“Break In Search Of Origin Of Complex Life” By Ed Yong

In Norse mythology, humans and our world were created by a pantheon of gods who lived in the realm of Asgard. As it turns out, these stories have a grain of truth to them.

Thanks to a team of scientists led by Thijs Ettema, Asgard is now also the name of a large clan of microbes. Its members, which are named after Norse gods like Odin, Thor, Loki, and Heimdall, are found all over the world. Many of them are rare and no one has actually seen them under a microscope. But thanks to their DNA, we know they exist. And we know that they are singularly important to us, because they may well be the group from which we evolved.

If Ettema is right, then around two billion years ago, an Asgardian microbe (or an incredibly close relative) took part in a unique event that gave rise to the eukaryotes. That’s the group which includes humans, our fellow animals, plants, fungi, and every living thing made from large, complex cells—all the living things we’re most familiar with, and all the ones we can actually see. Our origins lie either in Asgard, or next door to it.

To understand this story, we have to go back to the very beginning. The Earth was created around 4.5 billion years ago, and judging by some astonishingly ancient fossils, life emerged relatively soon after. For the longest time, living things belonged to two great domains: the bacteria and the archaea, both microscopic and both comprising single cells. That was the status quo for at least 1.7 billion years, until the two domains were joined by a third: the eukaryotes. And they were very different.

Eukaryotic cells are generally much bigger than either bacteria or archaea. They also have larger genomes. They have internal compartments that act like our organs, each with its own special job. They have an internal skeleton that acts as a transport network for molecules. There’s this huge gulf of complexity that separates them from the other two domains. It’s a gulf that has only ever been crossed once in life’s history. Bacteria and archaea are capable of amazing feats of evolution, but in over 3.7 billion years of existence, none of them have ever evolved into anything approaching a eukaryote-like cell—except that one time. Why?

One possible answer, which I’ve written about before, says that eukaryotes were created through an incredibly unlikely merger between members of the other two domains. Somehow, a bacterium found its way inside an archaeon and, rather than being digested or destroyed, became a permanent part of its host. In doing so, it provided the archaeon with an extra source of energy, which allowed it to get bigger, accumulate more genes, and evolve down new paths that were previously inaccessible to it. That fusion cell gave rise to the eukaryotes, and the bacterium eventually turned into the mitochondria—little bean-shaped structures that still power eukaryotic cells to this day.

Once the eukaryotes evolved, they repeatedly engulf microbes and fused with them—a process called endosymbiosis. But that’s much easier to do when the host cell is already big, and can engulf smaller neighbors. If the host is an archaeon, the feat becomes much harder and far more improbable. That’s maybe why the merger between an archaeon and a bacterium—the one that gave rise to mitochondria and may have spawned the eukaryotes—has only happened once.

What were those two ancient partners like? We know that the bacterium belonged to a group called the alphaproteobacteria (which also includes Wolbachia, a microbe that I’ve repeatedly written about here.) But until recently, no one knew anything about the archaeon host.

Full Article Click Here

posted by f. sheikh

Aristotle was wrong and so are we: there are far more than five senses

Worth watching short video about how many senses we have.

Aristotle was wrong and so are we: there are far more than five senses

Scientists have long known that there’s much more to our experience than the five senses (or ‘outward wits’) described by Aristotle – hearing, sight, smell, touch and taste. Yet the myth of five senses persists, perhaps because a clearer understanding of our sensory experience at the neurological level has only recently started to take shape. In this instalment of Aeon’s In Sight series, the British philosopher Barry C Smith argues that the multisensory view of human experience that’s currently emerging in neuroscience could make philosophising about our senses much more accurate, and richer, allowing philosophers to complement the work of scientists in important ways. But first, philosophy must catch up to the major advances being made in brain science.


posted by f. Sheikh

Is Evolution Predictable? By Elizabeth Pennisi

Is Evolution Predictable? | Science | AAAS

If the clock rewound, would organisms evolve the same way they did before? Humble stick insects may hold the answer to that long-running question in biology. Through studies of these bugs, whose bodies match the leaves the insects live on, researchers have found that although groups of the bug have evolved similar appearances, they achieved that mostly via different changes in their DNA. “I think it says that repeatability of evolution is very low,” says Andrew Hendry, an evolutionary biologist at McGill University in Montreal, Canada, who was not involved with the work.

A few studies have suggested that, when exposed to the same environmental conditions, organisms evolve in the same way. As glaciers have receded, for example, a tiny marine fish called the stickleback has invaded many lakes and rivers, and in each spot, they became sleeker with less body armor. Other researchers have looked beyond changes in behavior or physical features for “parallel evolution” in the genes, finding, for instance, that different insects alter the same DNA to help them feed on toxic plants. Yet critics have argued that these examples represent the exception and that evolution is not really predictable because too many chance events can knock it off course.

