Advertisement

Evolution, Tout de Suite

Epigenetic perturbations could jump-start heritable variation.

By | October 1, 2011

A large population of Arabidopsis epigenetic recombinant inbred lines (epiRILs) growing in a common garden. FABRICE ROUX

A central tenet of evolution is that small changes in an organism’s genome can be passed on to subsequent generations. Generally, we accept that this happens through the DNA sequences: small, random mutations are inherited by offspring. Indeed, many inherited characteristics, such as fruit color, flower shape, body size, or the direction a snail’s shell whorls are encoded in genes, but they do not always obey the simple laws of Mendelian inheritance. While transposable elements, extragenomic DNA, and—as was the case for the hawkweed that tormented Gregor Mendel himself—parthenogenesis can explain some of these anomalies, recently the spotlight has fallen on another type of inheritance altogether—epigenetic modifications.

Frank Johannes at the University of Groningen in The Netherlands has been trying to understand the intricacies of epigenetic inheritance—specifically, how methylation of DNA bases can contribute to the inheritance of particular characteristics in Arabidopsis. “People are beginning to speculate,” he says. “ ‘ Wait a minute. What’s going on in nature? Does this contribute significantly to adaptation?’ ”

But it’s hard to tell in most natural populations whether inheritance is due to DNA sequence variation or epigenetic changes. “We cannot delineate these two causes very well,” Johannes says. So with his collaborator, Fabrice Roux at the University of Science and Technology in Lille, France, he has been studying a large population of Arabidopsis plants with disrupted methylation patterns. The plants were derived from two Arabidopsis parents with essentially identical genomes, but with one having a mutated DDM1 DNA methylation gene. DDM1 is required for normal methylation—the conversion of cytosine, in cytosine-guanine pairs in the DNA, into 5-methylcytosine—and its mutation reduces genomic methylation by 70 percent.

A team headed by Vincent Colot, now at the École Normale Supérieure in Paris, backcrossed the first generation offspring and selected progeny that were homozygous for the wild type DDM1 gene; in other words, with fully functional methylation machinery. They propagated the plants through a further six rounds of inbreeding, creating “epigenetic recombinant inbred lines” (epiRILs), which carried a mosaic of the parental epigenome. When Roux grew them in a common garden in northern France to subject the almost 6,000 plants to “realistic” ecological selection, they found that the epiRILs yielded plants with distinctly different phenotypes despite being effectively genetically identical.

The segregation and heritability of these traits—which included flowering time and plant height—mirrored those found in naturally divergent Arabidopsis populations, in which phenotypic variation represents adaptations to different environmental conditions. But natural populations have had thousands of years to generate these variations: the epiRILs managed to do it in just eight generations. Andrew Hudson at the University of Edinburgh says there is a clear implication that “DNA methylation and epigenetic changes are important in evolution.”

Johannes explains that there are at least two processes that can influence the epigenome: point mutations in genes that control methylation such as DDM1 that create an additional layer of variation; and environmental impacts that can influence the methylation state, which can then be inherited. New variations of plants, perhaps better adapted to a change in environment, could therefore arise much more quickly than previously thought. Research in this area is “still correlative but nevertheless very interesting,” Hudson says.

But epigenetic changes are not typically as stable as changes in DNA sequence. Some stretches of DNA do remain unmethylated for at least ten generations, Johannes says, but other sequences revert to their “wild type” methylation state due to random fluctuations, or reversion brought about by small RNAs that try to correct the defects. It may be that epigenetic changes could be reinforced by mutations in the DNA, making them stable and heritable in the conventional way. Indeed, some of the sequences affected by the DDM1 mutation are likely to be associated with the mobilization of transposable elements, which would result in immediate—and heritable—DNA sequence changes.

Another complication arises because some traits, particularly those associated with seed production, don’t seem to dabble in epigenetic inheritance. Johannes speculates that there might be an “obscure epigenetic editing process going on” that repairs disadvantageous epigenetic states for crucial genes. “You can imagine,” he says, that there’s “some sort of rescue mechanism,” particularly for gene networks that control a process as important as seed production.

In collaboration with Colot, Johannes hopes to answer such questions by performing genome-wide measurements to establish exactly which genetic elements in the genome are affected by epigenetic perturbation. He already has measurements of genome-wide methylation from more than a hundred individual plants, and is performing what he thinks is the first genome-wide epigenetic linkage study—the epigenetic equivalent of genome-wide association studies of human disease. In parallel, he wants to mathematically model the epigenetic effects and incorporate them into population genetics models, to understand dynamic inheritance patterns that cannot be explained by purely Mendelian genetics.

