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Friday 10 November 2017

A primeval internet v. Darwin?

Internet of Cells: The Next Revolution?
Evolution News @DiscoveryCSC





Cells are the fundamental units of biology. They have long seemed like individuals. Sure, they communicate, like humans, and they build structures together, sharing the work with division of labor. But like factory workers going home at the end of the day, cells can be treated as independent units with their own lives to live. To evolutionary biologists, cells divide alone and evolve independently. Isn’t that one of the basic premises of modern biological science?

Take heed: the next biological revolution is coming. Nature calls it “The Internet of Cells” and says that it has biologists buzzing.

The revolution began, Monya Baker writes, when biologists noticed that proteins engineered to appear in certain cells appeared to have “teleported” to a different group of cells entirely. Then came the discovery of molecular nanotubes that appear to transmit genetic information and even organelles between cells. Gradually, cells seemed to be losing their independence.

Yamashita’s tubes joined a growing catalogue of cryptic conduits between cells. Longer tubes, reported in mammalian cells, seem to transport not just molecular signals but much larger cargo, such as viral particles, prions or even mitochondria, the cell’s energy-generating structures. These observations suggest an unanticipated level of connectivity between cells, says Amin Rustom, a neurobiologist at the University of Heidelberg in Germany, who first spotted such tubes as a graduate student almost 20 years ago. If correct, he says, “it would change everything in medical applications and biology, because it would change how we see tissues”

A short video clip reveals what appear to be “interstate highways” reaching out and connecting between cells, passing material between them. The concept of intercellular trafficking through conduits is controversial, because no one knows exactly what is being transported and how often this occurs. The nanotubes, a mere 200 nm in diameter (wide enough to transport protein scraps), have been observed in the lab, but not as clearly in living organisms. They are hard to see. What are they doing?

Baker recounts lab findings in 2004 that showed “something even more radical: nanotubes in mammalian cells that seemed to move cargo such as organelles and vesicles back and forth.” Since then, more “membrane nanotubes” have been found.

Meanwhile, other labs have reported cell-connecting tubes in neurons, epithelial cells, mesenchymal stem cells, several sorts of immune cell and multiple cancers. Further types of tube have been spotted as well. In 2010, Gerdes and his team reported that some tubes end in gap junctions: gateways that bestow the neuron-like ability to send electrical signals and can also pass along peptides and RNA molecules.

The “internet of cells” might also explain how disease agents, such as viruses, spread among tissue cells, or how cancer cells hijack their neighbors. Not everyone is jumping aboard the new paradigm, because the implications are huge. Eliseo Eugenin at Rutgers Medical School

thinks that other researchers are sceptical of nanotubes because they are unable to reconcile themselves to the idea that cells are constantly exchanging materials, including genetic information. “Our definition of a cell is falling apart,” Eugenin says. “That is why people don’t believe in these tubes, because we have to change the definition of a cell.”

The race is on to convince skeptics with better imaging of functional transport within multicellular organisms. Baker doesn’t say much about evolution. She notes that one researcher speculated, “Membrane protrusions might have evolved first, and higher organisms could have started upgrading them to make neurons for more complicated functions.” Such personification language is not particularly helpful for materialists. Baker quickly pivots and says, “Most researchers who study these cellular pipelines care less about their evolutionary origin than about their role in human health and disease.” As such, the “internet of cells” looks like it will be a boon for design research, and a challenge to Darwinian evolution.

Sharing Genetic Information
A separate paper in PNAS discusses “Intercellular mRNA trafficking via membrane nanotube-like extensions in mammalian cells.” Notice how this team of Americans and Israelis describes the finding as a revolutionary development in biology:

mRNA molecules convey genetic information within cells, beginning from genes in the nucleus to ribosomes in the cell body, where they are translated into proteins. Here we show a mode of transferring genetic information from one cell to another. Contrary to previous publications suggesting that mRNAs transfer via extracellular vesicles, we provide visual and quantitative data showing that mRNAs transfer via membrane nanotubes and direct cell-to-cell contact. We predict that this process has a major role in regulating local cellular environments with respect to tissue development and maintenance and cellular responses to stress, interactions with parasites, tissue transplants, and the tumor microenvironment.

