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On a vast stretch on chromosome eleven, for instance, there is a causeway dedicated entirely to the sensation of smell. Here, a cluster of 155 closely related genes encodes a series of protein receptors that are professional smell sensors. Each receptor binds to a unique chemical structure, like a key to a lock, and generates a distinctive sensation of smell in the brain—spearmint,
It is encrusted with history. Embedded within it are peculiar fragments of DNA—some derived from ancient viruses—that were inserted into the genome in the distant past and have been carried passively for millennia since then. Some of these fragments were once capable of actively “jumping” between genes and organisms, but they have now been largely inactivated and silenced.
Naming a gene cystic fibrosis (or CF), as Ridley observed, is “as absurd as defining the organs of the body by the diseases they get: livers are there to cause cirrhosis, hearts to cause heart attacks, and brains to cause strokes.”
The Human Genome Project allowed geneticists to invert this mirror writing on itself.
scientists propose that mitochondria originated from some ancient bacteria that invaded single-celled organisms. These bacteria formed a symbiotic alliance with the organism; they provided energy, but used the organism’s cellular environment for nutrition, metabolism, and self-defense. The genes lodged within mitochondria are left over from this ancient symbiotic relationship; indeed, human mitochondrial genes resemble bacterial genes more than human ones.)
The exclusively female origin of all the mitochondria in an embryo has an important consequence. All humans—male or female—must have inherited their mitochondria from
their mothers, who inherited their mitochondria from their mothers, and so forth, in an unbroken line of female ancestry stretching indefinitely into the past.
For modern humans, that number has reached one: each of us can trace our mitochondrial lineage to a single human female who existed in Africa about two hundred thousand years ago. She is the common mother of our species. We do not know what she looked like, although her closest modern-day relatives are women of the San tribe from Botswana or Namibia.
Genes can certainly tell us
about race, but can race tell us anything about genes?
most recent estimates suggest that the vast proportion of genetic diversity (85 to 90 percent) occurs within so-called races (i.e., within Asians or Africans) and only a minor proportion (7 percent) between racial groups (the geneticist Richard Lewontin had estimated a similar distribution as early as 1972).
For race and genetics, then, the genome is a strictly one-way street. You can use genome to predict where X or Y came from. But, knowing where A or B came from, you can predict little about the person’s genome.
every genome carries a signature of an individual’s ancestry—but an individual’s racial ancestry predicts little about the person’s genome.
shift the black-white IQ score discrepancy. And therein lies the rub. The tricky thing about the notion of g is that it pretends to be a biological quality that is measurable and heritable, while it is actually strongly determined by cultural priorities. It is—to simplify it somewhat—the most dangerous of all things: a meme masquerading as a gene.
mutation in any other chromosome can be repaired by copying the intact gene from the other chromosome. But a Y chromosome gene cannot be fixed, repaired, or recopied from another chromosome; it has no backup or guide (there is, however, a unique internal system to repair genes in the Y chromosome).
strategy does not solve the problem completely). As information was lost, the Y chromosome itself shrank—whittled down piece by piece by the mirthless cycle of mutation and gene loss. That the Y chromosome is the smallest of all chromosomes is not a coincidence: it is largely a victim of planned obsolescence
that a few extremely important
In genetic terms, this suggests a peculiar paradox. Sex, one of the most complex of human traits, is unlikely to be encoded by multiple genes. Rather, a single gene, buried rather precariously in the Y chromosome, must be the master regulator of maleness.I Male...
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What we call gender, then, is an elaborate genetic and developmental cascade, with SRY at the tip of the hierarchy, and modifiers, integrators, instigators, and interpreters below. This geno-developmental cascade specifies gender identity.
starting with SRY on top and then fanning out into thousands of rivulets of information below—then whether nature predominates or nurture is not absolute, but depends quite acutely on the level of organization one chooses to examine.
men do not pass on the X chromosome to their male children (in all human males, the X chromosome must come from the mother). But one of his sister’s sons might be gay, and that son’s sister’s son might also be gay: a man shares parts of his X chromosome with his sister and with his sister’s sons.
Perhaps the most intriguing feature of all these studies is that, thus far, no one has isolated an actual gene that influences sexual identity.