A Hidden Jewel refers to an article, published in a specialist journal, which has been evaluated in Faculty of 1000, a post-publication peer review service of the Science Navigation Group. Read the evaluation of Johannes’ article.

Correction (10/04/2011): The original version of this article incorrectly stated that Fabrice Roux created the epiRILs used to demonstrate the effects of methylation on the phenotypic variation that can arise in just 8 generations within a population of Arabidopsis plants grown in the same environment. In fact, a team led by Vincent Colot created the plants, and the story has been corrected to reflect this. The Scientist regrets the error.

Add a Comment

Avatar of: You

You

Processing...
Processing...

Sign In with your LabX Media Group Passport to leave a comment

Not a member? Register Now!

LabX Media Group Passport Logo

Comments

Avatar of: BaronP

Anonymous

October 5, 2011

Advanced members of the evolutionary biologist community have long described this as adaptive mutation, i.e., self-engineering to serve some immediate behavioral needs and purposes.  

Avatar of:

Posts: 0

October 5, 2011

Advanced members of the evolutionary biologist community have long described this as adaptive mutation, i.e., self-engineering to serve some immediate behavioral needs and purposes.  

Avatar of:

Posts: 0

October 5, 2011

Advanced members of the evolutionary biologist community have long described this as adaptive mutation, i.e., self-engineering to serve some immediate behavioral needs and purposes.  

Avatar of:

Posts: 0

November 18, 2011

How gratifying it is to me that biologists are coming around to addressing an issue I have had with bio-evolutionary theory for many, many years:  this issue of how any adaptation "need" may be transmitted to germ cells.  When I first studied biology, over half a century ago, I was told that the way evolution worked was that random mutations come along, and those mutations that yielded no disadvantage were tolerated in a species, whereas advantageous mutations were robustly conserved because offspring so fortunate as to inherit them were "more fit."  Not much mention was made of deleterious mutations, which are thousands of times the more likely -- today, at least -- which decrease fitness. Whether I was precocious, or just rebellious, I was NOT blinded in accepting the given wisdom by any non-scientific dogma.  As I accumulated a little more, and a little more, received wisdom, I was told that germ line cells are sequestered in a sexually perpetuated species, and behave according to their own segregated perpetuation dynamic.  That suggested to me that if the somatic cells mutate in any way, that is not what is passed on to offspring, because that would violate the principle of non-transmission of acquired characteristics.

So, okay, I reasoned, how, then, if a mutation is passed on to offspring that are independent from, and unaffected by, somatic cells, then all mutations that will make any difference WHATSOEVER in what gets passed on to offspring, are totally oblivious and unresponsive to anything that happens to the rest of the body.  Right?  Okay, if I were to buy that story carte blanch, then evolution of a species, insofar as experience of the whole organism is involved, is totally controlled by nothing other than whether a parent survives to reproductive age. The changes are germ line accidents. (And, sorry, but Dawkins strikes me as having failed in providing any explanation for any connection between experience and his suggested "will" of a selfish gene to adapt. For he showed no CONNECTION whereby one's gene either know, or give a damn. And without some connection, no number of books for the gullible anti-theist explain anything one way or another. No mechanism, not explanation. Empty words.)

But, anyhow, the waters of the proactive kind of connection IMPLIED (yet nowhere stated nor supported by any genetic mechanism taught me) were muddied by my being taught that most mutations are deleterious and decrease any current or future "fitness."  Also, the bulk of all mutations, if they are TOTALLY RANDOM, have nothing to do with what KIND of characteristic comes from a mutation.  To view this from another direction, totally random mutations would have zero "targeting capacity" insofar as coming up with any pure chance mutation that would be "adaptation appropriate."  The theory, in short, held then (as it seems to many to hold even today) that all species who have increase their fitness for these many, many millennia just won a veritable MUTATION LOTTERY time after time after time after time...  They just HAPPENED to come up with a pure chance, random mutation in their germ cells (okay, in the capacity of their germ cells to produce a "useful" characteristic at best, and a non-deleterious characteristic at second best.  Only those pure chance TOLERATED non-beneficial RNA or DNA mutations were, in a sense, more important in the LONG TERM than the ones immediately beneficial.  Why?  Well there are such things as long, long, long transduction paths in physiology that would not have worked effectively or efficiently (at least not as they do now) in having any other arrangement than the highly complex and ORDER-CONSTRAINED set-up than they now have.

