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the subject is taught bafflingly minimally and late in the curriculum even today; evolution by natural selection is crucial to every aspect of the living world. In the words of the Russian scientist Theodosius Dobzhansky: “Nothing in biology makes sense except in the light of evolution.”

his true legacy is The Selfish Gene and its profound effect on multiple generations of scientists and lay readers. In a sense, The Selfish Gene and Dawkins himself are bridges, both intellectually and chronologically, between the titans of mid-century biology – Ronald Fisher, Trivers, Hamilton, Maynard Smith and Williams – and our era of the genome, in which the interrogation of DNA dominates the study of evolution.

Since 1976, our understanding of why life is the way it is has blossomed and changed. Once the gene became the dominant idea in biology in the 1990s there followed a technological goldrush – the Human Genome Project – to find them all.

Genes aren’t what they used to be either. In 1976 they were simply stretches of DNA that encoded proteins. We now know about genes made of DNA’s cousin, RNA; we’ve discovered genes that hop from genome to genome

None of the complications of modern genomes erodes the central premise of the selfish gene.

Much of the enmity stems from people misunderstanding that selfishness is being used as a metaphor. The irony of these attacks is that the selfish gene metaphor actually explains altruism. We help others who are not directly related to us because we share similar versions of genes with them.

In the scientific community, the chief objection maintains that natural selection can operate at the level of a group of animals, not solely on genes or even individuals

To my mind, and that of the majority of evolutionary biologists, the gene-centric view of evolution always emerges intact.

the premise remains exciting that a gene’s only desire is to reproduce itself, and that the complexity of genomes makes that reproduction more efficient.

working on more broadly applying [the therapy] to other forms of genetic hearing loss,” he said. But in contrast to VGLUT3 mutant mice, which are missing the protein entirely, humans with missense mutations expressed a defective transporter, making it unclear whether Lustig’s strategy could translate to human VGLUT3-linked deafness.

Taste and smell are two of the senses that have received less attention from gene therapy researchers—but that’s changing

In olfactory dysfunction, there are few curative therapies,

Treating the mice intra-nasally with gene therapy vectors carrying the wildtype Ift88 gene, researchers saw significant regrowth of nasal cilia, whereas control mice given empty vectors showed no regrowth. Treated mice almost doubled in weight compared to controls.

So far, no scientists have designed a gene therapy to target taste buds, but at least one team is tackling an important factor in taste: saliva. If a person’s saliva production drops below 50 percent of normal, “you get tooth decay and trouble swallowing,”

Scientists are also developing gene therapies for disorders involving touch—or at least pain-sensing—neurons, with one drug candidate

Wolfe envisions that someday pain treatment could be as simple as visiting the doctor every few months for a quick skin prick “wherever it hurts”—choosing between a variety of genes to get the best effect.

Hedonic well-being comes from an experience a person seeks out that gives them pleasure.

Eudaimonic well-being is a kind of happiness that comes not from consuming something but from a sustained effort at working toward something bigger than you.

they can and do influence each other, so it has been hard for scientists to measure which kind has had a greater positive influence on someone's physical or psychological well-being.

there is an increased expression of genes involved in inflammation and a decreased antiviral response. People who are subjected to long periods of stress have white blood cells that make slightly more pro-inflammatory proteins on a constant basis.

Bottom line? Happiness that comes from working for the greater good has a much more positive genetic impact.

The people who found happiness by pursuing a greater good had a lower level of this inflammatory gene expression and strong antiviral and antibody gene expression.

in most parts of the world, languages and genes occupy the same areas and even appear to have traveled along similar trajectories.

These data have been available for some time, but never examined in the same place. “The thing we’ve done that no one else has is match worldwide genetic populations to their languages, so that you’re looking at a comparable set,”

Another finding is related to isolation: When small populations separate from the gene pool, genetic diversity falls. In language, the opposite is true. The study shows that isolation leads to more diversity in phonemes.

