Archive for the ‘Evolution’ Category
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. . .
Emily Singer reports at Quanta:
A stores our genetic code in an elegant double helix. But some argue that this elegance is overrated. “DNA as a molecule has many things wrong with it,” saidSteven Benner, an organic chemist at the Foundation for Applied Molecular Evolution in Florida.
Nearly 30 years ago, Benner sketched out better versions of both DNA and its chemical cousin RNA, adding new letters and other additions that would expand their repertoire of chemical feats. He wondered why these improvements haven’t occurred in living creatures. Nature has written the entire language of life using just four chemical letters: G, C, A and T. Did our genetic code settle on these four nucleotides for a reason? Or was this system one of many possibilities, selected by simple chance? Perhaps expanding the code could make it better.
Benner’s early attempts at synthesizing new chemical letters failed. But with each false start, his team learned more about what makes a good nucleotide and gained a better understanding of the precise molecular details that make DNA and RNA work. The researchers’ efforts progressed slowly, as they had to design new tools to manipulate the extended alphabet they were building. “We have had to re-create, for our artificially designed DNA, all of the molecular biology that evolution took 4 billion years to create for natural DNA,” Benner said.
Now, after decades of work, Benner’s team has synthesized artificially enhanced DNA that functions much like ordinary DNA, if not better. In two papers published in theJournal of the American Chemical Society last month, the researchers have shown that two synthetic nucleotides called P and Z fit seamlessly into DNA’s helical structure, maintaining the natural shape of DNA. Moreover, DNA sequences incorporating these letters can evolve just like traditional DNA, a first for an expanded genetic alphabet.
The new nucleotides even outperform their natural counterparts. When challenged to evolve a segment that selectively binds to cancer cells, DNA sequences using P and Z did better than those without.
“When you compare the four-nucleotide and six-nucleotide alphabet, the six-nucleotide version seems to have won out,” said Andrew Ellington, a biochemist at the University of Texas, Austin, who was not involved in the study.
Benner has lofty goals for his synthetic molecules. He wants to create an alternative genetic system in which proteins — intricately folded molecules that perform essential biological functions — are unnecessary. Perhaps, Benner proposes, instead of our standard three-component system of DNA, RNA and proteins, life on other planets evolved with just two.
Better Blueprints for Life
The primary job of DNA is to store information. Its sequence of letters contains the blueprints for building proteins. Our current four-letter alphabet encodes 20 amino acids, which are strung together to create millions of different proteins. But a six-letter alphabet could encode as many as 216 possible amino acids and many, many more possible proteins.
Why nature stuck with four letters is one of biology’s fundamental questions. Computers, after all, use a binary system with just two “letters” — 0s and 1s. Yet two letters probably aren’t enough to create the array of biological molecules that make up life. “If you have a two-letter code, you limit the number of combinations you get,” said Ramanarayanan Krishnamurthy, a chemist at the Scripps Research Institute in La Jolla, Calif.
On the other hand, additional letters could make the system more error prone. DNA bases come in pairs — G pairs with C and A pairs with T. It’s this pairing that endows DNA with the ability to pass along genetic information. With a larger alphabet, each letter has a greater chance of pairing with the wrong partner, and new copies of DNA might harbor more mistakes. “If you go past four, it becomes too unwieldy,” Krishnamurthy said.
But perhaps the advantages of a larger alphabet can outweigh the potential drawbacks. Six-letter DNA could densely pack in genetic information. And perhaps six-letter RNA could take over some of the jobs now handled by proteins, which perform most of the work in the cell.
Proteins have a much more flexible structure than DNA and RNA and are capable of folding into an array of complex shapes. A properly folded protein can act as a molecular lock, opening a chamber only for the right key. Or it can act as a catalyst, capturing and bringing together different molecules for chemical reactions.
Adding new letters to RNA could give it some of these abilities. “Six letters can potentially fold into more, different structures than four letters,” Ellington said.
Back when Benner was sketching out ideas for alternative DNA and RNA, it was this potential that he had in mind. According to the most widely held theory of life’s origins, . . .