As always, theoretical evo biologists were able to rationalize along the thought lines of, well since we KNOW the theory cannot be flawed, we KNOW accordingly that there has to be some explanation.  Theory, as it were, constrains the way things are and, consequently, what must somehow be proved through "scientific" testing.  And, a good rationale for how PHYSIOLOGICAL TRANSDUCTION SEQUENCES had to have (unless the theory was flawed) been useful for some other purpose, at every step of the way.  My problem with that was that it already seemed, even absent that theory rationalization, that species had to have been immensely fortunate to have won the germ line mutation lottery a time after time after time... as if I were to go to a crap table in a casino and roll a seven... or, okay, my SPECIES all went to the casino, and at least some of us rolled a seven, in at least a sufficient proportion of generations for a few million years.

Okay.  Probability doesn't rule that out I guess.  But at THIS juncture I was, if I was to be an open-minded and cooperative student (formal or otherwise) that to this already seemingly strained belief that such a series of lottery winnings occurred by the coming up with single mutations... each of the interstitial mutations resulting in an enormously complex and many-faceted physiological transduction sequence today ALSO had to pass through -- now get this -- one immediately beneficial stage of mutational change, after another beneficial stage, after another, after another, after another...  In other words, it didn't have to just come up with a single mutation that yielded an advantage but rather, had to come up with a useful new progressive change to an increasingly complex set.  And, mind you, not only does the mathematical probability of such a fortuitous add-on or deletion or re-ordering have to increase fitness (as in produce offspring that are better able to cope than their predecessors, but better able than their contemporaries.  Wow!  That increases the number of required lottery winnings exponentially, doesn't it!

Now, lest any evo-biology theorist think I am non-scientific.  Think on.  The feeling is mutual.  But let me qualify that.  I am NOT saying Darwin was unobservant.  I am NOT saying science does not have to come up with rationalizations (theories) as WORKING HYPOTHESES.  I have done much reading about the history of science, and totally appreciate, for example, Thomas Kuhn's observations about "revolutions" in science, and about how thoroughly useful it is in science for a paradigm to emerge, for anomalies such as those implied above to be played down, for scientists to have some kind of consensus in order to have something to test to come up with more anomalies, to begin to recognize them as indicative of the need for a NEW IMPROVED paradigm... and ultimately along comes a great synthesist who takes the puzzle (the affirmative test results AND the anomalies both) and puts the puzzle together in a way that MORE pieces fit than are seen to fit the older model.

I git it.  The question that haunts me, however, is "Do educators and other apologists for the current "narrative framing" of bio-evolutionary theory git it, too? 

And THIS brings me to how refreshing it is, for me, that some one (or some several?) are looking for MECHANISMS whereby epigenetic experience can somehow operate INTERACTIVELY with environment in such a way as to influence what the germ line cells may come up with that is not as PURELY RANDOM as waling into a casino and breaking the bank by such things as winning more rounds of the games than the probabilities of pure chance would suffice to explain that is even remotely "scientific."

Even this article speaks of epigenetics as though the germ-line cells are coincidental, or all inclusive in the "game play." 

Unlike a dogmatic objector, I am one who WELCOMES any and all NON-DOGMATIC effort to recognize, accept, and seek after... answers as to how in blazes species have beat mere odds of chance mutation in germ line RNA and DNA.  If anyone is dogmatic and closed minded, it is a person inside or outside the science professions who is so committed to a paradigm or a theoretical model that he/she would view someone who challenges it as the one who is dogmatic. 

Just as would the owner of a casino, if someone were to come in and beat the arithmetic odds against winning in blackjack, and I could find nothing in the game plan that enables him/her to do that "by the rules," I would be highly interested in how that person is "gaming the game."  (I know a man who got barred from every casino in America, but after winning more than a million by card counting.  Nowadays multiple decks are used.  But he is still barred.  But he invested that million by becoming a venture capitalist investor.  He is endowed with an eidetic memory, and has good money-judgement to boot.  But, you see, THERE'S THE MECHANISM.  That man has NOT gotten where he is today by being lucky.  He has done so by CHANGING the odds.

Now if I've made that clear, let me argue that sexually-reproducing species ALSO have had to change the odds by some mechanism or mechanisms, too. 

