Posted on 01/26/2006 11:47:13 AM PST by PatrickHenry
Jeffrey H. Schwartz's Sudden Origins closed Darwin's gaps; cell biology explains how.
An article by University of Pittsburgh Professor of Anthropology Jeffrey H. Schwartz and University of Salerno Professor of Biochemistry Bruno Maresca, to be published Jan. 30 in the New Anatomist journal, shows that the emerging understanding of cell structure lends strong support to Schwartz's theory of evolution, originally explained in his seminal work, Sudden Origins: Fossils, Genes, and the Emergence of Species (John Wiley & Sons, 2000).
In that book, Schwartz hearkens back to earlier theories that suggest that the Darwinian model of evolution as continual and gradual adaptation to the environment glosses over gaps in the fossil record by assuming the intervening fossils simply have not been found yet. Rather, Schwartz argues, they have not been found because they don't exist, since evolution is not necessarily gradual but often sudden, dramatic expressions of change that began on the cellular level because of radical environmental stressors-like extreme heat, cold, or crowding-years earlier.
Determining the mechanism that causes those delayed expressions of change is Schwartz's major contribution to the evolution of the theory of evolution. The mechanism, the authors explain, is this: Environmental upheaval causes genes to mutate, and those altered genes remain in a recessive state, spreading silently through the population until offspring appear with two copies of the new mutation and change suddenly, seemingly appearing out of thin air. Those changes may be significant and beneficial (like teeth or limbs) or, more likely, kill the organism.
Why does it take an environmental drama to cause mutations? Why don't cells subtly and constantly change in small ways over time, as Darwin suggests?
Cell biologists know the answer: Cells don't like to change and don't do so easily. As Schwartz and Maresca explain: Cells in their ordinary states have suites of molecules- various kinds of proteins-whose jobs are to eliminate error that might get introduced and derail the functioning of their cell. For instance, some proteins work to keep the cell membrane intact. Other proteins act as chaperones, bringing molecules to their proper locations in the cell, and so on. In short, with that kind of protection from change, it is very difficult for mutations, of whatever kind, to gain a foothold. But extreme stress pushes cells beyond their capacity to produce protective proteins, and then mutation can occur.
This revelation has enormous implications for the notion that organisms routinely change to adapt to the environment. Actually, Schwartz argues, it is the environment that knocks them off their equilibrium and as likely ultimately kills them as changes them. And so they are being rocked by the environment, not adapting to it.
The article's conclusions also have important implications for the notion of “fixing” the environment to protect endangered species. While it is indeed the environment causing the mutation, the resulting organism is in an altogether different environment by the time the novelty finally escapes its recessive state and expresses itself.
“You just can't do a quick fix on the environment to prevent extinction because the cause of the mutation occurred some time in the past, and you don't know what the cause of the stress was at that time,” Schwartz said.
“This new understanding of how organisms change provides us with an opportunity to forestall the damage we might cause by unthinking disruption of the environment,” added Schwartz. “The Sudden Origins theory, buttressed by modern cell biology, underscores the need to preserve the environment-not only to enhance life today, but to protect life generations from now.”
Schwartz, with his colleague Ian Tattersall, curator of anthropology at the American Museum of Natural History in New York, also authored the four-volume The Human Fossil Record (Wiley-Liss, 2002-05). Together, the volumes represent the first study of the entire human fossil record. Volume 1 was recognized by the Association of American Publishers with its Professional Scholarly Publishing Award. In 1987, Schwartz's The Red Ape: Orang-utans and Human Origin (Houghton Mifflin Company) was met with critical acclaim.
Schwartz, who also is a Pitt professor of the history and philosophy of science, was named a fellow in Pitt's Center for the Philosophy of Science and a fellow of the prestigious World Academy of Arts and Science.
The journal, The New Anatomist, is an invitation-only supplement to the Anatomical Record.
Er, no. The only way that a higher mutation rate could "assist" the expression of a mutant recessive allele is if the mutation rate is so insanely high that there's a decent chance of the exact same mutation occurring within the population within a few generations, and a mutation rate *that* high is so vastly huge that it's just as likely to destroy the original mutation as to add another one like it (not to mention making successful reproduction impossible due to mutation load).
