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Author Topic: How big a role does the epigenome play in evolution?  (Read 56090 times)

Offline echochartruse

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Re: How big a role does the epigenome play in evolution?
« Reply #50 on: 02/04/2010 06:17:29 »
Quote from: http://www.ncbi.nlm.nih.gov/pubmed/20216571
Evidence that disease-induced population decline changes genetic structure and alters dispersal patterns in the Tasmanian devil.

Lachish S, Miller KJ, Storfer A, Goldizen AW, Jones ME.

School of Biological Sciences, University of Queensland, St Lucia, Brisbane, Queensland, Australia.

Infectious disease has been shown to be a major cause of population declines in wild animals. However, there remains little empirical evidence on the genetic consequences of disease-mediated population declines, or how such perturbations might affect demographic processes such as dispersal. Devil facial tumour disease (DFTD) has resulted in the rapid decline of the Tasmanian devil, Sarcophilus harrisii, and threatens to cause extinction. Using 10 microsatellite DNA markers, we compared genetic diversity and structure before and after DFTD outbreaks in three Tasmanian devil populations to assess the genetic consequences of disease-induced population decline. We also used both genetic and demographic data to investigate dispersal patterns in Tasmanian devils along the east coast of Tasmania. We observed a significant increase in inbreeding (F(IS) pre/post-disease -0.030/0.012, P<0.05; relatedness pre/post-disease 0.011/0.038, P=0.06) in devil populations after just 2-3 generations of disease arrival, but no detectable change in genetic diversity. Furthermore, although there was no subdivision apparent among pre-disease populations (theta=0.005, 95% confidence interval (CI) -0.003 to 0.017), we found significant genetic differentiation among populations post-disease (theta=0.020, 0.010-0.027), apparently driven by a combination of selection and altered dispersal patterns of females in disease-affected populations. We also show that dispersal is male-biased in devils and that dispersal distances follow a typical leptokurtic distribution. Our results show that disease can result in genetic and demographic changes in host populations over few generations and short time scales. Ongoing management of Tasmanian devils must now attempt to maintain genetic variability in this species through actions designed to reverse the detrimental effects of inbreeding and subdivision in disease-affected populations.Heredity advance online publication, 10 March 2010; doi:10.1038/hdy.2010.17.

PMID: 20216571 [PubMed - as supplied by publisher]

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Offline echochartruse

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Re: How big a role does the epigenome play in evolution?
« Reply #51 on: 02/04/2010 06:26:02 »
If epigenomic markers actually allow life to direct mutation to any extent whatsoever, would that qualify as "intelligent design"?

If any process (epigentics)is involved rather than 'random change', you would think there is some 'intelligents'about it?

I think so.
 

Offline JP

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Re: How big a role does the epigenome play in evolution?
« Reply #52 on: 02/04/2010 16:45:53 »
echochartruse, I think the main point is still this:
Quote from: http://www.time.com/time/health/article/0,8599,1951968,00.html
"You're going to have the same chip in there, the same genome, but different software. And the outcome is a different cell type."

Maybe I'm missing something obvious, but I can't find a point in any of those sources that says that epigenetics are causing genetic mutations.
 

Offline norcalclimber

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Re: How big a role does the epigenome play in evolution?
« Reply #53 on: 02/04/2010 19:17:56 »
echochartruse, I think the main point is still this:
Quote from: http://www.time.com/time/health/article/0,8599,1951968,00.html
"You're going to have the same chip in there, the same genome, but different software. And the outcome is a different cell type."


Maybe I'm missing something obvious, but I can't find a point in any of those sources that says that epigenetics are causing genetic mutations.

To be honest, I can't find anything in them about epigenetics causing genetic mutations.  I still haven't had a chance to put together a decent post with a lot of sources(hopefully later today), but I haven't seen anywhere that said epigenetics for sure caused genetic mutation.  My support comes from the evidence that some form of directed mutation exists, and I think logically epigenetics is the likely culprit.  Here is a quick example of the types of things I will post later today:

http://www.pnas.org/content/88/13/5882.full.pdf

Abstract: A previous study has demonstrated that
adaptive missense mutations occur in the tip operon of Escherichia
coli. In this study it is shown that, under conditions of
intense selection, a strain carrying missense mutations in both
trpA and trpB reverts to Trp+ 108 times more frequently than
would be expected if the two mutations were the result of
independent events. Comparison of the single mutation rates
with the double mutation rate and information obtained by
sequencing DNA from double revertants show that neither our
classical understanding of spontaneous mutation processes nor
extant models for adaptive mutations can account for all of the
observations. Despite a current lack of mechanistic understanding,
it is clear that adaptive mutations can permit advantageous
phenotypes that require multiple mutations to arise
and that they appear enormously more frequently than would
be expected.
« Last Edit: 02/04/2010 19:28:41 by norcalclimber »
 

Offline echochartruse

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Re: How big a role does the epigenome play in evolution?
« Reply #54 on: 02/04/2010 23:08:03 »
Quote from: http://www.ncbi.nlm.nih.gov/pubmed/20216571
Evidence that disease-induced population decline changes genetic structure and alters dispersal patterns in the Tasmanian devil.