Want a fancy sensationalist name for it?  Okay, in reference to the Higgs particle in particle physics, someone called it "the God particle."  It appears more likely the Higgs particle will not be the last one found (to complex to explain the reasoning on that here).  Maybe you could call the mechanism whereby the history of bio-evolution (not the theory, but the actual occurrence we barely have any understanding of as yet) the "God mechanism."  But, no, that might give someone the notion you were one of those dogmatists you and I know to be non-scientific in their reasoning.  Maybe we could just call it the biggest most glaringly obvious un-answer, to date, to the question of how species PROACTIVELY alter the odds against mutating themselves to death without coming up with effective adaptive changes in the time allowed for them to do so without perishing.

Avatar of:

Posts: 0

November 18, 2011

How gratifying it is to me that biologists are coming around to addressing an issue I have had with bio-evolutionary theory for many, many years:  this issue of how any adaptation "need" may be transmitted to germ cells.  When I first studied biology, over half a century ago, I was told that the way evolution worked was that random mutations come along, and those mutations that yielded no disadvantage were tolerated in a species, whereas advantageous mutations were robustly conserved because offspring so fortunate as to inherit them were "more fit."  Not much mention was made of deleterious mutations, which are thousands of times the more likely -- today, at least -- which decrease fitness. Whether I was precocious, or just rebellious, I was NOT blinded in accepting the given wisdom by any non-scientific dogma.  As I accumulated a little more, and a little more, received wisdom, I was told that germ line cells are sequestered in a sexually perpetuated species, and behave according to their own segregated perpetuation dynamic.  That suggested to me that if the somatic cells mutate in any way, that is not what is passed on to offspring, because that would violate the principle of non-transmission of acquired characteristics.

So, okay, I reasoned, how, then, if a mutation is passed on to offspring that are independent from, and unaffected by, somatic cells, then all mutations that will make any difference WHATSOEVER in what gets passed on to offspring, are totally oblivious and unresponsive to anything that happens to the rest of the body.  Right?  Okay, if I were to buy that story carte blanch, then evolution of a species, insofar as experience of the whole organism is involved, is totally controlled by nothing other than whether a parent survives to reproductive age. The changes are germ line accidents. (And, sorry, but Dawkins strikes me as having failed in providing any explanation for any connection between experience and his suggested "will" of a selfish gene to adapt. For he showed no CONNECTION whereby one's gene either know, or give a damn. And without some connection, no number of books for the gullible anti-theist explain anything one way or another. No mechanism, not explanation. Empty words.)

But, anyhow, the waters of the proactive kind of connection IMPLIED (yet nowhere stated nor supported by any genetic mechanism taught me) were muddied by my being taught that most mutations are deleterious and decrease any current or future "fitness."  Also, the bulk of all mutations, if they are TOTALLY RANDOM, have nothing to do with what KIND of characteristic comes from a mutation.  To view this from another direction, totally random mutations would have zero "targeting capacity" insofar as coming up with any pure chance mutation that would be "adaptation appropriate."  The theory, in short, held then (as it seems to many to hold even today) that all species who have increase their fitness for these many, many millennia just won a veritable MUTATION LOTTERY time after time after time after time...  They just HAPPENED to come up with a pure chance, random mutation in their germ cells (okay, in the capacity of their germ cells to produce a "useful" characteristic at best, and a non-deleterious characteristic at second best.  Only those pure chance TOLERATED non-beneficial RNA or DNA mutations were, in a sense, more important in the LONG TERM than the ones immediately beneficial.  Why?  Well there are such things as long, long, long transduction paths in physiology that would not have worked effectively or efficiently (at least not as they do now) in having any other arrangement than the highly complex and ORDER-CONSTRAINED set-up than they now have.

As always, theoretical evo biologists were able to rationalize along the thought lines of, well since we KNOW the theory cannot be flawed, we KNOW accordingly that there has to be some explanation.  Theory, as it were, constrains the way things are and, consequently, what must somehow be proved through "scientific" testing.  And, a good rationale for how PHYSIOLOGICAL TRANSDUCTION SEQUENCES had to have (unless the theory was flawed) been useful for some other purpose, at every step of the way.  My problem with that was that it already seemed, even absent that theory rationalization, that species had to have been immensely fortunate to have won the germ line mutation lottery a time after time after time... as if I were to go to a crap table in a casino and roll a seven... or, okay, my SPECIES all went to the casino, and at least some of us rolled a seven, in at least a sufficient proportion of generations for a few million years.

