[Paleopsych] is evolutionary change stockpiled?
dsmith06 at maine.rr.com
Mon Nov 22 23:50:15 UTC 2004
This looks fascinating. I must find time to read it (easier said than done).
----- Original Message -----
From: HowlBloom at aol.com
To: paleopsych at paleopsych.org
Sent: Monday, November 22, 2004 6:41 PM
Subject: [Paleopsych] is evolutionary change stockpiled?
Greg Bear just sent me an amazing paper he delivered to the American Philosophical Society. I've enclosed a copy below.
The paper points out that evolution appears to occur in short bursts followed by long periods of stability. He points out that this is more meaningful than at first it seems. Evolutionary changes, he says, are apparently stored up but are kept from expressing themselves. Then, when the right signal comes, they come out of hiding and change the organism in which they've been hiding. They don't just change one organism. They make that change in a massive crowd of organisms--and in crowds of crowds.
In one of my papers, The Xerox Effect (see http://physicaplus.org.il/view_eng1.html), I've called the spontaneous and simultaneous precipitation of protons, galaxies, and stars supersimultaneity and supersynchrony. In Greg's view, this supersimultaneity and supersychrony also occurs in the evolution of life.
But how does it work? How do evolutionary changes stack up in storage? Do they go through any sort of pretesting, any process of natural selection, any tryouts in the obstacle course of the real world? How do they do this if they're not expressed in bodyplans or bodychanges that can be put through their paces to see if they work?
And, as Greg asks, when this host of changes comes out of hiding in a bunch of creatures simultaneously, what's the trigger that sets off the explosion of change? Howard
ps the boldfaced sections and those in yellow are my ways of highlighting material for myself. Ignore the bolding and yellowing.
WHEN GENES GO WALKABOUT
By Greg Bear
I’m pleased and honored to be asked to appear before the American Philosophical Society, and especially in such august company. Honored... and more than a little nervous! I am not, after all, a scientist, but a writer of fiction--and not just of fiction, but of science fiction. That means humility is not my strong suit. Science fiction writers like to be provocative. That’s our role. What we write is far from authoritative, or final, but science fiction works best when it stimulates debate.
I am an interested amateur, an English major with no degrees in science. And I am living proof that you don’t have to be a scientist to enjoy deep exploration of science. So here we go--a personal view.
A revolution is under way in how we think about the biggest issues in biology--genetics and evolution. The two are closely tied, and viruses--long regarded solely as agents of disease--seem to play a major role.
For decades now, I’ve been skeptical about aspects of the standard theory of evolution, the neo-Darwinian Modern Synthesis. But without any useful alternative--and since I’m a writer, and not a scientist, and so my credentials are suspect--I have pretty much kept out of the debate. Nevertheless, I have lots of time to read--my writing gives me both the responsibility and the freedom to do that, to research thoroughly and get my facts straight. And over ten years ago, I began to realize that many scientists were discovering key missing pieces of the evolutionary puzzle.
Darwin had left open the problem of what initiated variation in species. Later scientists had closed that door and locked it. It was time to open the door again.
Collecting facts from many sources--including papers and texts by the excellent scientists speaking here today--I tried to assemble the outline of a modern appendix to Darwin, using ideas derived from disciplines not available in Darwin’s time: theories of networks, software design, information transfer and knowledge, and social communication--lots of communication.
My primary inspiration and model was variation in bacteria. Bacteria initiate mutations in individuals and even in populations through gene transfer, the swapping of DNA by plasmids and viruses.
Another inspiration was the hypothesis of punctuated equilibrium, popularized by Stephen Jay Gould and Niles Eldredge. In the fossil record--and for that matter, in everyday life--what is commonly observed are long periods of evolutionary stability, or equilibrium, punctuated by sudden change over a short span of time, at least geologically speaking--ten thousand years or less. And the changes seem to occur across populations.
Gradualism--the slow and steady accumulation of defining mutations, a cornerstone of the modern synthesis--does not easily accommodate long periods of apparent stability, much less rapid change in entire populations. If punctuated equilibrium is a real phenomenon, then it means that evolutionary change can be put on hold. How is that done? How is the alleged steady flow of mutation somehow delayed, only to be released all at once?
I was fascinated by the possibility that potential evolutionary change could be stored up. Where would it be kept? Is there a kind of genetic library where hypothetical change is processed, waiting for the right moment to be expressed? Does this imply not only storage, but a kind of sorting, a critical editing function within our DNA, perhaps based on some unknown genetic syntax and morphology?