“A surprisingly high genetic component was found in the ability to be enthralled by an esthetic experience such as listening to a symphonic concert.”
Separated by geographic and economic continents, when two brothers, estranged at birth, were brought to tears by the same Chopin nocturne at night, they seemed to be responding to some subtle, common chord struck by their genomes.
The D4DR-7 repeat variant has been associated with bursts of focused creativity, and also with attention deficit disorder—a seeming paradox until you understand that both can be driven by the same impulse.
Perhaps the subtle drive caused by the D4DR variant drove the “out-of-Africa” migration, by throwing our ancestors out to sea.
Many attributes of our restless, anxious modernity, perhaps, are products of a restless, anxious gene.
It is a testament to the unsettling beauty of the genome that it can make the real world “stick.”
There is an exquisite precision in that mad scheme. Genes must carry out programmed responses to environments—otherwise, there would be no conserved form. But they must also leave exactly enough room for the vagaries of chance to stick.
Epigenetics, not genetics, solves the conundrum of a female tortoiseshell cat. (If humans carried the skin color gene on their X chromosomes, then a female child of a dark-skinned and light-skinned couple would be born with patches of light and dark skin.)
These marks may function like notes written above a sentence, or like marginalia recorded in a book—pencil lines, underlined words, scratch marks, crossed-out letters, subscripts, and endnotes—that modify the context of the genome without changing the actual words.
When Yamanaka and his colleagues analyzed the progression (or rather regression) of the skin cell to the embryo-like cell, they uncovered a cascade of events. Circuits of genes were activated or repressed. The metabolism of the cell was reset. Then, epigenetic marks were erased and rewritten. The cell changed shape and size. Its wrinkles unmarked, its stiffening joints made supple, its youth restored, the cell could now climb up Waddington’s slope. Yamanaka had expunged a cell’s memory, reversed biological time.
But myc is also one of the most potent cancer-causing genes known in biology; it is also activated in leukemias and lymphomas, and in pancreatic, gastric, and uterine cancer.
the quest for eternal youthfulness appears to come at a terrifying collateral cost.
“It sometimes seems as if curbing entropy is our quixotic purpose in the universe,” James Gleick wrote.
Since the mitochondria were derived from the donor, the maternal mitochondrial genes were intact, and the babies born would no longer carry the maternal mutations. Humans born from this procedure thus have three parents. The fertilized nucleus, formed by the union of the “mother” and “father” (parents 1 and 2), contributes virtually all the genetic material. The third parent—i.e., the egg donor—contributes only mitochondria, and the mitochondrial genes. In 2015, after a protracted national debate, Britain legalized the procedure, and the first cohorts of “three-parent children” are now being
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As Edvard Munch put it, “[My troubles] are part of me and my art. They are indistinguishable from me, and [treatment] would destroy my art. I want to keep those sufferings.”
Depraved dictators and predatory states are not an absolute requirement for eugenics. In the case of India, perfectly “free” citizens, left to their own devices, are capable of enacting grotesque eugenic programs—against females, in this case—without any state mandate.
The history of human genetics has reminded us, again and again, that “knowing apart” often begins with an emphasis on “knowing,” but often ends with an emphasis on “parting.”
The war between viruses and bacteria has gone on for so long, and with such ferocity, that like ancient, conjoined enemies, each has become defined by the other: their mutual animosity has been imprinted in their genes.
An arcane microbial defense, devised by microbes, discovered by yogurt engineers, and reprogrammed by RNA biologists, has created a trapdoor to the transformative technology that geneticists had sought so longingly for decades: a method to achieve directed, efficient, and sequence-specific modification of the human genome.
The crux, then, is not genetic emancipation (freedom from the bounds of hereditary illnesses), but genetic enhancement (freedom from the current boundaries of form and fate encoded by the human genome). The distinction between the two is the fragile pivot on which the future of genome editing whirls.
Illness might progressively vanish, but so might identity. Grief might be diminished, but so might tenderness. Traumas might be erased but so might history. Mutants would be eliminated but so would human variation. Infirmities might disappear, but so might vulnerability. Chance would become mitigated, but so, inevitably, would choice.