Okay.  Probability doesn't rule that out I guess.  But at THIS juncture I was, if I was to be an open-minded and cooperative student (formal or otherwise) that to this already seemingly strained belief that such a series of lottery winnings occurred by the coming up with single mutations... each of the interstitial mutations resulting in an enormously complex and many-faceted physiological transduction sequence today ALSO had to pass through -- now get this -- one immediately beneficial stage of mutational change, after another beneficial stage, after another, after another, after another...  In other words, it didn't have to just come up with a single mutation that yielded an advantage but rather, had to come up with a useful new progressive change to an increasingly complex set.  And, mind you, not only does the mathematical probability of such a fortuitous add-on or deletion or re-ordering have to increase fitness (as in produce offspring that are better able to cope than their predecessors, but better able than their contemporaries.  Wow!  That increases the number of required lottery winnings exponentially, doesn't it!

Now, lest any evo-biology theorist think I am non-scientific.  Think on.  The feeling is mutual.  But let me qualify that.  I am NOT saying Darwin was unobservant.  I am NOT saying science does not have to come up with rationalizations (theories) as WORKING HYPOTHESES.  I have done much reading about the history of science, and totally appreciate, for example, Thomas Kuhn's observations about "revolutions" in science, and about how thoroughly useful it is in science for a paradigm to emerge, for anomalies such as those implied above to be played down, for scientists to have some kind of consensus in order to have something to test to come up with more anomalies, to begin to recognize them as indicative of the need for a NEW IMPROVED paradigm... and ultimately along comes a great synthesist who takes the puzzle (the affirmative test results AND the anomalies both) and puts the puzzle together in a way that MORE pieces fit than are seen to fit the older model.

I git it.  The question that haunts me, however, is "Do educators and other apologists for the current "narrative framing" of bio-evolutionary theory git it, too? 

And THIS brings me to how refreshing it is, for me, that some one (or some several?) are looking for MECHANISMS whereby epigenetic experience can somehow operate INTERACTIVELY with environment in such a way as to influence what the germ line cells may come up with that is not as PURELY RANDOM as waling into a casino and breaking the bank by such things as winning more rounds of the games than the probabilities of pure chance would suffice to explain that is even remotely "scientific."

Even this article speaks of epigenetics as though the germ-line cells are coincidental, or all inclusive in the "game play." 

Unlike a dogmatic objector, I am one who WELCOMES any and all NON-DOGMATIC effort to recognize, accept, and seek after... answers as to how in blazes species have beat mere odds of chance mutation in germ line RNA and DNA.  If anyone is dogmatic and closed minded, it is a person inside or outside the science professions who is so committed to a paradigm or a theoretical model that he/she would view someone who challenges it as the one who is dogmatic. 

Just as would the owner of a casino, if someone were to come in and beat the arithmetic odds against winning in blackjack, and I could find nothing in the game plan that enables him/her to do that "by the rules," I would be highly interested in how that person is "gaming the game."  (I know a man who got barred from every casino in America, but after winning more than a million by card counting.  Nowadays multiple decks are used.  But he is still barred.  But he invested that million by becoming a venture capitalist investor.  He is endowed with an eidetic memory, and has good money-judgement to boot.  But, you see, THERE'S THE MECHANISM.  That man has NOT gotten where he is today by being lucky.  He has done so by CHANGING the odds.

Now if I've made that clear, let me argue that sexually-reproducing species ALSO have had to change the odds by some mechanism or mechanisms, too. 

Want a fancy sensationalist name for it?  Okay, in reference to the Higgs particle in particle physics, someone called it "the God particle."  It appears more likely the Higgs particle will not be the last one found (to complex to explain the reasoning on that here).  Maybe you could call the mechanism whereby the history of bio-evolution (not the theory, but the actual occurrence we barely have any understanding of as yet) the "God mechanism."  But, no, that might give someone the notion you were one of those dogmatists you and I know to be non-scientific in their reasoning.  Maybe we could just call it the biggest most glaringly obvious un-answer, to date, to the question of how species PROACTIVELY alter the odds against mutating themselves to death without coming up with effective adaptive changes in the time allowed for them to do so without perishing.