“In their study, they found that some of these gene variants were significantly more associated with being trans women, and not just being male. That doesn’t establish causality, and it is just an association. And in fact, its a weak association,”

genetic markers are not assumed to be the only factor in what shapes something like gender.

When publishing material that supports the idea that there is a biological element to gender identity, scientists, policy makers and the general public are less inclined to listen to trans activists.

Trans activists seek to educate people on their fundamental human right to experiment with dress, movement, identity and presentation.

“The way that science, technology and science is progressing can be incredibly dangerous in regards to things like eugenics.”

Until 2013, trans people in Sweden were required to undergo sterilization before they could access gender-affirming treatment.

Given the rising accessibility of gene testing, this sort of research can easily be weaponised as justification for sterilisation, persecution or the abortion of fetuses with these genes.

It also further troubles the tenuous relationship that the scientific and medical community have with the trans community.

Fostering the notion of a genetic factor to gender dysphoria threatens to further complicate trans people’s access to appropriate care.

it takes away their right to self determination and the right to bodily autonomy in regards to gender expression and creativity.”

raises questions about the repeated and unchecked power discrepancies between science, medicine and the trans and gender diverse community.

prevent patients from examining their own genetic information” and “made it impossible to obtain second opinions.”

he legal question for the justices is whether isolated genes are “products of nature” that may not be patented or “human-made inventions” eligible for patent protection.

“The isolated DNA molecules before us are not found in nature,” wrote Judge Alan D. Lourie, who was in the majority. “They are obtained in the laboratory and are man-made, the product of human ingenuity.”

Americans could account for as much as 20% of these populations' increased prevalence of type 2 diabetes - the origins of which are complex and poorly understood.

It is not unusual to find Neanderthal genes. About 2% of the genomes of present-day non-Africans were inherited from this distinctive human group, which lived across Europe and western Asia from about 400,000-300,000 years ago until 30,000 years ag

His theory draws upon many of the most prominent views of how humans emerged. These range from our evolution of the ability to run long distances to our development of the earliest weapons, which involved the improvement of hand-eye coordination. Dramatic climate change in Africa over the course of a few tens of thousands of years also may have forced Australopithecus and Homo to adapt rapidly. And over roughly the same span, humans became cooperative hunters and serious meat eaters, vastly enriching our diet and favoring the development of more-robust brains. By themselves, Wilson says, none of these theories is satisfying. Taken together, though, all of these factors pushed our immediate prehuman ancestors toward what he called a huge pre-adaptive step: the formation of the earliest communities around fixed camps.

“When humans started having a camp—and we know that Homo erectus had campsites—then we know they were heading somewhere,” he told me. “They were a group progressively provisioned, sending out some individuals to hunt and some individuals to stay back and guard the valuable campsite. They were no longer just wandering through territory, emitting calls. They were on long-term campsites, maybe changing from time to time, but they had come together. They began to read intentions in each other’s behavior, what each other are doing. They started to learn social connections more solidly.”

“The humans become consistent with all the others,” he said, and the evolutionary steps were likely similar—beginning with the formation of groups within a freely mixing population, followed by the accumulation of pre-adaptations that make eusociality more likely, such as the invention of campsites. Finally comes the rise to prevalence of eusocial alleles—one of two or more alternative forms of a gene that arise by mutation, and are found at the same place on a chromosome—which promote novel behaviors (like communal child care) or suppress old, asocial traits. Now it is up to geneticists, he adds, to “determine how many genes are involved in crossing the eusociality threshold, and to go find those genes.”

Wilson posits that two rival forces drive human behavior: group selection and what he calls “individual selection”—competition at the level of the individual to pass along one’s genes—with both operating simultaneously. “Group selection,” he said, “brings about virtue, and—this is an oversimplification, but—individual selection, which is competing with it, creates sin. That, in a nutshell, is an explanation of the human condition.

“Within groups, the selfish are more likely to succeed,” Wilson told me in a telephone conversation. “But in competition between groups, groups of altruists are more likely to succeed. In addition, it is clear that groups of humans proselytize other groups and accept them as allies, and that that tendency is much favored by group selection.” Taking in newcomers and forming alliances had become a fundamental human trait, he added, because “it is a good way to win.”

