Picard’s famous challenge from STNG Measure of a Man inverts the question most asked about AI, “Prove it’s sentient.” There is a growing drumbeat about the Singularity, the day the machines take over. My own take is the Mitochondrial Singularity, the argument that the singularity is ongoing, ever since humans invented letters and numbers; or, to be fair to artists, perhaps when they drew the first image on the wall of a cave. As we outsource our abilities, eventually we’ll be left with the mitochondrial role of powering the machine; that is, turning it on.
Another sign of our growing mitochondrialization is the appropriation of our organic tissue nature, our “water ware”, into machines. The proto-mitochondrial bacteria, after all, had all sorts of useful genes that got appropriated into their host nuclei–for the host benefit, or the benefit of the mitochondrion, the question is unclear.
In our human context, twentieth century robot builders would have scorned the idea that human tissue might have properties useful for a silicon ship. Human tissue is wet and slimy, nothing like the clean, dry shininess of silicon. Yet Stanford scientist are now building computers out of water, in which water flow replaces electron flow in generating logic gates. At least, that’s what I understand from the PacMan-like image above. “Little bags” of water, for logical manipulation of matter. Um, how are those not like human cells?
More to the point, NIH is building Tissue Chip for Drug Screening. The ideas is to incorporate human tissues into a computer chip and design instruments to test the effect of toxins. A more advanced idea is Organs-on-Chip, funded by DARPA and others. Known officially as the innocuous-sounding mouthful Human Toxicology Project Consortium, the stated goal is to model organs, even a “human-on-a-chip” using stem cells. And of course, we’re all about building organs for transplant. Printing out organs on our cute 3D printer.
Excuse me–Human on a chip? Does the word “being” fit in there, as in, “human being on a chip”? Even with the best of intentions, what does this mean?
Suppose we wish to test toxicity and brain exposure, the effect of toxins on brain function, cognition, affect etc. Brain on a chip? Prove to the court that I am (not) sentient.
At the climax of Data’s trial, Maddox argues (spoiler) that Data is a machine, a Pinocchio with a human pulling the strings. Data is “an idea conceived of by the mind of a man. Its purpose is to serve human needs and interests. It’s a collection of neural nets and heuristic algorithms. Its responses dictated by an elaborate software program written by a man. Its hardware built by a man. And now a man will shut it off.”
Any mitochondrion can shut off a cell. In fact, it happens all the time; as our mitochondria mutate, they shut down the cell, causing disease or aging. Likewise, we humans slide down our own mitochondrial vortex. Then what will our sentience mean?
This remarkable report claims that scientists have built a new limb from the collagen matrix of a rat’s paw. They started with the limb from one rat, and used a detergent to wash away all the cells from the collagen that holds the limb’s shape. Presumably they kept the bone too; I’ve not yet got through the paywall for the details. Then they added cells from a new rat, and the cells grew out, forming all the requisite muscle and blood vessels. A graft to the new rat behaved as native tissue. It doesn’t sound like the researchers connected nerves yet, but still impressive.
While this feat sounds remarkable, in fact, collagen matrix (a natural mesh of protein) has been used for many years to restore tissue; for example, receded gum tissue. Collagen from a cadaver is stripped of cells (which harbor the MHC genes and proteins of tissue type) then pasted onto the roots of your teeth. New gum cells migrate into it, restoring the gums.
Who knows; maybe a head transplant‘s not so far away. We know a lot of political candidates who could use one. The ultimate answer to climate change denial. More on climate change this week.
My appearance on Inside Story didn’t work out (travel mixup–someone confused Kenyon with Ohio State) but still generated some blog discussion on one of our favorite themes:
- When will computers be as smart as humans?
- What about their lack of common sense, intuition, and other intrinsically human qualities?
- What happens to humans once singularity is achieved?
Bacteria Lab students are wrapping up a paper on “polar aging” of E. coli. What does that mean? Every time a bacterial cell divides, each daughter cell inherits an old pole (preexisting cell division) and a new pole (formed by division). Inevitably, a line of cells inherits an old pole for many generations. In the colony above, the old poles are marked yellow; the new poles are green, and inbetween generations are marked other colors. The white line marks the divide between two half-lineages of the original ancestral cell, for which we don’t know which pole was old or new. A small portion of a colony lineage is diagrammed:
Under certain conditions, the cell with the superannuated pole (yellow) tires out. You can see where the green-yellow cell has given up dividing. The old-pole cell division slows, and the cell eventually dies of old age–despite inheriting a new pole too. It’s like Rowling’s Death Eater that got its head stuck in a time-turner jar, and turned into a baby’s head: half old and half newborn.
Can bacteria ever “reverse” their “polar age”? Not E. coli, we think–but other kinds of bacteria do. Mycobacteria, which cause tuberculosis, grow differently by extending one pole only (Bree Aldridge, Science 2012).
The extending mycobacterial pole makes a newborn cell that accelerates cell division (Age 2) while leaving behind an old-pole cell that pauses (Age 1). But then–in the next generation, the old pole accelerates division–leaving its new pole behind, suddenly old. In effect, a mycobacterium is a time-turner, its young pole growing old and its old pole growing new. Though not an endless loop, the lineage endlessly generates deadly infectious cells showing age-dependent resistance to various antibiotics.