Lachish S, Miller KJ, Storfer A, Goldizen AW, Jones ME.

School of Biological Sciences, University of Queensland, St Lucia, Brisbane, Queensland, Australia.

............. Our results show that disease can result in genetic and demographic changes in host populations over few generations and short time scales.........

PMID: 20216571 [PubMed - as supplied by publisher]

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They must be wrong then
 

Offline norcalclimber

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Re: How big a role does the epigenome play in evolution?
« Reply #55 on: 02/04/2010 23:59:57 »
I'm not sure that this really supports directed mutation by epigenetic causation.  I can see how it is talking about evolution, but what it is saying doesn't really seem surprising, nor different from what has been previously thought.  If I am misunderstanding, please explain.
Quote from: http://www.ncbi.nlm.nih.gov/pubmed/20216571
Evidence that disease-induced population decline changes genetic structure and alters dispersal patterns in the Tasmanian devil.

Lachish S, Miller KJ, Storfer A, Goldizen AW, Jones ME.

School of Biological Sciences, University of Queensland, St Lucia, Brisbane, Queensland, Australia.

............. Our results show that disease can result in genetic and demographic changes in host populations over few generations and short time scales.........

PMID: 20216571 [PubMed - as supplied by publisher]

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They must be wrong then
 

Offline echochartruse

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Re: How big a role does the epigenome play in evolution?
« Reply #56 on: 03/04/2010 05:27:30 »
In my words...... Tassie Devil's genetics, prior to the toxins in their water, were all the same throughout their species. After the toxins from the mono culture effected their water, their genetics changed over 2-3 generations to cope with the toxins and to survive and reproduce.

So if you go to the zoo where these animals are kept away from the toxins, you will find their genes are different from the ones in the wild.

The toxins are not leaving their water system any time in the near future, so if they continue to breed their genes will be passed down throughout many generations. While the captive Tassie Devils reproduce without the altered genes.

1.Cancer is an epigentic disease characterised by the break down of DNA.
2.Prior to the environmental change all the Tassie Devils genes were the same.
3. No change in Tassie Devil's genes in zoos or that have never come in contact with the toxic environment.
4. It took 2-3 generations for the environment to effect change in their genes.
5. If the captured, zoo's Tassie devils were released and returned to their native environment they would not survive. Their environment has directly effected their evolution.
6. As I believe, if the ones in the zoos continue to reproduce together without bringing in the new genes from their wild counterparts then 2 distinct species of Tassie Devils may occur over time. One group unable to live/reproduce/survive in it's natural habitat.
Survival of the fittest!

Anyway this example was for JP, to show that epigentics does change genes.
« Last Edit: 03/04/2010 05:38:07 by echochartruse »
 

Offline Geezer

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Re: How big a role does the epigenome play in evolution?
« Reply #57 on: 03/04/2010 06:28:54 »
Tassie Devil's genetics, prior to the toxins in their water, were all the same throughout their species. After the toxins from the mono culture effected their water, their genetics changed over 2-3 generations to cope with the toxins and to survive and reproduce.

That is truly remarkable. If I understand what you are saying;

a) All Tasmanian Devils had identical genes.

b) The Tasmanian Devils that were subjected to toxins in their water showed significant changes in their genes in two to three generations.

Did I get that right?
 

Offline norcalclimber

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Re: How big a role does the epigenome play in evolution?
« Reply #58 on: 03/04/2010 07:19:25 »
Here is a few more examples which I feel indicate epigenetics causing mutation:

http://www.gate.net/~rwms/EvoMutations.html

In the section about exotic 5 carbon sugars we see a possible example of an overall mutation which may have started off with an epigenetic mutation, then had a genetic mutation, then had an epigenetic mutation (the author doesn't attribute epigenetics, merely states what effects occurred)
Quote

"Some five carbon sugars are very rare in nature, so very few organisms have the ability to use these exotic compounds in their metabolism. Robert Mortlock determined that the bacteria Klebsiella aerogenes was not immediately able to metabolize D-arabinose and xylitol by growing strains in media containing those compounds and noting the strains that were able to grow only after a lag time. This indicated that the original strain did not have the ability to process the compounds, but was able to evolve such a capability. Mortlock then went on to see how this capability was evolved.