Avatar of: Guest

Anonymous

November 18, 2011

How gratifying it is to me that biologists are coming around to addressing an issue I have had with bio-evolutionary theory for many, many years:  this issue of how any adaptation "need" may be transmitted to germ cells.  When I first studied biology, over half a century ago, I was told that the way evolution worked was that random mutations come along, and those mutations that yielded no disadvantage were tolerated in a species, whereas advantageous mutations were robustly conserved because offspring so fortunate as to inherit them were "more fit."  Not much mention was made of deleterious mutations, which are thousands of times the more likely -- today, at least -- which decrease fitness. Whether I was precocious, or just rebellious, I was NOT blinded in accepting the given wisdom by any non-scientific dogma.  As I accumulated a little more, and a little more, received wisdom, I was told that germ line cells are sequestered in a sexually perpetuated species, and behave according to their own segregated perpetuation dynamic.  That suggested to me that if the somatic cells mutate in any way, that is not what is passed on to offspring, because that would violate the principle of non-transmission of acquired characteristics.

So, okay, I reasoned, how, then, if a mutation is passed on to offspring that are independent from, and unaffected by, somatic cells, then all mutations that will make any difference WHATSOEVER in what gets passed on to offspring, are totally oblivious and unresponsive to anything that happens to the rest of the body.  Right?  Okay, if I were to buy that story carte blanch, then evolution of a species, insofar as experience of the whole organism is involved, is totally controlled by nothing other than whether a parent survives to reproductive age. The changes are germ line accidents. (And, sorry, but Dawkins strikes me as having failed in providing any explanation for any connection between experience and his suggested "will" of a selfish gene to adapt. For he showed no CONNECTION whereby one's gene either know, or give a damn. And without some connection, no number of books for the gullible anti-theist explain anything one way or another. No mechanism, not explanation. Empty words.)

But, anyhow, the waters of the proactive kind of connection IMPLIED (yet nowhere stated nor supported by any genetic mechanism taught me) were muddied by my being taught that most mutations are deleterious and decrease any current or future "fitness."  Also, the bulk of all mutations, if they are TOTALLY RANDOM, have nothing to do with what KIND of characteristic comes from a mutation.  To view this from another direction, totally random mutations would have zero "targeting capacity" insofar as coming up with any pure chance mutation that would be "adaptation appropriate."  The theory, in short, held then (as it seems to many to hold even today) that all species who have increase their fitness for these many, many millennia just won a veritable MUTATION LOTTERY time after time after time after time...  They just HAPPENED to come up with a pure chance, random mutation in their germ cells (okay, in the capacity of their germ cells to produce a "useful" characteristic at best, and a non-deleterious characteristic at second best.  Only those pure chance TOLERATED non-beneficial RNA or DNA mutations were, in a sense, more important in the LONG TERM than the ones immediately beneficial.  Why?  Well there are such things as long, long, long transduction paths in physiology that would not have worked effectively or efficiently (at least not as they do now) in having any other arrangement than the highly complex and ORDER-CONSTRAINED set-up than they now have.

As always, theoretical evo biologists were able to rationalize along the thought lines of, well since we KNOW the theory cannot be flawed, we KNOW accordingly that there has to be some explanation.  Theory, as it were, constrains the way things are and, consequently, what must somehow be proved through "scientific" testing.  And, a good rationale for how PHYSIOLOGICAL TRANSDUCTION SEQUENCES had to have (unless the theory was flawed) been useful for some other purpose, at every step of the way.  My problem with that was that it already seemed, even absent that theory rationalization, that species had to have been immensely fortunate to have won the germ line mutation lottery a time after time after time... as if I were to go to a crap table in a casino and roll a seven... or, okay, my SPECIES all went to the casino, and at least some of us rolled a seven, in at least a sufficient proportion of generations for a few million years.

Okay.  Probability doesn't rule that out I guess.  But at THIS juncture I was, if I was to be an open-minded and cooperative student (formal or otherwise) that to this already seemingly strained belief that such a series of lottery winnings occurred by the coming up with single mutations... each of the interstitial mutations resulting in an enormously complex and many-faceted physiological transduction sequence today ALSO had to pass through -- now get this -- one immediately beneficial stage of mutational change, after another beneficial stage, after another, after another, after another...  In other words, it didn't have to just come up with a single mutation that yielded an advantage but rather, had to come up with a useful new progressive change to an increasingly complex set.  And, mind you, not only does the mathematical probability of such a fortuitous add-on or deletion or re-ordering have to increase fitness (as in produce offspring that are better able to cope than their predecessors, but better able than their contemporaries.  Wow!  That increases the number of required lottery winnings exponentially, doesn't it!