If Wilson is right, the human impulse toward racism and tribalism could come to be seen as a reflection of our genetic nature as much as anything else—but so could the human capacity for altruism, and for coalition- and alliance-building. These latter possibilities may help explain Wilson’s abiding optimism—about the environment and many other matters. If these traits are indeed deeply written into our genetic codes, we might hope that we can find ways to emphasize and reinforce them, to build problem-solving coalitions that can endure, and to identify with progressively larger and more-inclusive groups over time.

“Building a more complex cortex likely involves several things: making more cells, modifying the functions of cortical areas, and changing the connections neurons make with each other

Scientists have become adept at comparing the genomes of different species to identify the DNA sequence changes that underlie those differences. But many human genes are very similar to those of other primates, which suggests that changes in the way genes are regulated — in addition to changes in the genes themselves — is what sets human biology apart.

First, Noonan and his colleagues mapped active regulatory elements in the human genome during the first 12 weeks of cortical development by searching for specific biochemical, or “epigenetic” modifications

same in the developing brains of rhesus monkeys and mice, then compared the three maps to identify those elements that showed greater activity in the developing human brain.

wanted to know the biological impact of those regulatory changes.

They used those data to identify groups of genes that showed coordinated expression in the cerebral cortex.

“While we often think of the human brain as a highly innovative structure, it’s been surprising that so many of these regulatory elements seem to play a role in ancient processes important for building the cortex in all mammals, said first author Steven Reilly

The rodent at the top of this story is being studied with a technique called optogenetics, which Deisseroth pioneered.

genetically engineered the mouse so that its brain cells turn certain genes on or off when scientists shine laser light onto them. The light enters the mouse's brain through that optical fiber you see in the photo.

For example, say 20 percent of people with autism don't have Gene A, but scientists aren't sure what Gene A does. They could turn off Gene A in a mouse's brain and see what happens next. The mouse's reaction could provide a clue about what Gene A does in people and why it's missing in certain patients

The technique holds the power to repair or enhance any human gene. “It raises the most fundamental of issues about how we are going to view our humanity in the future and whether we are going to take the dramatic step of modifying our own germline and in a sense take control of our genetic destiny, which raises enormous peril for humanity,”

The paper’s authors, however, are concerned about countries that have less regulation in science. They urge that “scientists should avoid even attempting, in lax jurisdictions, germline genome modification for clinical application in humans” until the full implications “are discussed among scientific and governmental organizations.”

Though such a moratorium would not be legally enforceable and might seem unlikely to exert global influence, there is a precedent. In 1975, scientists worldwide were asked to refrain from using a method for manipulating genes, the recombinant DNA technique, until rules had been established.

Though highly efficient, the technique occasionally cuts the genome at unintended sites. The issue of how much mistargeting could be tolerated in a clinical setting is one that Dr. Doudna’s group wants to see thoroughly explored before any human genome is edited.

“We worry about people making changes without the knowledge of what those changes mean in terms of the overall genome,” Dr. Baltimore said. “I personally think we are just not smart enough — and won’t be for a very long time — to feel comfortable about the consequences of changing heredity, even in a single individual.”

Many ethicists have accepted the idea of gene therapy, changes that die with the patient, but draw a clear line at altering the germline, since these will extend to future generations. The British Parliament in February approved the transfer of mitochondria, small DNA-containing organelles, to human eggs whose own mitochondria are defective. But that technique is less far-reaching because no genes are edited.

There are two broad schools of thought on modifying the human germline, said R. Alta Charo, a bioethicist at the University of Wisconsin and a member of the Doudna group. One is pragmatic and seeks to balance benefit and risk. The other “sets up inherent limits on how much humankind should alter nature,” she said. Some Christian doctrines oppose the idea of playing God, whereas in Judaism and Islam there is the notion “that humankind is supposed to improve the world.” She described herself as more of a pragmatist, saying, “I would try to regulate such things rather than shut a new technology down at its beginning.

