation. First, the researchers studied the relationship between mineral diversity and the abundance of individual elements in Earth’s crust. They found that the more abundant the element, the more minerals it formed, a relationship that was published last month in The Canadian Mineralogist. They then performed the same exercise with minerals from the moon. A similar relationship held, even though the number of known minerals there is much smaller. This common trend suggested an element of determinism: Given starting chemical conditions, one could predict, to a certain extent, which minerals would form.
The team did find outliers, however. For instance, . . .
Kevin Hartnett reports in Quanta:
It used to be that to find new forms of life, all you had to do was take a walk in the woods. Now it’s not so simple. The most conspicuous organisms have long since been cataloged and fixed on the tree of life, and the ones that remain undiscovered don’t give themselves up easily. You could spend all day by the same watering hole with the best scientific instruments and come up with nothing.
Maybe it’s not surprising, then, that when discoveries do occur, they sometimes come in torrents. Find a different way of looking, and novel forms of life appear everywhere.
A team of microbiologists based at the University of California, Berkeley, recently figured out one such new way of detecting life. At a stroke, their work expanded the number of known types — or phyla — of bacteria by nearly 50 percent, a dramatic change that indicates just how many forms of life on earth have escaped our notice so far.
“Some of the branches in the tree of life had been noted before,” said Chris Brown, a student in the lab of Jill Banfield and lead author of the paper. “With this study we were able to fill in many gaps.”
Life’s Finest Net
As an organizational tool, the tree of life has been around for a long time. Lamarck had his version. Darwin had another. The basic structure of the current tree goes back 40 years to the microbiologist Carl Woese, who divided life into three domains: eukaryotes, which include all plants and animals; bacteria; and archaea, single-celled microorganisms with their own distinct features. After a point, discovery came to hinge on finding new ways of searching.
“We used to think there were just plants and animals,” said Edward Rubin, director of the U.S. Department of Energy’s Joint Genome Institute. “Then we got microscopes, and got microbes. Then we got small levels of DNA sequencing.”
DNA sequencing is at the heart of this current study, though the researchers’ success also owes a debt to more basic technology. . .
I have great difficulty understanding why anyone would reject the theory of evolution since it so clearly explains so many things about organisms and lifeforms. The question of why we are mortal has a clear answer in evolutionary terms, well expressed by Suzanne Sandedin in this answer on Quora to the question “According to the theory of evolution, why do we die?”:
Excellent question. And before I explain the real answer, which is rather mind-bending, here are some previous arguments and why they are wrong.
Myth 1: We die to make room for younger generations.
Genes are selfish, and each individual body is a vehicle for a collection of genes. These genes are selected to favor the survival of copies of themselves. Since parents and offspring use the same resources, the death of a parent creates room ecologically for just one offspring. Each gene in the parent has a 50% chance of appearing in this offspring. But it has a 100% chance of appearing in the parent, because it’s already there. It’s never, then, in the evolutionary interests of a parent to die so an offspring can replace it.
Myth 2: We die because our cells/DNA get damaged with age.
This like saying bad drivers die because of blood loss. It’s a proximate mechanism of death, not the evolutionary cause of mortality.
Our somatic cells (the cells that are part of our body) do indeed suffer occasional mutations as they divide. These mutations can kill or damage cells, which is annoying but not generally a big problem as we can make more. However, the worst mutations do something much more dangerous: they help cells to survive and proliferate. That’s how you get cancer. Because this risk accumulates over time, cells are normally allowed only a limited number of divisions before they undergo cellular senescence, that is, they die. But the genes that cause cellular senescence can also stop working. So that’s one of the ways in which we get old: our somatic cell lineages get older, damaged and mutated, and some become cancerous.
However, the cell/DNA damage idea assumes that this isn’t something evolution can counteract. And that’s clearly false. Lifespan and cancer rates differ between species, and not in the ways you would expect if they were determined by cell/DNA damage. For instance, once you take into account body size and phylogeny, DNA repair doesn’t correlate with lifespan. Lifespan does, however, correlate with ecology: mammal species who typically lead risky lives die younger (even if you protect them from those risks). At one extreme, in the harsh Australian bush we find the male agile antechinus, who dies of stress at the end of a single breeding season. At the other extreme, the naked mole rat can live for three decades in its peaceful underground colonies.
This gets even more puzzling when you start to look at genomics. We have a whole suite of genes devoted to keeping our genome pristine. My favorite is a clever gene called P53 that acts as a “gatekeeper” for cell division. If the cell has too many mutations, P53 will halt division and activate repair mechanisms. If that doesn’t fix things, it will make the cell commit suicide. Mutations that break P53 are involved in about half of all human cancers. Now, here’s the rub: there’s a whole family of genes related to P53 in other mammals, and some work better than others. Naked mole rats, as it happens, have two particularly awesome versions that completely protect them against cancer.
We also know that it’s perfectly feasible for genetic modification to immortalize cell lineages, and that going through a haploid stage is not essential for maintaining cell viability. How do we know this? From the strange case of the 11,000 year old dog. The dog as an individual is long dead, but her cells survive today as an infectious cancer on other dogs’ genitalia. There’s also a quaking aspen in Utah whose roots are at least 80,000 years old.
The same applies to permanent organ damage. Some organs heal and regenerate, some don’t. Some species can regenerate organs that others can’t. A salamander can grow a whole new leg. There’s even a jellyfish that can reverse its development when it’s damaged. All in all, natural selection is clearly capable of creating creatures who can fix cellular and DNA damage and repair damaged organs.
So: evolution can fix these problems for us, and it doesn’t. What the heck, evolution, aren’t we friends?
Well, no, actually, evolution is not our friend. If anything, it’s our genes’ friend. And there’s a very good reason our genes don’t actually care about us. . .
Evolution produces interesting solutions. Michael Byrne reports at Motherboard:
It’s a shrewd but certainly dark adaptive strategy. The serpentine columbine, a pretty herbaceous plant endemic to California’s wet coastal regions, doesn’t defend against or attack its enemies directly. Instead, it sends out a chemical signal, which attracts random nearby bugs who then detour to the columbine to check things out but suddenly find themselves ensnared on the plant’s “sticky” surfaces—which are leaves and appendages coated with layers of hairlike barbs. These insect passerby, known to biologists as “tourists,” are trapped and eventually die,
The result is that the columbine winds up with a beneficial coating of death. This sheen of corpses is more properly referred to as carrion and it serves to attract carnivorous bugs and spiders, who then unwittingly protect the plant by attacking and-or repelling herbivores that would otherwise pose a threat to the columbine. This strategy, described in the current issue of Ecology, is the only indirect defensive mechanism of its type that’s so-far been observed, though the researchers behind the report note that it may be quite common.
The general idea is known as carrion provisioning. . .