The team admits that “The biological importance of mRNA transfer between cells is still unknown,” but the concept of sharing of genetic information between cells appears to overturn long-held assumptions about the independence of cells.

As for what cells are sharing, many possibilities come to mind. For instance, “the transfer of mRNAs involved in cell differentiation during embryonic development might act as means to induce or repress neighboring cells.” Conceptualizing the rapid transfer of genetic information via “nanotubular highways” between cells opens up many new avenues for research. “Determining the scope of this process and deciphering the mechanism and physiological outcome of mRNA transfer will be the goal of future studies,” they conclude.

More Evidence
Hormones and signal molecules have long been known to travel between cells, but direct transport by contact is fairly new. Science Daily reported on work at Vanderbilt to learn how cells communicate during wound healing. The cell’s signals are “surprisingly complex”, the headline says. One hypothesis had been that cells send proteins to their neighbors that trigger them to boost their calcium levels.

The second hypothesis proposes that the trigger signal spreads from cell to cell through gap junctions, specialized intercellular connections that directly link two cells at points where they touch. These are microscopic gates that allow neighboring cells to exchange ions, molecules and electrical impulses quickly and directly.

“What is extremely exciting is that we found evidence that cells use both mechanisms,” said Shannon. “It turns out cells have a number of different ways to signal injury. This may allow them to differentiate between different kinds of wounds.”

Implications for Design Research
Darwinian theory presupposes some kind of “unit of selection” in biology. Evolutionists have long debated whether the unit of selection is a gene, a cell, an organism, or (less commonly proposed) a population of organisms. Neo-Darwinism has long focused on cells as units of selection, because that’s where genetic mutations take place that might be beneficial. Essential to the theory, though, is some degree of independence of the unit of selection, so that whatever beneficial variation appears can be victorious in the struggle for existence.

If organisms routinely share their information, however, all evolutionary bets are off. There won’t be competition if all the players share the benefit. We saw this conundrum when evidence grew for rampant horizontal gene transfer between microbes, and then between higher organisms. Some biologists considered the existence of a “quasi-species” in which a population could rapidly recover from individual stresses because of information sharing.


The “internet of cells” bears more similarity to “cloud computing” than to classical notions of Darwinian evolution. If functional information is routinely shared throughout the internet of cells, that looks a lot more like cooperation than competition. Prospects for research in this hot new paradigm appear wide open for non-Darwinian interpretations.

The Iconoclasm continues?

Upsetting Another Evolutionary Icon — Blindness in Cave Fish Is Due to Epigenetics
Cornelius Hunter

A recent paper out of Brant Weinstein’s and William Jeffery’s laboratories on eye development, or the lack thereof, in blind cave fish has important implications for evolutionary theory (the paper is discussed  here). The study finds that the loss of eyes in fish living in dark Mexican caves is not due to genetic mutations, as evolutionists have vigorously argued for many years, but due to genetic regulation. Specifically, methylation of key development genes represses their expression and with it eye development in this venerable icon of evolution. But the finding is causing yet more problems for evolutionary theory.

Darwin appealed to the blind cave fish in his one long argument for evolution. It is a curious argument in many ways, and the first sign of problems was in Darwin’s presentation where he flipped between two different explanations. At one point he explained the loss of vision in the cave fish as an example of evolutionary change not due to his key mechanism, natural selection. Instead, the Sage of Kent resorted to using the Lamarckian mechanism or law of “use and disuse.” Privately, Darwin despised and harshly criticized Lamarck, but when needed he occasionally employed his French forerunner’s ideas.Elsewhere Darwin hit upon a natural selection-based mechanism for the blind cave fish, explaining that elimination of the costly and unneeded vision system would surely raise the fitness of the hapless creatures.

This latter explanation would become a staple amongst latter-day evolutionary apologists, convinced that it mandates the fact of evolution. Anyone who has discussed or debated evolutionary theory with today’s Epicureans has likely encountered this curious argument that because blind cave fish lost their eyes, therefore the world must have arisen by itself.