If so, then what triggers the change?
Most often, it appears that the trigger is either environmental challenge or opportunity. Niches go away, new niches open up. Food and energy becomes scarce. New sources of food and energy become available. Lacking challenge or change, evolution tends to go to sleep--perhaps to dream, and sometimes to rumple the covers, but not to get out of bed and go for coffee.
Because bacteria live through many generations in a very short period of time, their periods of apparent stability are not millennia, but years or months or even days.
The most familiar mutational phenomenon in bacteria--resistance to antibiotics--can happen pretty quickly. Bacteria frequently exchange plasmids that carry genes that counteract the effects of antibiotics. Bacteria can also absorb and incorporate raw fragments of DNA and RNA, not packaged in nice little chromosomes. The members of the population not only sample the environment, but exchange formulas, much as our grandmothers might swap recipes for soup and bread and cookies. How these recipes initially evolve can in many instances be attributed to random mutation--or to the fortuitous churning of gene fragments--acting through the filter of natural selection. Bacteria do roll the dice, but recent research indicates that they roll the dice more often when they’re under stress--that is, when mutations will be advantageous. Interestingly, they also appear to roll the dice predominantly in those genetic regions where mutation will do them the most good! Bacteria, it seems, have learned how to change more efficiently.
Once these bacterial capabilities evolve, they spread rapidly. However, they spread only when a need arises--again, natural selection. No advantage, no proliferation. No challenge, no change.
But gene swapping is crucial. And it appears that bacteria accept these recipes not just through random action, but through a complicated process of decision-making. Bacterial populations are learning and sharing. In short, bacteria are capable of metaevolution--self-directed change in response to environmental challenges.
Because of extensive gene transfer, establishing a strict evolutionary tree of bacterial types has become difficult, though likely not impossible. We’re just going to have to be clever, like detectives solving crimes in a town where everyone is a thief.
Perhaps the most intriguing method of gene swapping in bacteria is the bacteriophage, or bacterial virus. Bacteriophages--phages for short--can either kill large numbers of host bacteria, reproducing rapidly, or lie dormant in the bacterial chromosome until the time is right for expression and release. Lytic phages almost invariably kill their hosts. But these latter types--known as lysogenic phages--can actually transport useful genes between hosts, and not just randomly, but in a targeted fashion. In fact, bacterial pathogens frequently rely on lysogenic phages to spread toxin genes throughout a population. Cholera populations become pathogenic in this fashion. In outbreaks of E. coli that cause illness in humans, lysogenic phages have transported genes from shigella--a related bacterial type--conferring the ability to produce shiga toxin, a potent poison.
Thus, what at first glance looks like a disease--viral infection--is also an essential method of communication--FedEx for genes.
When genes go walkabout, bacteria can adapt quickly to new opportunities. In the case of bacterial pathogens, they can rapidly exploit a potential marketplace of naïve hosts. In a way, decisions are made, quorums are reached, genes are swapped, and behaviors change.
What lies behind the transfer of bacterial genes? Again, environmental challenges and opportunities. While some gene exchange may be random, bacterial populations overall appear to practice functions similar to education, regimentation, and even the execution of uncooperative members. When forming bacterial colonies, many bacteria--often of different types--group together and exchange genes and chemical signals to produce an organized response to environmental change. Often this response is the creation of a biofilm, a slimy polysaccharide construct complete with structured habitats, fluid pathways, and barriers that discourage predators. Biofilms can even provide added protection against antibiotics. Bacteria that do not go along with this regimen can be forced to die--either by being compelled to commit suicide or by being subjected to other destructive measures. If you don’t get with the picture, you break down and become nutrients for those bacterial brothers who do, thus focusing and strengthening the colony.
A number of bacteriologists have embraced the notion that bacteria can behave like multicellular organisms. Bacteria cooperate for mutual advantage. Today, in the dentist’s office, what used to be called plaque is now commonly referred to as a biofilm. They’re the same thing--bacterial cities built on your teeth.
In 1996, I proposed to my publishers a novel about the coming changes in biology and evolutionary theory. The novel would describe an evolutionary event happening in real-time--the formation of a new sub-species of human being. What I needed, I thought, was some analog to what happens in bacteria. And so I would have to invent ancient viruses lying dormant in our genome, suddenly reactivated to ferry genes and genetic instructions between humans.
To my surprise, I quickly discovered I did not have to invent anything. Human endogenous retroviruses are real, and many of them have been in our DNA for tens of millions of years. Even more interesting, some have a close relationship to the virus that causes AIDS, HIV.