Instead, single mutations (recessive or otherwise) actually have a counter-intuitively high chance of "fixing" in the population through chance alone. "Fixing" means that the mutation (which originally starts as a single copy in a single individual, of course) eventually reaches the point where it has not only "found" another copy of itself (in subsequent generations, due to parents producing multiple offspring with the mutation), but has actually managed to *replace* every alternate version (allele) of the same gene.
The odds of a new mutation eventually fixing in the population works out to 1/N, where N is the size of the breeding population. That's for the case where the mutation is entirely neutral (which is of course the case for recessive genes "masked" by a dominant version) - for mutations which confer a benefit, the odds of fixation are even greater, of course, because then natural selection kicks in to "help" the mutant relative to non-mutant copies of the gene.
So although it might seem intuitive that "Otherwise, of course, the recessive gene disappears after just a few generations" if it is not aided by natural selection, it actually has a decent chance of not just persisting, but of actually becoming *ubiquitous* in the population. In a breeding population of 1000 individuals, for example, a non-harmful mutation has a 0.1% chance of spreading through the entire population and replacing all "competitors", which is far higher than most people would guess (many would presume it would have an effectively zero chance of persisting, as you have).
An interesting corollary is that while the odds of any one mutation "fixing" in the population drop as the population size rises, the *number* of novel mutations per generation goes up (since there are more individuals in which mutations can occur), in a way that exactly cancels the increased "difficulty" of a particular mutation fixing. The end result is that for populations of ALL sizes, the number of new (neutral) mutations achieving fixation per generation (on average) is *exactly* equal to the rate of new mutations per individual. So for example in a breeding population of 1,000,000 individuals, if 2 new mutations occur in each individual, that's 2,000,000 new mutations per generation in the whole population, each of which has a 1/1,000,000 chance of reaching fixation by pure chance, meaning that 2 of those 2 million new mutations will eventually "take over" the whole population and become ubiquitous. And likewise for the mutations in the next generation, etc. So while a lot of mutations get "shuffled out", a significant number in every new generation always "make it" and eventually become universal in the population.
The only effect that higher mutation rates (due to stress, or whatever) will have on that is to increase the total number of new mutations in each generation (and ultimately the number of mutations which will achieve fixation), but won't increase the odds of any particular mutation "making it", because that depends *only* on population size (and in the case of beneficial mutations, on natural selection as well).
That certainly is counter-intuitive. Can you give me a readily-accessible source for that? I'm not challenging what you say, but would like to understand how that result comes about.
and, that's why I say evolution is not random, because the "survival" mechanism of a life form provides bias.
Hans Selye, endocrinologist and author of the General Adaptation Syndrome," defined stressor by the physiologic response. That was back in the 40's. Today it has been shown that stressors can be vague, diffuse (e.g., chronic anxiety) and yet be deleterious (and yet a selective pressure). Mice in a colony will kill certain others, mostly low ranking contenders for alpha status. If you watch the process carefully, you'll see the mice mob the victim and harass by posturing and hisses. The victim eventually succumbs by dying...but with not a mark of violence. Later they'll eat his carcass...the stressor? (vagal death). I could go on absurdum with examples which illustrate the essence of evolution is not found in the stressor but within the response.
So, yes, ...higher mutation rates can also be induced by more mundane environmental conditions...
Thanks for the ping!
That certainly is counter-intuitive. Can you give me a readily-accessible source for that? I'm not challenging what you say, but would like to understand how that result comes about.
Sure. I don't know what level of explanation you'd prefer, so here are several good introductions to the subject, of varying levels of detail:
Random Genetic Drift (talk.origins)Genetic Drift (Wikipedia)
Population Size and Genetic Drift (detailed math)
Genetic Drift Simulation (Java applet, simulation)
Population Genetics of Plant Pathogens: Genetic Drift (more math)
Genetic Drift (EvoWiki)
Random Genetic Drift (yet more math)
GENETIC DRIFT (mostly graphs)
It's been in The List-O-Links since yesterday, stashed away in the section called SOME LINKS DEBUNKING "YOUNG EARTH" BELIEFS.
Very neat. It somehow feels the same as a game of musical chairs. But there must be a better model.