Now, lest any evo-biology theorist think I am non-scientific.  Think on.  The feeling is mutual.  But let me qualify that.  I am NOT saying Darwin was unobservant.  I am NOT saying science does not have to come up with rationalizations (theories) as WORKING HYPOTHESES.  I have done much reading about the history of science, and totally appreciate, for example, Thomas Kuhn's observations about "revolutions" in science, and about how thoroughly useful it is in science for a paradigm to emerge, for anomalies such as those implied above to be played down, for scientists to have some kind of consensus in order to have something to test to come up with more anomalies, to begin to recognize them as indicative of the need for a NEW IMPROVED paradigm... and ultimately along comes a great synthesist who takes the puzzle (the affirmative test results AND the anomalies both) and puts the puzzle together in a way that MORE pieces fit than are seen to fit the older model.

I git it.  The question that haunts me, however, is "Do educators and other apologists for the current "narrative framing" of bio-evolutionary theory git it, too? 

And THIS brings me to how refreshing it is, for me, that some one (or some several?) are looking for MECHANISMS whereby epigenetic experience can somehow operate INTERACTIVELY with environment in such a way as to influence what the germ line cells may come up with that is not as PURELY RANDOM as waling into a casino and breaking the bank by such things as winning more rounds of the games than the probabilities of pure chance would suffice to explain that is even remotely "scientific."

Even this article speaks of epigenetics as though the germ-line cells are coincidental, or all inclusive in the "game play." 

Unlike a dogmatic objector, I am one who WELCOMES any and all NON-DOGMATIC effort to recognize, accept, and seek after... answers as to how in blazes species have beat mere odds of chance mutation in germ line RNA and DNA.  If anyone is dogmatic and closed minded, it is a person inside or outside the science professions who is so committed to a paradigm or a theoretical model that he/she would view someone who challenges it as the one who is dogmatic. 

Just as would the owner of a casino, if someone were to come in and beat the arithmetic odds against winning in blackjack, and I could find nothing in the game plan that enables him/her to do that "by the rules," I would be highly interested in how that person is "gaming the game."  (I know a man who got barred from every casino in America, but after winning more than a million by card counting.  Nowadays multiple decks are used.  But he is still barred.  But he invested that million by becoming a venture capitalist investor.  He is endowed with an eidetic memory, and has good money-judgement to boot.  But, you see, THERE'S THE MECHANISM.  That man has NOT gotten where he is today by being lucky.  He has done so by CHANGING the odds.

Now if I've made that clear, let me argue that sexually-reproducing species ALSO have had to change the odds by some mechanism or mechanisms, too. 

Want a fancy sensationalist name for it?  Okay, in reference to the Higgs particle in particle physics, someone called it "the God particle."  It appears more likely the Higgs particle will not be the last one found (to complex to explain the reasoning on that here).  Maybe you could call the mechanism whereby the history of bio-evolution (not the theory, but the actual occurrence we barely have any understanding of as yet) the "God mechanism."  But, no, that might give someone the notion you were one of those dogmatists you and I know to be non-scientific in their reasoning.  Maybe we could just call it the biggest most glaringly obvious un-answer, to date, to the question of how species PROACTIVELY alter the odds against mutating themselves to death without coming up with effective adaptive changes in the time allowed for them to do so without perishing.

Avatar of: primativewriter

primativewriter

Posts: 22

November 20, 2011

how much did this search cost?

Avatar of:

Posts: 0

November 20, 2011

how much did this search cost?

Avatar of:

Posts: 0

November 20, 2011

how much did this search cost?

Follow The Scientist

icon-facebook icon-linkedin icon-twitter icon-vimeo icon-youtube
Advertisement

Stay Connected with The Scientist

  • icon-facebook The Scientist Magazine
  • icon-facebook The Scientist Careers
  • icon-facebook Neuroscience Research Techniques
  • icon-facebook Genetic Research Techniques
  • icon-facebook Cell Culture Techniques
  • icon-facebook Microbiology and Immunology
  • icon-facebook Cancer Research and Technology
  • icon-facebook Stem Cell and Regenerative Science
Advertisement
Thermo Scientific
Thermo Scientific
Advertisement
Mettler Toledo
Mettler Toledo
Life Technologies