The Doudna group calls for public discussion, but is also working to develop some more formal process, such as an international meeting convened by the National Academy of Sciences, to establish guidelines for human use of the genome-editing technique.“We need some principled agreement that we want to enhance humans in this way or we don’t,” Dr. Jaenisch said. “You have to have this discussion because people are gearing up to do this.”

Dr. Krogan and his colleagues set about finding proteins in our cells that the coronavirus uses to grow. Normally, such a project might take two years. But the working group, which includes 22 laboratories, completed it in a few weeks.

In 2011, Dr. Krogan and his colleagues developed a way to find all the human proteins that viruses use to manipulate our cells — a “map,” as Dr. Krogan calls it. They created their first map for H.I.V.

That virus has 18 genes, each of which encodes a protein. The scientists eventually found that H.I.V. interacts, in one way or another, with 435 proteins in a human cell.

In February, the research group synthesized genes from the coronavirus and injected them into cells. They uncovered over 400 human proteins that the virus seems to rely on.

The flulike symptoms observed in infected people are the result of the coronavirus attacking cells in the respiratory tract.

The new map shows that the virus’s proteins travel throughout the human cell, engaging even with proteins that do not seem to have anything to do with making new viruses.

Kevan Shokat, a chemist at U.C.S.F., is poring through 20,000 drugs approved by the Food and Drug Administration for signs that they may interact with the proteins on the map created by Dr. Krogan’s lab.

If promising drugs are found, investigators plan to try them in an animal infected with the coronavirus — perhaps ferrets, because they’re known to get SARS, an illness closely related to Covid-19.

Even if some of these drugs are effective treatments, scientists will still need to make sure they are safe for treating Covid-19. It may turn out, for example, that the dose needed to clear the virus from the body might also lead to dangerous side effects.

In past studies on animals, remdesivir blocked a number of viruses. The drug works by preventing viruses from building new genes.

In February, a team of researchers found that remdesivir could eliminate the coronavirus from infected cells. Since then, five clinical trials have begun to see if the drug will be safe and effective against Covid-19 in people.

Other researchers have taken startling new approaches. On Saturday, Stanford University researchers reported using the gene-editing technology Crispr to destroy coronavirus genes in infected cells.

A major concern with any type of gene therapy is that the inserted genetic material could have dangerous side effects, like turning off an essential gene or turning on one that could lead to cancer.

This kind of modeling is already in use to study individual cellular processes like metabolism. But Dr. Covert said: “Where I think our work is different is that we explicitly include all of the genes and every known gene function. There’s no one else out there who has been able to include more than a handful of functions or more than, say, one-third of the genes.”

The simulation, which runs on a cluster of 128 computers, models the complete life span of the cell at the molecular level, charting the interactions of 28 categories of molecules — including DNA, RNA, proteins and small molecules known as metabolites, which are generated by cell processes.

They called the simulation an important advance in the new field of computational biology, which has recently yielded such achievements as the creation of a synthetic life form — an entire bacterial genome created by a team led by the genome pioneer J. Craig Venter. The scientists used it to take over an existing cell.

A decade ago, scientists developed simulations of metabolism that are now being used to study a wide array of cells, including bacteria, yeast and photosynthetic organisms. Other models exist for processes like protein synthesis.

“Right now, running a simulation for a single cell to divide only one time takes around 10 hours and generates half a gigabyte of data,” Dr. Covert wrote. “I find this fact completely fascinating, because I don’t know that anyone has ever asked how much data a living thing truly holds. We often think of the DNA as the storage medium, but clearly there is more to it than that.”

scientists chose an approach called object-oriented programming, which parallels the design of modern software systems. Software designers organize their programs in modules, which communicate with one another by passing data and instructions back and forth.

