“My basic premise,” Wetherbee said, “is that you take a capable microörganism like Klebsiella and you put it through the gruelling test of being exposed to a broad spectrum of antibiotics and it will eventually defeat your efforts, as this one did.” Although Tisch Hospital has not had another outbreak, the bacteria appeared soon after at several hospitals in Brooklyn and one in Queens. When I spoke to infectious-disease experts this spring, I was told that the resistant Klebsiella had also appeared at Mt. Sinai Medical Center, in Manhattan, and in hospitals in New Jersey, Pennsylvania, Cleveland, and St. Louis.
…
Unlike resistant forms of Klebsiella and other gram-negative bacteria, however, MRSA can be treated. “There are about a dozen new antibiotics coming on the market in the next couple of years,” Moellering noted. “But there are no good drugs coming along for these gram-negatives.” Klebsiella and similarly classified bacteria, including Acinetobacter, Enterobacter, and Pseudomonas, have an extra cellular envelope that MRSA lacks, and that hampers the entry of large molecules like antibiotic drugs. “The Klebsiella that caused particular trouble in New York are spreading out,” Moellering told me. “They have very high mortality rates. They are sort of the doomsday-scenario bugs.”

For a long time, we were pretty dumb. Humans did little but make “the same very boring stone tools for almost 2 million years,” he said. Then, only about 150,000 years ago, a different type of spurt happened — our big brains suddenly got smart. We started innovating. We tried different materials, such as bone, and invented many new tools, including needles for beadwork. Responding to, presumably, our first abstract thoughts, we started creating art and maybe even religion.

To understand what caused the cognitive spurt, Khaitovich and colleagues examined chemical brain processes known to have changed in the past 200,000 years. Comparing apes and humans, they found the most robust differences were for processes involved in energy metabolism.

The finding suggests that increased access to calories spurred our cognitive advances, said Khaitovich, carefully adding that definitive claims of causation are premature.

They developed a mathematical model that attributed patterns of speciation to the way that closely related species divide up their environment. According to this model, when there are few relatives around to compete for resources, such as when an environment is first colonized, species differentiate rapidly.
…
This model is robust: even when the authors assumed that their phylogenetic tree contains only 25 percent of all Dendroica species, they found that their γ test was still valid, indicating that this genus experienced an explosive bout of adaptive radiation before settling down to a “more normal” rate of speciation.

This mathematical model provides an incisive tool to gain a clearer understanding of the pattern and rate of speciation for groups of closely related species, even in the absence of a fossil record, simply by analyzing their DNA.

“If you compare the 23 chromosomes of humans with the 19 chromosomes of amphioxus, you find that both genomes can be expressed in terms of 17 ancestral pieces. So, we can say with some confidence that 550 million years ago, the common ancestor of amphioxus and humans had 17 chromosomal elements.”
…
Each of those 17 ancestral segments was duplicated twice in the evolution of vertebrates, after which most of the routine “housekeeping” genes lost the extra copies. Those left, totaling a couple thousand genes, found new functions that, Putnam said, make us different from all other creatures.

“These few thousand genes have been retooled to make humans more elaborate than their simpler ancestors. They are involved in setting up the body plan of an animal and differentiating different parts of the animal,” he said. “The hypothesis, pretty strongly supported by this data, is that the multiplication of this particular kind of gene and differentiation into different functions was important in the formation of vertebrates as we know them.”

“The most exciting thing that the amphioxus genome does is provide excellent evidence for the idea that Ono proposed in 1970, that the human genome had undergone two rounds of whole-genome duplication with subsequent losses,”

The chicken molecule, an antibody called IgY, looks remarkably similar to the human antibody IgE. IgE is known to be involved in allergic reactions and humans also have a counterpart antibody called IgG that helps to destroy invading viruses and bacteria. Scientists know that both IgE and IgG were present in mammals around 160 million years ago because the corresponding genes are found in the recently published platypus genome. However, in chickens there is no equivalent to IgG and so IgY performs both functions.

Lead researcher, Dr. Rosy Calvert said: “Although these antibodies all started from a common ancestor, for some reason humans have ended up with two rather specialised antibodies, whereas chickens only have one that has a much more general function.
…
Professor Brian Sutton, head of the laboratory where the work was done said: “It might be that there was a nasty bug or parasite around at the time that meant that humans needed a really dramatic immune response and so there was pressure to evolve a tight binding antibody like IgE. The problem is that now we’ve ended up with an antibody that can tend to be a little over enthusiastic and causes us problems with apparently innocuous substances like pollen and peanuts, which can cause life-threatening allergic conditions.”

