It turns out that about 8 percent of the human genome is made up of viruses that once attacked our ancestors. The viruses lost. What remains are the molecular equivalents of mounted trophies, insects preserved in genomic amber, DNA fossils.

The thousands of human endogenous retroviruses, or HERVs, sketch a history of rough times during the 550 million years of vertebrate evolution. The best-preserved one, HERV-K113, probably arrived less than 200,000 years ago, long after human beings and chimpanzees diverged from a common ancestor.

But these retroviruses are more than just curiosities. They are some of the most important enemies we ever had. They helped mold the immune system that is one of the evolutionary marvels of life on Earth.

Researchers at the Ohio State University Comprehensive Cancer Center examined the effect of freeze-dried black raspberries on genes altered by a chemical carcinogen in an animal model of esophageal cancer
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“We have clearly shown that berries, which contain a variety of anticancer compounds, have a genome-wide effect on the expression of genes involved in cancer development,” says principal investigator Gary D. Stoner
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Stoner notes that black raspberries have vitamins, minerals, phenols and phytosterols, many of which individually are known to prevent cancer in animals. “Freeze drying the berries concentrates these elements about ten times, giving us a power pack of chemoprevention agents that can influence the different signaling pathways that are deregulated in cancer,” he says.
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Their analyses included measuring the activity, or expression levels, of 41,000 genes. In the carcinogen-treated animals, 2,261 of these genes showed changes in activity of 50 percent or higher.

Until recently that would also have been the opinion of most scientists. Genes, it was thought, were highly resilient. Even if people did wreck their own DNA through bad diet, smoking and getting fat, that damage was unlikely to be passed to future generations.

Now, however, those assumptions are being re-examined. At the heart of this revolution is a simple but controversial idea: that DNA can be modified or imprinted with the experiences of your parents and grandparents.

According to this new science, known as epigenetics, your ancestors’ diet, smoking habits, exposure to pollutants and levels of obesity could be affecting you today. In turn, your lifestyle could affect your children and grandchildren.
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If we drink heavily, take drugs, get fat or wait too long to reproduce, then epigenetics might start tying up some of the wrong genes and loosening the bonds on others. Sometimes those changes will affect sperm and egg cells.

For the new study, researchers first collected DNA samples collected in 1991 and again between 2002 and 2006 from 600 participants already enrolled in the AGES Reykjavik Study. The AGES study is renowned for its value to genetics research because of the historic isolation and reduced number of genetic “variables” among Iceland’s population, making certain patterns of genetic information easier to identify.

Among the 600, the research team measured the total amount of DNA methylation in each of 111 samples and compared total methylation from DNA collected in 2002 to 2005 to that person’s DNA collected in 1991.

They discovered that in almost one-third of the subjects, methylation changed over that 11-year span, with some gaining DNA methylation and others losing it.

“The key thing this part of the study told us is that levels changed over time, proof of principle that an individual’s epigenetic profile does change with age,” said M. Daniele Fallin, Ph.D., an associate professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health.

Still a puzzle, though, was why or how, Fallin said, “so we wondered whether the tendency to those changes was also inherited, right along with our DNA sequences. That would explain why certain families are more susceptible to certain diseases.”

“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.”
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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.
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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.”

Unlike the genome, which remains essentially static between cell types and over time, the proteome is tremendously dynamic, changing constantly in response to cell-cell signalling and environmental stimuli. Thus even though -with some small exceptions - every cell in your body carries the same genome, the proteome can be wildly different between different tissues and can change rapidly over time
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At the very least, large-scale analysis of the human proteome should allow researchers to tentatively place many of our currently anonymous genes into functional pathways. That’s a step forward for personal genomics: knowing that you have a loss-of-function mutation in a gene that may be involved in cholesterol biosynthesis is a lot more useful (in terms of guiding further clinical testing) than simply knowing that you have a mutation in hypothetical gene C11orf68.

the inside out organization of the cephalopod eye relative to ours: they have photoreceptors that face towards the light, while we have photoreceptors that are facing away from the light. There are other important differences, though, some of which came out in a recent Nature podcast with Adam Rutherford, which was prompted by a recent publication on the structure of squid rhodopsin.

Superficially, squid eyes resemble ours. Both are simple camera eyes with a lens that projects an image onto a retina, but the major details of these eyes evolved independently - the last common ancestor probably had little more than a patch of light sensitive cells with an opsin-based photopigment. The general properties of this ancient eye can still be seen in modern eyes. They detect light with a simple molecule called retinal that is capable of absorbing a photon, changing its shape from the 11-cis form to the all trans form; basically, it flips from a chain with a kink to a straight chain. Retinal is imbedded in a protein called opsin. When retinal changes shape, it changes the shape of the opsin protein, too, which can then interact with other proteins in the cell membrane.

The next protein in the sequence is called a G protein. G proteins are ubiquitous intermediates for many cellular processes; when a receptor, like opsin, is activated, it activates a G protein, which then activates other proteins, starting a signaling cascade. In the podcast, I compare this to starting an avalanche. Opsin is an agent standing on a hill; when it receives a light signal, it nudges a small boulder (the G protein), which then tumbles down setting a whole series of rocks in motion. The G protein is an intermediate which takes a small change, the initial nudge, and amplifies it into the activation of many other proteins.

A fish species, which is all female, has survived for 70,000 years without reproducing sexually, experts believe.
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The species, found in Texas and Mexico, interacts with males of other species to trigger its reproduction process. The offspring are clones of their mother and do not inherit any of the male’s DNA. Typically, when creatures reproduce asexually, harmful changes creep into their genes over many generations.
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One theory is that the fish may occasionally be taking some of the DNA from the males that trigger reproduction, in order to refresh their gene pool.

Dr Laurence Loewe, of the university’s School of Biological Sciences, said: “What we have shown now is that this fish really has something special going on and that some special tricks exist to help this fish survive. “Maybe there is still occasional sex with strangers that keeps the species alive. Future research may give us some answers.”

He added that their findings could also help them understand more about how other creatures operate. “I think one of the interesting things is that we are learning more about how other species might use these tricks as well,” he said. “It might have a more general importance.”

A good counterexample is E. coli, a species of bacteria that lives harmlessly in every person’s gut by the billions. A typical E. coli contains about 4,000 genes (we have about 20,000). Feeding on sugar, the microbe grows till it is ready to split in two. It makes two copies of its genome, almost always managing to produce perfect copies of the original. The single microbe splits in two, and each new E. coli receives one of the identical genomes. These two bacteria are, in other words, clones.
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A colony of genetically identical E. coli is, in fact, a mob of individuals. Under identical conditions, they will behave in different ways. They have fingerprints of their own.
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E. coli appears to follow a universal rule. Other microbes exploit noise, as do flies, worms and humans. Some of the light-sensitive cells in our eyes are tuned to green light, and others to red. The choice is a matter of chance. One protein may randomly switch on the green gene or the red gene, but not both.

In our noses, nerve cells can choose among hundreds of different kinds of odor receptors. Each cell picks only one, and evidence suggests that the choice is controlled by the unpredictable bursts of proteins within each neuron. It’s far more economical to let noise make the decision than to make proteins that can control hundreds of individual odor receptor genes.

Identical genes can also behave differently in our cells because some of our DNA is capped by carbon and hydrogen atoms called methyl groups. Methyl groups can control whether genes make proteins or remain silent. In humans (as well as in other organisms like E. coli), methyl groups sometimes fall off of DNA or become attached to new spots. Pure chance may be responsible for changing some methyl groups; nutrients and toxins may change others.

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.