Why have our immune systems become so sensitive that auto-immune diseases are on the rise? Moises Velasquez-Manoff has an interesting column in the NY Times:
AS many as one in three Americans tries to avoid gluten, a protein found in wheat, barley and rye. Gluten-free menus, gluten-free labels and gluten-free guests at summer dinners have proliferated.
Some of the anti-glutenists argue that we haven’t eaten wheat for long enough to adapt to it as a species. Agriculture began just 12,000 years ago, not enough time for our bodies, which evolved over millions of years, primarily in Africa, to adjust. According to this theory, we’re intrinsically hunter-gatherers, not bread-eaters. If exposed to gluten, some of us will develop celiac disease or gluten intolerance, or we’ll simply feel lousy.
Most of these assertions, however, are contradicted by significant evidence, and distract us from our actual problem: an immune system that has become overly sensitive.
Wheat was first domesticated in southeastern Anatolia perhaps 11,000 years ago. (An archaeological site in Israel, called Ohalo II, indicates that people have eaten wild grains, like barley and wheat, for much longer — about 23,000 years.)
Is this enough time to adapt? To answer that question, consider how some populations have adapted to milk consumption. We can digest lactose, a sugar in milk, as infants, but many stop producing the enzyme that breaks it down — called lactase — in adulthood. For these “lactose intolerant” people, drinking milk can cause bloating and diarrhea. To cope, milk-drinking populations have evolved a trait called “lactase persistence”: the lactase gene stays active into adulthood, allowing them to digest milk.
Milk-producing animals were first domesticated about the same time as wheat in the Middle East. As the custom of dairying spread, so did lactase persistence. What surprises scientists today, though, is just how recently, and how completely, that trait has spread in some populations. Few Scandinavian hunter-gatherers living 5,400 years ago had lactase persistence genes, for example. Today, most Scandinavians do.
Here’s the lesson: Adaptation to a new food stuff can occur quickly — in a few millenniums in this case. So if it happened with milk, why not with wheat?
“If eating wheat was so bad for us, it’s hard to imagine that populations that ate it would have tolerated it for 10,000 years,” Sarah A. Tishkoff, a geneticist at the University of Pennsylvania who studies lactase persistence, told me.
For Dr. Bana Jabri, director of research at the University of Chicago Celiac Disease Center, it’s the genetics of celiac disease that contradict the argument that wheat is intrinsically toxic.
Active celiac disease can cause severe health problems, from stunting and osteoporosis to miscarriage. It strikes a relatively small number of people — just around 1 percent of the population. Yet given the significant costs to fitness, you’d anticipate that the genes associated with celiac would be gradually removed from the gene pool of those eating wheat.
A few years ago, Dr. Jabri and the population geneticist Luis B. Barreiro tested that assumption and discovered precisely the opposite. Not only were celiac-associated genes abundant in the Middle Eastern populations whose ancestors first domesticated wheat; some celiac-linked variants showed evidence of having spread in recent millenniums.
People who had them, in other words, had some advantage compared with those who didn’t.
Dr. Barreiro, who’s at the University of Montreal, has observed this pattern in many genes associated with autoimmune disorders. They’ve become more common in recent millenniums, not less. As population density increased with farming, and as settled living and animal domestication intensified exposure to pathogens, these genes, which amp up aspects of the immune response, helped people survive, he thinks. . .
From an interesting article by Tania Lambrozo at NPR:
. . . A new paper by psychologist Will Gervais, just published in the journal Cognition, sheds new light on these questions. In two surveys conducted with hundreds of undergraduates attending a large university in Kentucky, Gervais found an association between cognitive style and beliefs about evolution. Gervais used a common task to measure the extent to which people engage in a more intuitivecognitive style, which involves going with immediate, intuitive judgments, versus a more analytic cognitive style, which involves more explicit deliberation, and which can often override an intuitive response.
In both studies, Gervais found a statistically significant relationship between the extent to which individuals exhibited a more analytic style and their endorsement of evolution. Importantly, the relationship remained significant even when controlling for other variables that predict evolutionary beliefs, including belief in God, religious upbringing and political conservatism.