The acronym HERV--human endogenous retrovirus--became my mantra. In 1997 and 1998, I searched the literature (and the internet) for more articles about these ancient curiosities--and located a few pieces here and there, occasional mention in monographs, longer discussions in a few very specialized texts. I was especially appreciative of the treatment afforded to HERV in the Cold Spring Harbor text Retroviruses, edited by Drs. Coffin, Varmus, and Hughes. But to my surprise, the sources were few, and there was no information about HERV targeted to the general layman.
As a fiction writer, however, I was in heaven--ancient viruses in our genes! And hardly anyone had heard of them.
If I had had any sense, I would have used that for what it seemed at face value--a ticking time bomb waiting to go off and destroy us all. But I had different ideas. I asked, what do HERV do for us? Why do we allow them to stay in our genome?
In fact, even in 1983, when I was preparing my novel Blood Music, I asked myself--what do viruses do for us? Why do we allow them to infect us? I suspected they were part of a scheme involving computational DNA, but could not fit them in...not just then. HIV was just coming into the public consciousness, and retroviruses were still controversial.
I learned that HERV express in significant numbers in pregnant women, producing defective viral particles apparently incapable of passing to another human host. So what were they--useless hangers-on? Genetic garbage? Instinctively, I could not believe that. I’ve always been skeptical of the idea of junk DNA, and certainly skeptical of the idea that the non-coding portions of DNA are deserts of slovenly and selfish disuse.
HERV seemed to be something weird, something wonderful and counter-intuitive--and they were somehow connected with HIV, a species-crossing retrovirus that had become one of the major health scourges on the planet. I couldn’t understand the lack of papers and other source material on HERV. Why weren’t they being investigated by every living biologist?
In my rapidly growing novel, I wrote of Kaye Lang, a scientist who charts the possible emergence of an HERV capable of producing virions--particles that can infect other humans. To her shock, the HERV she studies is connected by investigators at the CDC with a startling new phenomenon, the apparent mutation and death of infants. The infectious HERV is named SHEVA. But SHEVA turns out to be far more than a disease. It’s a signal prompting the expression of a new phenotype, a fresh take on humanity--a signal on Darwin’s Radio.
In 1999, the novel was published. To my gratified surprise, it was reviewed in Nature and other science journals. Within a very few months, news items about HERV became far more common. New scientific papers reported that ERV-related genes could help human embryos implant in the womb--something that has recently been given substantial credence. And on the web, I encountered the fascinating papers of Dr. Luis P. Villarreal.
I felt as if I had spotted a big wave early, and jumped on board just in time. Still, we have not found any evidence of infectious HERV--and there is certainly no proof that retroviruses do everything I accuse them of in Darwin’s Radio. But after four years, the novel holds up fairly well. It’s not yet completely out of date.
And the parallel of HERV with lysogenic phages is still startling.
But back to the real world of evolution and genetics.
The picture we see now in genetics is complex. Variation can occur in a number of ways. DNA sequence is not fate; far from it. The same sequence can yield many different products. Complexes of genes lie behind most discernible traits. Genes can be turned on and off at need. Non-coding DNA is becoming extremely important to understanding how genes do their work.
As well, mutations are not reliable indicators of irreversible change. In many instances, mutations are self-directed responses to the environment. Changes can be reversed and then reenacted at a later time--and even passed on as reversible traits to offspring.
Even such neo-Darwinian no-nos as the multiple reappearances of wings in stick insects points toward the existence of a genetic syntax, a phylogenetic toolbox, rather than random mutation. Wings are in the design scheme, the bauplan. When insects need them, they can be pulled from the toolbox and implemented once again.
We certainly don’t have to throw out Mr. Darwin. Natural selection stays intact. Random variation is not entirely excised. But the neo-Darwinian dogma of random mutation as a cause of all variation, without exception, has been proven wrong.
Like genetics, evolution is not just one process, but a collaboration of many processes and techniques. And evolution is not entirely blind. Nor must evolution be directed by some outside and supernatural intelligence to generate the diversity and complexity we see. Astonishing creativity, we’re discovering, can be explained by wonderfully complicated internal processes.
These newer views of evolution involve learning and teamwork. Evolution is in large part about communication--comparing notes and swapping recipes, as it were.
It appears that life has a creative memory, and knows when and how to use it.
Let’s take a look at what the scientists have discovered thus far.