Why do bacteria age? As best we can tell, they age for the same reason humans do. Humans are animals that partition their biomass into an immortal germ line (the sex cells) and a mortal soma (the rest of our body.) The mortal body (the bacterial old pole) “eats death” by inheriting all the mistakes, the misfolded proteins, while keeping the germ line young. In humans, similarly, our brains accumulate the misfolded proteins associated with Parkinson’s and Alzheimer’s. But our germ line (new pole) remains the potential baby, while it’s still part of one’s own body. Like E. coli, we’re all the hapless Death Eater stuck with half a baby.
A 3D tracheal splint was custom designed for each baby, suffering a rare disorder in which the baby can’t breathe out. The splint holds the trachea open, then dissolves naturally as the baby grows and no longer needs the help.
No doubt this is just one of many such ingenious devices to come out of future printers.
We’ve discussed before how ancient endogenous retroviruses evolved into our own human genes, including HERVs (human endogeount retroviral genes) that encode essential products such as placental syncitin. So far, though, it has been assumed that the viruses themselves were extinct; that only their nucleobase sequence (ATCG etc.) remained, adapted to a human function.
Now, researchers show that human embryos produce actual virions–virus particles–containing retroviral sequence and capsid. These truly endogenous retrovirus particles actually serve as part of the human immune system to protect us from viral infection. This is, bizarrely enough, the very opposite of what HIV (the most famous retrovirus) does to adult human immune systems.
The retrovirus studied was HERVK, which infected humans while we were still diverging from chimps–relatively recently in our evolution. Multiple infections left signs of their nucleobase sequence in our genome; in fact, since humans show different versions of HERVK in their genomes toda, the virus must continue some activity in our population, in the last 200,000 years. Thus, HERVK would be a good bet to exhibit some virus-producing ability. At Stanford, Joanna Wysocka and colleagues used fluorescence microscopy and various specific fluorophores (glowing molecules that bind specific proteins or genes) to show the presence of HERVK virus-like particles emerging from embryos.
Why embryos? In adult humans, HERVK appears to be suppressed by DNA methylation, a chemical modification of the nucleobases that generally turns of gene expression (the making of a gene’s product). But in the embryos, the HERVK DNA is free of methyl groups. So, the embryo condition allows expression of retroviral genes. The gene expression is not random, but is regulated by known embryonic regulators, such as the OCT4 transcription factor. The OCT4 is known as a gene expressed only during very early embryos–or in tumors, under abnormal conditions.
Surprisingly, the HERVK activation leads to production of virus-like particles (particles that look like viruse under electron microscopy). Even more surprising, HERVK activation causes upregulation of the anti-viral defense protein, Interferon-induced transmembrane protein 1 (IFITM1). Interferons are a class of protein that host cells commonly express in response to being infected–to tell their neighbor cells to avoid infection. In this case, however, the HERVK may be protecting the embryos from infection of other possible pathogens during a vulnerable period in the womb, before the adult immune system develops.
You may be wondering, where do the researchers get all these human embryos to study? Early human embryos at the stage of blastocyst (hollow ball of cells) are obtained from IVF donors; couples who seek in vitro fertilization for reasons of infertility or other causes. The IVF procedure routinely produces “supernumerary” embryos, a fancy word for “more than needed.” Such embryos are commonly donated to science, under government regulation.
Headlines promote a breakthrough in “artificial photosynthesis.” It’s exciting technology, but–artificial? So what are those bacteria doing twined around the photocathodes?
The Berkeley scientists’ article in Nano Letters is titled “Nanowire–Bacteria Hybrids for Unassisted Solar Carbon Dioxide Fixation to Value-Added Chemicals.” What they seem to have made is:
(1) A silicon-nanowire array (the “photoanode”) splits water (H2O) like chlorophyll does in photosynthesis. The light-absorbing reaction removes an electron. What you get is H+ and O2 (O2 being the good clean oxygen we breathe). Where the other H goes is not clear; presumably it also gives up an electron, without toxic oxidizing radicals, which real photosynthesis produces.
(2) The electrons travel down the nanowires to a source of CO2, in the presence of photocathode wires. But here’s where we need the bacteria, Sporomusa ovata. The bacteria use an ancient evolved pathway of metabolism to reduce (add electrons to) the CO2, making acetic acid, CH3CO2H. Notice a lot of extra steps in there.
The use of Sporomusa ovata in a fuel cell was actually shown a few years ago by Derek Lovley’s lab, which has a long history of pioneering work in bacterial electricity. Lovley’s students used an electrical current to make Sporomusa bacteria reduce CO2 to acetate, a building block for various industrial products.
Here are Lovley’s electrode biofilms of Sporomusa. The implication is that hybrid nanoelectrode-bacterial fixation of carbon could directly make fuels and plastics, without the usual production of biomass (sugar polymers etc.) and thus without all the carbon waste along way.