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evolve toward greater virulence, or antibiotic resistance, or transmissibility between human hosts, allows them to increase their Darwinian success. Fast evolution is generally better than slow evolution, and HGT represents the fastest way of adding major new possibilities to the heritable variation upon which evolution depends.
Their supposition, entirely reasonable, was that each close match of genes shared in two distant lineages signaled a relatively recent horizontal transfer event for that gene.
bacteria that live in our guts tend to trade genes with other gut bugs. Bacteria of the gums, likewise. Of the vagina, likewise. Skin bacteria, likewise. These gene transfers mainly happen at short spatial distances, even when the phylogenetic distance (between two very different bacterial lineages) is great.
ecology matters more than phylogeny,
This paper, coauthored with a young physicist named Kalin Vetsigian, appeared in 2006, bringing forward the subject with which Woese had grappled in his 1967 book. It offered the radical proposition that the universality of the code—all creatures using the same three-letter DNA combinations to call in the same amino acids—reflects a dynamic evolutionary process during the early history of life, not a “frozen accident” traceable to happenstance in one small population of universal ancestors,
HGT is not just an ancient and widespread phenomenon, according to Vetsigian, Woese, and Goldenfeld; it was one of the preeminent factors in early evolution, shaping life as we know it and the informational system from which all life is built.
“The available studies strongly indicate that microbes absorb and discard genes as needed, in response to their environment.” Because of that genetic fluidity, the two men argued, the concept of “species” is useless among bacteria and archaea. With genes flowing sideways, information moving across boundaries, and energy flowing upward from cells through communities and environments, the concept of an “organism”—an isolated creature, a discrete individual—seemed less valid too.
“evolution” in its familiar Darwinian sense. That also seemed obsolete. Their newer idea—that evolutionary innovation might occur by means other than incremental mutation, and spread by means other than vertical inheritance—called the Darwinian model into question, they claimed. By this time, Woese had been reading some brilliantly unconventional scientific thinkers, such as the biologist Stuart Kauffman and the physicist Ilya Prigogine, associated with the swirl of ideas known as chaos and complexity theory, who proposed that certain “emergent properties,” unpredictable and wondrously
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Somewhere amid the rich chaos of the RNA-world, Goldenfeld and Woese wrote, an “operating system” might have spontaneously taken form, by which the more promising innovations arising from random mistakes in RNA self-replication could be communicated and applied. They were alluding to the translation mechanism as seen eventually in cells, by which DNA information is turned into working proteins. At the core of that mechanism sits the ribosome, and at its core, Woese’s beloved 16S rRNA molecule.
That thought led to another: that early life evolved in what Goldenfeld and Woese called “a lamarckian way,” meaning the inheritance of acquired characteristics, with vertical inheritance less important than horizontal gene transfer.
Let’s pull Darwin down from his pillar. He may not have been wrong entirely, but his theory failed to cover the first two billion years.
(Coding sequences that produced actual proteins comprised only 5 percent of the genome.)
Other scientists knew them, more descriptively, as “transposable elements.” They were transposable in the sense that they seemed not just to have copied themselves many times, but also to have jumped around into different parts of the genome.
They were first detected by the visionary plant geneticist Barbara McClintock back in the 1940s as she studied the genetics of maize (corn). At that time, McClintock worked at Cold Spring Harbor Laboratory, on Long Island, where she grew and tended her own maize, raising a few hundred plants on an acre or so of ground every summer. She looked for mutations, induced artificially by X-raying the kernels, and traced those mutation from chromosome to chromosome,
Part of what makes maize still so apt for such research is that—unsuspected even by McClintock back in the 1940s and 1950s—transposons comprise 85 percent of its genome, and they jump around that genome frequently.
Among the big unknowns about all these transposons, intriguing to Feschotte, are (1) where they come from originally, (2) how they enter a new genome, and (3) why they copy themselves so profusely once they have gotten aboard. None of those three questions can be answered with certainty, but Feschotte has his preferred guesses.