So Patrik Nosil, an evolutionary biologist at the University of Sheffield in the United Kingdom, turned to a stick insect called Timema cristinae. In many places in California, this species has split into two forms, or ecotypes, on a hillside. One form is wide and lives on a wide-leaf plant; the other is narrow, with a stripe down its back, and lives on a plant with narrow leaves. Nosil and his colleagues sequenced the genomes of dozens of individuals of each ecotype from multiple hillsides to assess the genetic differences that arose to make them specialized for their particular host plant.

They discovered many genetic differences between the ecotypes. Yet to their surprise, they found that, even in stick insects that looked the same but were from different places, only 17% of their DNA had changed in the same way.  That suggests, Nosil and his colleagues report online today in Science, that although some evolution in the genes leading to host specialization is predictable, a lot of the changes are random.

Click for full article

posted by f.sheikh

Are Majority Of Cancers Matter Of Bad Luck?

Bad luck and cancer: A science reporter’s reflections on a controversial story

We reporters—or this one, at any rate—often fail to anticipate which stories will grip readers and which will quickly fade into oblivion. Given that, perhaps I shouldn’t have been surprised that a story I saw off to the printing press in the lull between Christmas and New Year’s engendered more comments than any other I’ve written.

The piece, which appeared online with the headline “The simple math that explains why you may (or may not) get cancer” (and in the magazine’s News section with the headline “The bad luck of cancer”), described a paper published in the 2 January issue of Science. As I and many other journalists explained, the study suggested that simple “bad luck”—random mutations accumulating in healthy stem cells—could explain about two-thirds of cancers, exceeding the risk conferred by environmental and genetic factors combined. One message was that some cancers could not be prevented and that detecting them early was key to combating them.

Readers wasted little time in skewering the authors, mathematician Cristian Tomasetti and cancer geneticist Bert Vogelstein of Johns Hopkins University in Baltimore, Maryland. Their statistics were faulty, some argued; they included many rare cancers and left out several common ones. Earlier today, the International Agency for Research on Cancer, the cancer arm of the World Health Organization, put out an unusual press release stating it “strongly disagrees” with the report. The agency said that “nearly half of all cancer cases worldwide can be prevented.” It charged that the authors’ push for early detection “if misinterpreted … could have serious negative consequences from both cancer research and public health perspectives.”

Reporters, if anything, fared worse. “Please, journalists, get a clue before you write about science,” pleaded an irate column in The Guardian, co-authored by an evolutionary biologist who goes by the Twitter handle @GrrlScientist and statistician Bob O’Hara at the Biodiversity and Climate Research Centre in Frankfurt, Germany.

Given the furor, I wondered: Had I gotten it wrong? Had the authors? Answering these apparently straightforward questions proved surprisingly difficult, exposing the challenges that come with communicating science, and the desire by scientist-authors and reporters to streamline the story they’re trying to tell.

I began with my own story, working backward to the science that spawned it. I’d written that the theory of random mutations in stem cells “explained two-thirds of all cancers.” Immediately, I knew that I had written part of that sloppily, to put it generously: The study didn’t include all cancers. In fact, it didn’t include two of the most common, prostate and breast, because the authors weren’t able to pin down the size of the stem cell compartment or the frequency of stem cell divisions in those tissues. Although my piece subsequently noted the number of cancer types in the study, I should have stressed the omissions early on.

Still, was “two-thirds” referring to the number of cases of cancers the study did include, as I and other journalists had suggested—or to something else? Journalists like numbers that abridge a study down to a bullet point. I’d wondered immediately if this two-thirds finding might be one such nugget. Tomasetti had explained to me in a lengthy interview that “if you go to the American Cancer Society website and you check what are the causes of cancer, you will find a list of either inherited or environmental things. We are saying two-thirds is neither of them.” I’d run the text of my “two-thirds” sentence by him prior to publication and he had had no objections (he had other clarifications).

Last week, we spoke again. Tomasetti had received more than 200 e-mails. Parents of children who had died of cancer were grateful that it might have occurred entirely by chance, suggesting that there was nothing they could have done. Biologists and statisticians were disputing his conclusions or simply surprised that so much of cancer might be random.

“We did not claim that two-thirds of cancer cases are due to bad luck,” Tomasetti told me gently. What the study argued, he explained, was that two-thirds of the variation in cancer rates in different tissues could be explained by random bad luck (a point made by others). What exactly did that mean, I wondered? Tomasetti, chatting by phone, had me draw some graphs to help me understand. By the end of the hour, I still wasn’t sure I grasped the essence.

Tomasetti was sympathetic. “There are lots of scientists that need clarification” on this paper, he said, along with some statisticians. He was busy preparing a technical report with additional details, and Johns Hopkins had just put out a press release explainer. “I honestly feel—and that’s what I told the BBC, and you can definitely quote me on this—overall, the reporters who interacted with us made a very honest and sincere effort to be as accurate as possible.”

Click for full article

posted by f. sheikh