In the case of D-arabinose, Mortlock showed that the arabinose could be utilized if it could be converted to D-ribulose by an enzyme (an isomerase). Unfortunately, K. aerogenes has no such isomerase for the conversion of D-arabinose. However, the isomerase for L-fucose has a low activity for D-arabinose.   But, the bad news is that the L-fucose isomerase is normally produced only when the cell is exposed to fucose. Nonetheless, in a few individuals, mutations occurred that allowed the fucose isomerase to be produced at all times - not just when L-fucose is present. This is normally a bad thing and would be selected against because it wastes the cells resources by constantly producing an unneeded enzyme. In this situation though, the mutation is a very good thing, and allows the cell to survive because it can now metabolize arabinose (albeit rather poorly). Although production of the fucose isomerase has been deregulated, the structure of the isomerase itself has not been changed. The next mutation was a change to the isomerase to make it more effective in the conversion of arabitol to ribulose. Finally (although I can't tell from Bell's description if this was actually done in the experiments), the culture could be selected to regain control of the expression of the isomerase - so that it is produced only when arabitol is present. "

It seems to me that perhaps the initial mutation which caused the isomerase for fucose to be produced without fucose present may have been epigenetic.  The next mutation seems to have been a genetic mutation which made the isomerase more efficient.  The final mutation seems to have been epigenetic again, to only produce the new isomerase when arabinose is present.

I am going off a limited understanding of the experiments involved, but it seems as if the bacteria was able to accomplish these mutations very quickly.

In another section of that page, we see this example of beneficial mutation(emphasis mine):

Quote
5.) Evidence of genetic divergence and beneficial mutations in bacteria after 10,000 generations
 

    Papadopoulos, D., Schneider, D., Meier-Eiss, J., Arber, W., Lenski, R. E., Blot, M. (1999). Genomic evolution during a 10,000-generation
    experiment with bacteria. Proc. Natl. Acad. Sci. U. S. A. 96: 3807-3812

    Edited by John R. Roth, University of Utah, Salt Lake City, UT, and approved February 3, 1999 (received for review July 21, 1998)

    Molecular methods are used widely to measure genetic diversity within populations and determine relationships among species. However, it is difficult to observe genomic evolution in action because these dynamics are too slow in most organisms. To overcome this limitation, we sampled genomes from populations of Escherichia coli evolving in the laboratory for 10,000 generations. We analyzed the genomes for restriction fragment length polymorphisms (RFLP) using seven insertion sequences (IS) as probes; most polymorphisms detected by this approach reflect rearrangements (including transpositions) rather than point mutations. The evolving genomes became increasingly different from their ancestor over time. Moreover, tremendous diversity accumulated within each population, such that almost every individual had a different genetic fingerprint after 10,000 generations. As has been often suggested, but not previously shown by experiment, the rates of phenotypic and genomic change were discordant, both across replicate populations and over time within a population. Certain pivotal mutations were shared by all descendants in a population, and these are candidates for beneficial mutations, which are rare and difficult to find. More generally, these data show that the genome is highly dynamic even over a time scale that is, from an evolutionary perspective, very brief.

The fact that each individual cell had its own genetic fingerprint, yet the pivotal mutations were shared by all descendants seems significant.

More from the same page:

Quote
4.) Adaptation to a Low Phosphate Chemostat Environment by a Clonal Line of Yeast
 

    P.E. Hansche and J.C. Francis set up chemosats to allow evolution of a single clonal line of beer yeast in a phosphate limited (due to high pH) environment. (A chemostat is a device that allows the propagation of microorganisms in an extremely constant environment.) The yeast clones grew slowly for about the first 180 generations when there was an abrupt increase in population density. This was later shown to be due to  better assimilation of the phosphate, presumably due to an improvement in the permease molecule. (Permease is an enzyme that controls what is allowed to come into the cell through the yeast's cell membrane.) After about 400 generations, a second improvement in cell growth rates occurred because of a mutation to the yeast's phosphatase (an enzyme that improves the cells ability to use phosphate). The phosphatase became more active overall, and its optimal pH (the pH where it is most active) was raised.  Finally, a third mutant appeared after 800 generations that caused the yeast cells to clump. This raised the population density in the chemostat because individual cells were no longer being washed out of chemostat (which is one of the methods that the chemostat uses to maintain very uniform conditions) as quickly as they had prior to the mutation. (This is just speculation on my part, but I wonder if it wasn't under some similar conditions that multi-cellularity became favored over unicellularity - perhaps on a sea bed or river bottom.)