A major evolutionary innovation has unfurled right in front of researchers’ eyes. It’s the first time evolution has been caught in the act of making such a rare and complex new trait. And because the species in question is a bacterium, scientists have been able to replay history to show how this evolutionary novelty grew from the accumulation of unpredictable, chance events.
…
sometime around the 31,500th generation, something dramatic happened in just one of the populations – the bacteria suddenly acquired the ability to metabolise citrate, a second nutrient in their culture medium that E. coli normally cannot use. Indeed, the inability to use citrate is one of the traits by which bacteriologists distinguish E. coli from other species.
…
The replays showed that even when he looked at trillions of cells, only the original population re-evolved Cit+ – and only when he started the replay from generation 20,000 or greater. Something, he concluded, must have happened around generation 20,000 that laid the groundwork for Cit+ to later evolve.

Lenski and his colleagues are now working to identify just what that earlier change was, and how it made the Cit+ mutation possible more than 10,000 generations later.

in 1971, scientists started an experiment. They took 5 male lizards and 5 female lizards of the species Podarcis sicula from a tiny Adriatic island called Pod Kopiste, 0.09km2, and they placed them on an even tinier island, Pod Mrcaru, 0.03km2, which was also inhabited by another lizard species, Podarcis melisellensis. Then a war broke out, the Croatian War of Independence, which went on and on and meant the little islands were completely neglected for 36 years, and nature took its course. When scientists finally returned to the island and looked around, they discovered that something very interesting had happened.

The original population of P. sicula was still present on Pod Kopiste, so we have a nice control population. These lizards are small, fast, insect-eaters in which the males defend territories. Sadly, P. melisellensis on Pod Mrcaru had been extirpated. So we had a few innocent casualties of the experiment.

The transplanted P. sicula thrived and swarmed over the island of Pod Mrcaru, but they were different, and they had evolved in multiple ways.

The original P. sicula were insectivores who occasionally munched on a leaf; approximately 4-7% of their diet was vegetation. The P. sicula of Pod Mrcaru, though, had adopted a more vegetarian diet: examining their gut contents revealed that 34% of their diet was plants in the spring, climbing to 61% in the summer…and much of this diet was hard-to-digest stuff, high in cellulose. This is a fairly radical shift.

There were concomitant changes. The lizards’ skulls were wider, deeper, and longer, and they had stronger bites — a necessity for chomping off bits of tough plants, instead of soft mosquitos. Instead of chasing bugs, they’re browsing stationary plants, and their legs are shorter and they are slower. Population densities are higher. The Pod Mrcaru lizards no longer seem to defend territories, so there have been behavioral changes.

Still just a lizard, I know.

Now here’s something really cool, though: these lizards have evolved cecal valves. What those are are muscular ridges in the gut that allow the animal to close off sections of the tube to slow the progress of food through them, and to act as fermentation chambers where plant material can be broken down by commensal organisms like bacteria and nematodes — and the guts of Pod Mrcaru P. sicula are swarming with nematodes not found in the guts of their Pod Kopiste cousins.

All living things, ourselves included, turn genes on and off in a similar way, by making switch-like proteins called transcription factors. And as scientists have identified more of these, they’ve discovered something remarkable: They form a chain of command. The job of some transcription factors is to switch others on and off, and they in turn are controlled by other transcription factors. Even a seemingly simple microbe like E. coli has an impressive hierarchy. Just nine genes rule over about half of the 4,000-odd genes in E. coli.

E. coli’s network allows it to respond quickly to the challenges it meets, from starvation to heat to the loss of oxygen. It can rapidly reorganize itself, switching on hundreds of genes and switching off hundreds of others. What makes this network all the more impressive are the feedback loops that keep it from spinning out of control. When one gene switches on, for example, it may make a protein that shuts down the gene that switched it on in the first place.

Yet even as scientists uncover this network, they discover yet another mystery. In the latest issue of Nature, scientists reported an experiment in which they wreaked havoc with E. coli’s network. They randomly added new links between the transcription factors at the top of the microbe’s hierarchy. Now a transcription factor could turn on another one that it never had before. The scientists randomly rewired the network in 598 different ways and then stepped back to see what happened to the bacteria.

You might expect that they all died. After all, if you were to pop open the back of an iPod and start linking its components together in random ways, you’d expect it to crash. But that’s not what happened.

About 95 percent of the rewired bacteria did just fine with their new networks. They went on with their lives, feeding, growing and dividing. Some even performed better than microbes with the original wiring, under some conditions.

The first recorded species of frog that breathes without lungs has been found in a clear, cold-water stream on the island of Borneo in Indonesia. The frog, named Barbourula kalimantanensis, gets all its oxygen through its skin.
…
Previously the only four-limbed creatures known to lack lungs were salamanders. A species of earthwormlike, limbless amphibian called a caecilian is also lungless. Tetrapods, or four-limbed creatures, that develop without lungs are rare evolutionary events, Bickford and colleagues write.

The trait in amphibians is likely an adaptation to life between water and land and their ability to respire through the skin. The researchers suggest lunglessness in B. kalimantanensis may be an adaptation to the higher oxygen content in fast-flowing, cold water.
…
Wake added that for most amphibians, the majority of gas exchange happens through the skin. A low but significant amount of respiration occurs via simple, sac-like lungs. Most species, he noted, have mating calls that require lungs. So biologists are unsure why a few species have entirely gotten rid of the organs, Wake said.