“The major modeling insight we had a few years ago was to break up the functionality of the cell into subgroups, which we could model individually, each with its own mathematics, and then to integrate these submodels together into a whole,”

In response, the National Academy of Sciences (NAS) and its Institute of Medicine will convene an international summit this fall where researchers and other experts will "explore the scientific, ethical, and policy issues associated with human gene-editing research," the academies said in a statement

It is a step reminiscent of one in 1975, when NAS convened the Asilomar Conference. That led to guidelines and federal regulations of recombinant DNA, the gene-splicing technology that underlay the founding of Genentech and other biotech companies and revolutionized the production of many pharmaceuticals

The researchers note that only a few modifier genes of disease mutations such as Ankrd16 have been identified and a modifier-based mechanism for understanding the underlying pathology of neurodegenerative diseases may be a promising route to understand disease development.

Over the course of many generations, the gene pool thickens with helpful alleles until—voila!—the overwhelming number of these alleles are helpful and learners guesses are so uncannily accurate as to seem instinctual. Makes sense, no? But now consider that languages change. (And in the real world they do—quickly.) If the language’s principles switch often, many of those helpfully biased alleles are suddenly not so helpful at all. For fast-changing languages, the model finds, neutral alleles win out:

when the language is programmed to hardly mutate at all, the genes have a chance to adapt to the new language. The two populations become genetically distinct, their alleles heavily biased toward the idiosyncrasies of their local language—precisely what we don’t see in the real world

when the language is programmed to change quickly, neutral alleles are again favored.

maybe our brains couldn’t have evolved to handle language’s more arbitrary properties, because languages never stay the same and, as far as we know, they never have. What goes unspoken here is that the simulations seem to suggest that truly universal properties—such as language’s hierarchical nature—could have been encoded in our brains.

"The classic finding — I would say it is the most replicated finding in psychology — is that people who are good at one type of mental task tend to be good at them all,"

G-factor is real in the sense it can predict outcomes in our lives — how much money you'll make, how productive of a worker you might be, and, most chillingly, how likely you are to die an earlier death.

According to the research, people with high IQs tend to be healthier and live longer than the rest of us

One is the fact that people with higher IQs tend to make more money than people with lower scores. Money is helpful in maintaining weight, nutrition, and accessing good health care.

IQ often beats personality when it comes to predicting life outcomes: Personality traits, a recent study found, can explain about 4 percent of the variance in test scores for students under age 16. IQ can explain 25 percent, or an even higher proportion, depending on the study.

Many of these correlations are less than .5, which means there's plenty of room for individual differences. So, yes, very smart people who are awful at their jobs exist. You're just less likely to come across them.

The correlation between IQ and happiness is usually positive, but also usually smaller than one might expect (and sometimes not statistically significant)," Ritchie says.

It could also be that people with higher IQs are smart enough to avoid accidents and mishaps. There's actually some evidence to support this: Higher-IQ people are less likely to die in traffic accidents.

Even though intelligence generally declines with age, those who had high IQs as children were most likely to retain their smarts as very old people.

"If we know the genes related to intelligence — and we know these genes are related to cognitive decline as well — then we can start to a predict who is going to have the worst cognitive decline, and devote health care medical resources to them," he says.

Studies comparing identical and fraternal twins find about half of IQ can be explained by genetics.

genetics seems to become more predictive of IQ with age.

The idea is as we age, we grow more in control of our environments. Those environments we create can then "amplify" the potential of our genes.

About half the variability in IQ is attributed to the environment. Access to nutrition, education, and health care appear to play a big role.

People’s lives are really messy, and the environments they are in are messy. There’s a possibility that a lot of the environmental effect on a person’s intelligence is random."

Hurray! Mean IQ scores appear to be increasing between 2 and 3 points per decade.

This phenomenon is know as the Flynn effect, and it is likely the result of increasing quality of childhood nutrition, health care, and education.

"The experiments are elegant and seem to show that in the mouse sperm production can be achieved when only two genes from the Y-chromosomes are present.

"Whilst this is of limited use in understanding human fertility, this kind of work is important if we are to unravel to complexities of how genes control fertility."