Huh?

To understand the evolutionary logic, or lack thereof, one must understand the history of ideas, and in particular the idea of fixity, or immutability, of species. According to evolutionists, species are either absolutely fixed in their designs, or otherwise there are no limits to their evolutionary changes and the biological world, and everything else for that matter, spontaneously originated.

Any evidence, for any kind of change, no matter how minor, is immediately yet another proof text for evolution, with all that the word implies.

Of course, from a scientific perspective, the evidence provides precisely zero evidence for evolution. Evolution requires the spontaneous (i.e., by natural processes without external input) creation of an unending parade of profound designs. The cave fish evidence shows the removal, not creation, of such a design.

The celebration of such evidence and argument by Darwin and his disciples reveals more about evolutionists than evolution. That they would find this argument persuasive reveals their underlying metaphysics and the heavy lifting it performs.

We are reminded of all this with the news of Weinstein’s new study. But we also see something new: The insertion, yet again, of Lamarck into the story. The irony is that the epigenetics, now revealed as the cause of repressed eye development in the cave fish, hearkens back to Lamarck.

Darwin despised Lamarck and later evolutionists made him the third rail in biology. Likewise they have pushed back hard against the scientific findings of epigenetics and their implications.

The environment must not drive biological change.

False.

Well then, such biological change must not be transgenerational.

False.

Well, such inheritance must not be long lasting, or otherwise robust.

False again.

This last failure is revealed yet again in the new blind cave fish findings.

False predictions count. A theory that is repeatedly wrong, over and over, in its fundamental expectations, will eventually be seen for what it is.

The rise of epigenetics is yet another such major failure. Evolutionists pushed back against it because it makes no sense on the theory, and that means it cannot now be easily accommodated.

One problem is that epigenetics is complex. The levels of coordination and intricacy of mechanism are far beyond evolution’s meager resources.

Another problem is the implied serendipity. For instance, one epigenetic mechanism involves the molecular tags placed on the tails of the DNA packing proteins called histones. While barcoding often seems to be an apt metaphor for epigenetics, the tagging of histone tails can influence the histone three-dimensional structures. It is not merely an information-bearing barcode. Like the tiny rudder causing the huge ship to change course, the tiny molecular tag can cause the much larger packing proteins to undergo conformational change, resulting in important changes in gene accessibility and expression.

This is all possible because of the special, peculiar structure and properties of the histone protein and its interaction with DNA. With evolution we must believe this just happened to evolve for no reason, and thus fortuitously enabled the rise of epigenetics.

Another problem with epigenetics is that it is worthless, in evolutionary terms that is. The various mechanisms that sense environmental shifts and challenges, attach or remove one of the many different molecular tags to one of the many different DNA or histone locations, propagate these messages across generations, and so forth, do not produce the much needed fitness gain upon which natural selection operates.

The incredible epigenetics mechanisms are helpful only at some yet to be announced future epoch when the associated environmental challenge presents itself. In the meantime, selection is powerless and according to evolution the incredible system of epigenetics, that somehow just happened to arise from a long, long series of random mutations, would wither away with evolution none the wiser.

These are the general problems with epigenetics. In the case of the blind cave fish, however, there is a possible explanation. It is a longshot, but since this case specifically involves the loss of a stage of embryonic development, evolutionists can say that genetic mutations caused changes in the methylating proteins, causing them to be overactive.

This explanation relies on the preexistence of the various epigenetic mechanisms, so does not help to resolve the question of how they could have evolved. What the explanation does provide is a way for evolutionists to dodge the bullet presented by the specter of the cave fish intelligently responding to an environmental shift.

Such teleology in the natural world is not allowed. So the evolutionary prediction is that these proteins will be found to have particular random changes causing an increase in their methylation function, in particular at key locations in key genes (i.e., the genes associated with eye development).


That’s a long shot, and an incredible violation of Occam’s razor. My predictions are that (i) this evolutionary prediction will fail just as the hundreds that came before, and (ii) as with those earlier failures, this failure will do nothing to open the evolutionist’s eyes.