No, he wasn't saying ANY of that. Go back and re-read....(without the blinders this time)
It would seem the Inteligent Designer is a bit red in tooth and claw.
http://www.freerepublic.com/focus/f-news/1565622/posts?page=59#59
Here's an excellent commentary from the editor of Creationsafaris regarding this study:
Heretic!
— Granville Sewall, professor of mathematics at Texas A&M University, Appendix D of textbook, The Numerical Solution of Ordinary and Partial Differential Equations, 2nd ed. (John Wiley & Sons, 2005)
Nah, it's just the thinking. Most scientists don't suffer under that burden.
I do have a theory, though. That the intelligence of the scientist is inversely proportional to the intelligence of the research subject. So you have the following partial ranking:
The "system" is set up to advance science. But any system can be abused. Note how the religious community was abused by folks like Jim Jones. But pointing that out is not an argument for eliminating religion because Jones was the exception, not the rule.
The Korean stem cell issue and the others you list are also exceptions, and should not be used to smear all of science, but only to correct it's flaws.
Ask any cop: For every guy you catch, a dozen get away with it.
Warmed over Dr. James Shapiro. These guys are years behind the good doctor, who has earned no respect from the usual suspects here.
Dr. Shapiro
http://shapiro.bsd.uchicago.edu/21st_Cent_View_Evol.html
A 21st Century View of evolution
The conventional view is that genetic change comes from stochastic, accidental sources: radiation, chemical, or oxidative damage, chemical instabilities in the DNA, or from inevitable errors in the replication process. However, the fact is that DNA proofreading and repair systems are remarkably effective at removing these non-biological sources of mutation. For example, consider that the E. coli cell replicates its 4.6 megabase genome every 40 minutes. That is a replication frequency of almost 2 kHz. Yet, due to the action of error-recognition and correction systems in the replication machine and in the cell to catch mistakes in already-replicated DNA, the error rate is reduced below one mistake in every 1010 base-pairs duplicated, and a similar low value is observed in mammalian cells (32). That is less than one base change in every 2000 cells, certainly well below the mutation frequencies I have measured in E. coli of about four mutations per every 100 to 1000 cells.
In addition to proofreading systems, cells have a wide variety of repair systems to prevent or correct DNA damage from agents that include superoxides, alkylating chemicals and irradiation (33). Some of these repair systems encode mutator DNA polymerases which are clearly the source of DNA damage-induced mutations and also appear to be the source of so-called "spontaneous" mutations that appear in the absence of an obvious source of DNA damage (34). Results illustrating the effectiveness of cellular systems for genome repair and the essential role of enzymes in mutagenesis emphasize the importance of McClintock?s revolutionary discovery of internal systems generating genome, particularly when an organism has been challenged by a stress affecting genome function (Fig. 4; 5).
McClintock recognized that genetic change is a cellular process, subject to regulation, and is not dependent on stochastic accidents. The idea of internally-generated, biologically regulated mutation has profound impacts for thinking about the process of evolution. Darwin himself acknowledged this point in later editions of Origin of Species, where he wrote about natural "sports" or "...variations which seem to us in our ignorance to arise spontaneously. It appears that I formerly underrated the frequency and value of these latter forms of variation, as leading to permanent modifications of structure independently of natural selection." (6th edition, Chapter XV, p. 395).
Readers may recall a discussion about the book "Sudden Origins" by Jeffrey Schwartz. A short review was published recently in the July issue of Trends in Genetics ("Error and Evolution" by Ian J.H. Roberts). Here are some quotations from the review. "Unfortunately, the author Jeffrey Schwartz, an accomplished paleoanthropologist, has failed to grasp in this book the fundamentals of of genetics or developmental biology; a handicap when trying to combine the recent advances in these fields with evolution."
(I love the way British writers express their criticism.) "The explanation given that crossing over between homologous chromosomes causes the small discrepencies observed in the Mendelian 3:1 ratio in hybrid crosses is again incorrect. Crossing over makes no difference to this ratio." "Readers, especially undergraduates, should proceed with caution - otherwise this book might explain the sudden origin of errors emerging in examination answers to come."
Larry Moran
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Is there any correlation between periods when the Earth's magnetic field is flipping and the rise of new species?
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