By this logic, transposons have acquired the capacity to self-copy because it improves their prospects of long-term survival. They replicate themselves more quickly than the host genome replicates, and they sometimes jump into other lineages, which enables them to evade extinction with the dying out of a single lineage. As a secondary effect, the redundant DNA that they add to a genome becomes available and might even prove useful, as it mutates, for cellular functions.
parasites and infection. Viruses may occasionally carry such bits of selfish DNA from one species to another, just as viruses sometimes carry whole genes in the process of HGT. The parallel is close enough that Feschotte and his team began calling the process horizontal transposon transfer (HTT).
parasitic insect (Rhodnius prolixus) in cases of transposon transfer. It’s a mean little critter, this insect, native to South America and Central America, that feeds on the blood of birds, reptiles, and mammals, including humans. It belongs to the group known as kissing bugs, because they tend to bite in the area near a victim’s mouth. Kissing bugs are despised in the American tropics not just for biting but also for their role in transmitting Chagas disease, a lingering and sometimes fatal affliction caused by a protozoan that replicates in a victim’s blood and tissues.
“horribly disgusting, to feel numerous creatures nearly an inch long & black & soft crawling in all parts of your person—gorged with your blood.” Typical of Darwin, when he was still young and robust, he shrugged that off with the aside “good to experience everything once.”
Chagas has been one hypothesis for the mysterious, chronic illness that punished Darwin throughout his middle years.
It suggested that the bug might be an intermediary, a vector, for the transposon. Next morning, he alerted two of his postdocs and invited them to investigate. Further scanning the bug’s genome, they found not just Space Invaders, represented in more than two hundred copies, but also three other transposons known previously in mammals. From the evidence of mutation rates, the transfers seemed to have happened within a time range of fifteen million to forty-six million years ago.
selfish DNA passing from the genome of one species of mammal, through the belly of a blood-sucking insect, into another species of mammal, where it inserts itself into that genome. The transposed DNA becomes part of the second mammal’s heritable legacy. And once the self-copying of the transposon begins, it adds masses of DNA to the genome. This could be bad or, much less probably, good. If bad, it disarranges the genome, destroys necessary gene functions, induces congenital diseases, and maybe even causes the mammal lineage to go extinct. Science will never see that transposon, because it has
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transposons that have entered the primate lineage, most likely by horizontal transfer, over the past eighty million years. They found forty. Each has copied itself abundantly. Those copies now constitute about 98,000 distinct elements, 98,000 stretches of alien DNA, amounting to 1 percent of the human genome. They’re still with us, changing slowly, and their effects too are largely unknown.
“Consider too,” Sapp wrote, “that a great percentage of our own DNA is of viral origin.” The figure most commonly cited is 8 percent: roughly 8 percent of the human genome consists of the remnants of retroviruses that have invaded our lineage—invaded the DNA, not just the bodies, of our ancestors—and stayed. We are at least one-twelfth viral, at the deepest core of our identities. Consider that, Sapp urged.
A retrovirus is a virus that works backward relative to the usual DNA transcription process. Instead of DNA-makes-RNA-makes-protein, the normal path from genetic information to living application, a retrovirus uses its RNA genome to make DNA, the double-stranded molecule. That trick, plus a few others, allows it not only to invade a cell but also to enter the cell nucleus and patch a DNA version of itself into the cell’s DNA, becoming a permanent part of the cell’s genome. Whenever the cell or its descendants replicate, that alien stretch is copied too. If the retrovirus happens to infect
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Such viruses are known as endogenous retroviruses (ERVs) because they become endogenous to the lineage of creatures they have infected. If a retrovirus inserts itself into the human genome, then that’s a human endogenous retrovirus, or HERV. Those are the viruses, HERVs, that constitute 8 percent of the human genome.
Some retroviruses cause cancer. Mouse leukemia virus, for instance. Heidmann studied that one. The most notorious of retroviruses, of course, is HIV-1, which causes AIDS.
some HERVs, if not that one, have indeed acquired roles as human genes.
capacity to cause cells (cyt) to fuse together (syn). This effect had been proven with laboratory cell cultures. Fusion of cells into aggregate cell masses with multiple nuclei instead of individual walls is a crucial step in building one layer of the human placenta. That layer, a sort of permeable protoplasmic cushion, is the part of the placenta that mediates between the maternal blood and the fetal blood. (Brace yourself for a fancy bit of lingo: it’s called the syncytiotrophoblast.