The study also replicated prior work that has found a relationship between religiosity and evolutionary beliefs, and between cognitive style and religious disbelief: Participants with a more analytic style were not only more likely to accept evolution, but also to indicate lesser belief in God.
These findings are consistent with at least three possibilities. The first — suggested by the clever title of Gervais’ paper, “Override the Controversy” — is that all individuals have a tendency to reject evolution on an intuitive level, but that some individuals engage in a form of analytic or reflective thinking that allows them to “override” this intuitive response.
A second possibility is that some individuals have stronger intuitive responses than others. Such individuals are likely to experience a stronger pull toward purposive thinking, a greater aversion to uncertainty and other cognitive preferences at odds with evolution. If their intuitive responses are generally stronger, they’re also less likely to succeed in overriding them by engaging in analytic or reflective thought.
Yet, a third possibility . . .
Analytic thought is for most something that must be learned, since it is a skill—that is, thinking analytically does not come naturally but requires training and practice. It seems to be the case with all skills (i.e., with things that must be learned through practice) that self-taught learners will fall into certain common traps, which is why good coaching can result in rapid improvements in performance. Whether the skill is golf, swimming, analytic thinking, decision making, or whatever, self-taught learners almost inevitably will discover certain counter-productive shortcuts that undermine proficiency. Russo and Schoemaker’s wonderful little book, Decision Traps discusses this in detail and points out ten specific common errors to avoid in making important decisions.
UPDATE: I should mention that Edward de Bono has developed a well-regarded curriculum specifically to teach creativity and critical-thinking skills in the early grades. The materials involve one session per week to develop skills in thinking. For more information, see his site. The site also includes an on-line course of 24 lessons to teach thinking skills.
Emily Singer has a very interesting article in Quanta:
Benjamin de Bivort’s lab at Harvard University is Groundhog Day for fruit flies. In de Bivort’s version, a fly must choose to walk down a dark tunnel or a lighted one. Once it has made the choice — THWOOP! — a vacuum sucks the fly back to the starting point, where it has to decide again… and again… and again.
The contraption, which tracks scores of individual flies, makes it possible to analyze how behavior varies from fly to fly. What de Bivort found when he first used it surprised him: The animals’ behavior varied much more than he expected, even when the flies were more or less genetically identical and raised under the same conditions. “If you hold genetics constant and the environment mostly constant, you still see a lot of variation,” de Bivort said.
De Bivort and his team are now exploring this phenomenon in detail, hoping to discover what drives that unexpected individuality. He’s found that different fly strains show different levels of variability. Some strains are like a troop of well-trained soldiers, with each fly mirroring its neighbor. Other strains resemble a wild group of dancers, with individuals moving to their own beat. By comparing soldier and dancer strains, de Bivort thinks he’s identified both a gene and a neural circuit that may underlie some of these differences.
“They are suggesting that variation itself might be a genetic trait,” said Gerd Kempermann, a neurobiologist at the German Center for Neurodegenerative Diseases in Dresden. “That’s a new and interesting twist.” In other words, natural selection might sometimes favor genetic variants that produce a mix of behaviors — the wild dancers — over variants that create the same outcomes.
De Bivort’s work is part of a larger effort to understand why nature produces so much variability. Is it merely a side effect of the random mutations that affect all living things? Or does natural selection reward variability and favor mutations that produce it? A diverse population might be more likely to survive changing conditions. A stand of trees that seeds at different times during the season is more resistant to an early frost or late rains than one that disperses all its seeds at once.
“Whether variance itself is a trait that can vary among individuals or genotypes has important implications and is potentially fascinating, but is very difficult to study,” said Alison Bell, a biologist at the University of Illinois, Urbana-Champaign. Comparing genetically identical, or almost identical, lines of flies, as de Bivort is doing, “is really the best tactic for getting at this question.”
A Bad Breed
Buff Orpington chickens are the lapdogs of the chicken world, known for their extreme friendliness. But the breed occasionally hatches an ornery clucker, much to breeders’ dismay. The Buffs aren’t alone.