Viruses can and do ferry useful genes between organisms. Viruses can also act as site-specific regulators of genetic expression. Within a cell, transposable elements--jumping genes similar in some respects to endogenous retroviruses--can also be targeted to specific sites and can regulate specific genes. Both viruses and transposable elements can be activated by stress-related chemistry, either in their capacity as selfish pathogens--a stressed organism may be a weakened organism--or as beneficial regulators of gene expression--a stressed organism may need to change its nature and behavior.
Viral transmission occurs not just laterally, from host to host (often during sex), but vertically through inherited mobile elements and endogenous retroviruses.
Chemical signals between organisms can also change genetic expression. As well, changes in the environment can lead to modification of genetic expression in both the individual and in later generations of offspring. These changes may be epigenetic--factors governing which genes are to be expressed in an organism can be passed on from parent to offspring--but also genetic, in the sequence and character of genes.
Our immune system functions as a kind of personal radar, sampling the environment and providing information that allows us to adjust our immune response--and possibly other functions, as well.
These pathways and methods of regulation and control point toward a massive natural network capable of exchanging information--not just genes themselves, but how genes should be expressed, and when. Each gene becomes a node in a genomic network that solves problems on the cellular level. Cells talk to each other through chemistry and gene transfer. And through sexual recombination, pheromonal interaction, and viruses, multicellular organisms communicate with each other and thus become nodes in a species-wide network.
On the next level, through predation and parasitism, as well as through cross-species exchange of genes, an ecosystem becomes a network in its own right, an interlinking of species both cooperating and competing, often at the same time.
Neural networks from beehives to brains solve problems through the exchange and the selective cancellation and modification of signals. Species and organisms in ecosystems live and die like signals in a network. Death--the ax of natural selection--is itself a signal, a stop-code, if you will.
Networks of signals exist in all of nature, from top to bottom--from gene exchange to the kinds of written and verbal communication we see at this event. Changes in genes can affect behavior. Sometimes even speeches can affect behavior.
Evolution is all about competition and cooperation--and communication.
Traditional theories of evolution emphasize the competitive aspect and de-emphasize or ignore the cooperative aspect. But developments in genetics and molecular biology render this emphasis implausible.
Genes go walkabout far too often. We are just beginning to understand the marvelous processes by which organisms vary and produce the diversity of living nature.
For now, evolution is a wonderful mystery, ripe for further scientific exploration. The gates have been blown open once again.
And as a science fiction writer, I’d like to make two provocative and possibly ridiculous predictions.
The first is that the more viruses may be found in an organism and its genome, the more rapid will be that organism’s rate of mutation and evolution.
And the second: Bacteria are such wonderful, slimmed-down organisms, lacking introns and all the persiflage of eukaryotic biology. It seems to me that rather than bacteria being primitive, and that nucleated cells evolved from them, the reverse could be true. Bacteria may once have occupied large, primitive eukaryotic cells, perhaps similar to those seen in the fossil Vendobionts--or the xenophyophores seen on ocean bottoms today. There, they evolved and swam within the relative safety of the membranous sacs, providing various services, including respiration. They may have eventually left these sacs and become both wandering minstrels and predators, serving and/or attacking other sacs in the primitive seas.
Eventually, as these early eukaryotic cells advanced, and perhaps as the result of a particularly vicious cycle of bacterial predation, they shed nearly all their bacterial hangers-on in a protracted phase of mutual separation, lasting hundreds of millions or even billions of years.
And what the now trim and super-efficient bacteria--the sports cars of modern biology--left behind were the most slavish and servile members of that former internal community: the mitochondria.
Which group will prove to have made the best decision, to have taken the longest and most lasting road?
Author of The Lucifer Principle: A Scientific Expedition Into the Forces of History and Global Brain: The Evolution of Mass Mind From The Big Bang to the 21st Century
Visiting Scholar-Graduate Psychology Department, New York University; Core Faculty Member, The Graduate Institute
Founder: International Paleopsychology Project; founding board member: Epic of Evolution Society; founding board member, The Darwin Project; founder: The Big Bang Tango Media Lab; member: New York Academy of Sciences, American Association for the Advancement of Science, American Psychological Society, Academy of Political Science, Human Behavior and Evolution Society, International Society for Human Ethology; advisory board member: Youthactivism.org; executive editor -- New Paradigm book series.
For information on The International Paleopsychology Project, see: www.paleopsych.org
for two chapters from
The Lucifer Principle: A Scientific Expedition Into the Forces of History, see www.howardbloom.net/lucifer
For information on Global Brain: The Evolution of Mass Mind from the Big Bang to the 21st Century, see www.howardbloom.net
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