All of these genes have four things in common. Each one derives from the envelope gene of a retrovirus that inserted itself in the mammal genome. Each one expresses itself as a protein suffusing the placenta. Each one causes cell-to-cell fusion (at least in lab cultures), suggesting that it can create that special fused-cell protoplasmic layer, which helps mediate between placenta and fetus, letting nutrients and gases seep in from the mother, letting wastes seep out. And each is an ancient gene, preserved for many millions of years in functional form (against the disarray of random mutations)
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They all came from different sources. They represent independent captures, independent domestications, of viral genes from entirely different retroviruses.
how did the mammalian lineage arise at all—how did the first placenta evolve—before those gene captures occurred? They have been acquired intermittently and by chance, through the course of mammal evolution, but they have always been necessary. You can’t be a placental mammal without a placenta. Which came first, chance or necessity? “Yeah. Exactly,” said Heidmann. “This is the paradox.”
Besides their ability to cause cell-to-cell fusion, they can also suppress the antiviral immune response of a host. This has obvious value to an invading virus. It has other value, less obvious, to a mammal for use in its placenta. Both the fetus and the placenta of an individual mammal carry a different genome from the mother’s. Half their DNA comes from the father. If the mother’s immune system were entirely on alert, her white blood cells might attack the fetus and reject it. Part of the role of the placenta, a uniquely adaptive organ among placental mammals, is to keep peace between the
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What this all suggests, according to Heidmann’s hypothesis, is that the earliest syncytial gene that was captured in preplacental mammals may have served such a purpose of immunosuppression toward the fetus, and then gradually acquired its additional role also as an intermediating layer in the evolving placenta. Later syncytins may then have been substituted into mammalian lineages as improvements upon the first one.
CRISPR stands for clustered regularly interspaced short palindromic repeats. A palindrome, of course, is a sequence of letters that spell the same words in either direction, front to back or vice versa. In the verbal realm, that’s wordplay, yielding gambits of strained cleverness such as “Able was I ere I saw Elba,” in the voice of Napoléon, and “A man, a plan, a canal: Panama,” referring
By performing the edit very early during in vitro fertilization—one human egg in a dish, one human sperm, plus a dose of the CRISPR magic. Such germline engineering is especially powerful and controversial because it affects populations, not just individuals. A
high-tech eugenics.
he found other matches among bacterial plasmids, those infective little particles of horizontally transferable DNA. So it seemed that CRISPR might represent a record of past infections, during which bacteria and archaea captured fragments of foreign DNA and incorporated those fragments into their own genomes. But for what purpose?
A memory of infection, as defense against future infection? There’s a word for this in our own realm. We call it vaccination.
These CRISPR-associated genes (cas genes, for short) were conspicuously absent from microbial genomes that lacked CRISPR sequences. They seemed to have some functional relationship to CRISPRs—something
cas genes perform the function, guided by CRISPR spacers, of attacking and dismantling invasive DNA.
CRISPR-cas among microbes, as it has naturally evolved, is a defense mechanism against infection and infective heredity. It’s their version of an adaptive immune system. We have antibodies and white blood cells; they have CRISPR. It protects bacteria and archaea from killer viruses, and it serves as a barrier (sometimes useful, sometimes limiting) against horizontal gene transfer.
All the experts agree nowadays that endosymbiosis played an essential role: somehow a bacterium got captured and domesticated inside another cell, a host, where it became a mitochondrion. Once present and abundant within early eukaryotic cells, mitochondria delivered vast quantities of energy, far beyond anything previously available, allowing increases in size and complexity among these new cells and the multicellular creatures that evolved from them. A salient feature of the increased complexity was containment—in particular, containment of genetic material. More specifically, that meant
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So the mystery of eukaryotic origins encompasses three main questions. (1) What was the original host cell? (2) Did mitochondria acquisition trigger the most crucial changes—or, alternatively, did it result from them? (3) From what sources did the nucleus arise?
(Phyla are big divisions; all vertebrate animals, for instance, belong to a single phylum.)
Ettema’s team placed the origin of Eukarya within the Archaea, not beside it. If correct, that meant we were back to a two-limb tree of life, neither of which is the limb we have long cherished as our own. That meant we ourselves are descended from archaeans, a separate form of life, unimagined before 1977. (There are intricate complications to this scenario, involving horizontal gene transfer of bacterial genes into our archaean ancestors before our lineage even began,
mitochondria as secondary to the big transition, and human ancestry rooted within the Archaea, on a two-limb tree of life.
“Species are groups of actually or potentially interbreeding natural populations, which are reproductively isolated from other such groups.”
isolation is a useful and intuitive standard, yes, but not an absolute one.