This week’s revelation is androgenesis. Androgenesis is what happens when kids get all their genes from their father.
…
Androgenesis, it turns out, transforms fatherhood into a parasitic invasion. It begins like normal fertilization, with a sperm fusing to an egg. But then the egg’s DNA gets hurled out of its nucleus, so that the sperm’s genes are the only ones left in the egg. The egg begins to develop into an embryo, but only after it has lost the mother’s DNA.

I’m going to wave a magic wand and reduce the mutation rate to zero, instantly, in all species, and forever. Then I’m going to watch to see how long it takes for evolution to stop.
…
Actually stopping mutations is a physical impossibility - hence the need for a magic wand. But if they were to stop, so would raw invention. But evolution would not. Not for a long time.
…
And sometimes natural selection actively promotes the persistence of genetic variation. This can happen when there’s an advantage to having genes that are rare. Among guppies, for example, males with rare color patterns are much more likely to survive than those with common color patterns, presumably because predators get good at spotting the patterns they encounter often. In such situations, the rare type does well, begins to become common - and then becomes the victim of its own success and starts to do badly. In situations like this, the frequencies of different genes can rise and fall, cycling indefinitely.
…
Among lifestyles that promote genetic diversity, far and away the most important is sex. Sex shuffles up genes, continually producing new gene combinations. (An important difference between sex and mutation is that sex can only create genetic novelty if it already exists in the population. If everyone is genetically identical, sex will have no effect.) Sex also - and this is important - decouples the fates of genes from one another.

The odds of growing up aren’t good for baby sand dollars. Smaller than the head of a pin, the larvae drift in the ocean — easy prey for anything with a mouth.

But a University of Washington graduate student has discovered the tiny animal has a surprising survival strategy: Faced with the threat of being gobbled up, it makes like Dr. Evil from the Austin Powers movies and clones itself. The resulting “mini-me” may escape hungry fish because it is even teenier than the original — and harder to see.

“If you are eaten, but the smaller version of you survives, you’re still a winner from an evolutionary standpoint,” said Dawn Vaughn.
…
Familiar inhabitants of Washington’s subtidal zone, sand dollars start life though the chance encounter of sperm and egg, simultaneously released into the water by mature adults. The larvae free-float for about six weeks before metamorphosing into miniature sand dollars that settle in colonies and eventually grow to full size.
…
The white shells that wash up on the beach are the creatures’ external skeletons. Living sand dollars are covered with velvety, purple spines used to grab food particles. Vaughn knew many other marine invertebrates shift their shape to avoid being eaten. Colonial animals called bryozoans grow spikes when voracious sea slugs crawl across them. Barnacles take on a bent posture to repel snails. Vaughn’s own previous research showed periwinkle larvae narrow their shell openings to keep out marauding crab larvae.

Seven dino-era feathers found perfectly preserved in amber in western France highlight a crucial stage in feather evolution, scientists report. The hundred-million-year-old plumage has features of both feather-like fibers found with some two-legged dinosaurs known as theropods and of modern bird feathers, the researchers said.
…
The find provides a clear example “of the passage between primitive filamentous down and a modern feather,” said team member Didier Néraudeau of the University of Rennes in France. The study team isn’t sure yet whether the feathers belonged to a dino or a bird. But fossil teeth from two dino families thought to have been feathered were excavated from rocks just above the layer that contained the amber, Perrichot said. “It is entirely plausible that the feathers come from a dinosaur rather than from a bird,” he said.

What are the leading causes of death in humans? Four of the top ten causes—heart disease, diabetes, obesity, and stroke - have some sort of genetic basis and, likely, a historical one. Much of the difficulty is almost certainly due to our having a body built for an active animal but the lifestyle of a spud.
…
The problem is that the brain stem originally controlled breathing in fish; it has been jerry-rigged to work in mammals… This works well in fish, but it is a lousy arrangement for mammals.
…
The example from microbes is not unique. Judging by the Nobel Prizes awarded in medicine and physiology in the past 13 years, I should have called this book Your Inner Fly, Your Inner Worm, or Your Inner Yeast. Pioneering research on flies won the 1995 Nobel Prize in medicine for uncovering a set of genes that builds bodies in humans and other animals. Nobels in medicine in 2002 and 2006 went to people who made significant advances in human genetics and health by studying an insignificant-looking little worm (C. elegans). Similarly, in 2001, elegant analyses of yeast (including baker’s yeast) and sea urchins won the Nobel in medicine for increasing our understanding of some of the basic biology of all cells. These are not esoteric discoveries made on obscure and unimportant creatures. These discoveries on yeast, flies, worms, and, yes, fish tell us about how our own bodies work, the causes of many of the diseases we suffer, and ways we can develop tools to make our lives longer and healthier.