    This experiment was repeated, and the same mutations occurred, but in different orders. Also, in one replication, the processing of phosphate was improved by a duplication of the gene that produces phosphatase. This is experimental evidence of an extremely important mechanism in evolutionary history! It is also a particularly elegant experiment because not only was all of this adaptation shown to occur in clonal lines (descended from a single individual), but the authors also determined the exact mutations that caused the improved adaptations by sequencing the genes and proteins involved.

    Francis, J.E., & Hansche, P.E. (1972) Directed evolution of metabolic pathways in microbial populations. I. Modification of the acid phosphatase pH optimum in Saccharaomyces cervisiae. Genetics, 70: 59-73.

    Francis, J.E., & Hansche, P.E. (1973) Directed evolution of metabolic pathways in microbial populations. II. A repeatable adaptation in Saccharaomyces cervisiae. Genetics, 74:259-265.

    Hansche, P.E. (1975) Gene duplication as a mechanism of genetic adaptation in Saccharaomyces cervisiae. Genetics, 79: 661-674.



These seem to be describing abrupt mutations which occur to a lot of the population at once, not gradual changes.  Also, the same mutations occurred when the experiment was repeated.  It seems so ordered, and quick, which to me implies some sort of direction.  I personally do not believe in a "higher power" so that is why I lean strongly towards something like epigenetics.


Here is an example where 2 separate mutations were required in order to metabolize salicin, and not only did they happen, but the initial mutation was not beneficial and only occurred in populations grown on mediums containing salicin:

Quote
http://www.ncbi.nlm.nih.gov/pubmed/2852143?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubmed
Adaptive evolution that requires multiple spontaneous mutations. I. Mutations involving an insertion sequence.

Hall BG.

Molecular and Cell Biology, University of Connecticut, Storrs 06268.

Escherichia coli K12 strain chi 342LD requires two mutations in the bgl (beta-glucosidase) operon, bglR0----bglR+ and excision of IS103 from within bglF, in order to utilize salicin. In growing cells the two mutations occur at rates of 4 x 10(-8) per cell division and less than 2 x 10(-12) per cell division, respectively. In 2-3-week-old colonies on MacConkey salicin plates the double mutants occur at frequencies of 10(-8) per cell, yet the rate of an unselected mutation, resistance to valine, is unaffected. The two mutations occur sequentially. Colonies that are 8-12 days old contain from 1% to about 10% IS103 excision mutants, from which the Sal+ secondary bglR0----bglR+ mutants arise. It is shown that the excision mutants are not advantageous within colonies; thus, they must result from a burst of independent excisions late in the life of the colony. Excision of IS103 occurs only on medium containing salicin, despite the fact that the excision itself confers no detectable selective advantage and serves only to create the potential for a secondary selectively advantageous mutation.


Really I could go on and on, the evidence supporting some form of directed mutation is everywhere.  Yes, each individual event can have a possible different explanation, but it seems to happen over and over.  If we as scientists are constantly searching for a new way to explain why something observed isn't impossible, maybe we need to go back to the fundamentals and look at why we thought something was impossible to begin with.
 

Offline BenV

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Re: How big a role does the epigenome play in evolution?
« Reply #59 on: 03/04/2010 10:24:03 »
In my words...... Tassie Devil's genetics, prior to the toxins in their water, were all the same throughout their species. After the toxins from the mono culture effected their water, their genetics changed over 2-3 generations to cope with the toxins and to survive and reproduce.
In that case, I think you've got entirely the wrong end of the stick with that paper.

Quote
So if you go to the zoo where these animals are kept away from the toxins, you will find their genes are different from the ones in the wild.

The toxins are not leaving their water system any time in the near future, so if they continue to breed their genes will be passed down throughout many generations. While the captive Tassie Devils reproduce without the altered genes.

That's not what the paper says.

Quote
1.Cancer is an epigentic disease characterised by the break down of DNA.

No it's not.  And in particular, DTFD is a contagious cancer - tumour cells from one individual can cause tumours in another.

Cancer is a disease that can be caused by DNA damage - not the other way around.

Quote
2.Prior to the environmental change all the Tassie Devils genes were the same.
No they weren't - that would make them clones.

Quote
3. No change in Tassie Devil's genes in zoos or that have never come in contact with the toxic environment.
Well, it's not a toxin in the environment - if DTFD isn't introduced, why would you expect any change?
Quote
4. It took 2-3 generations for the environment to effect change in their genes.
The abstract says:
"We observed a significant increase in inbreeding in devil populations after just 2-3 generations of disease arrival, but no detectable change in genetic diversity."

Quote
5. If the captured, zoo's Tassie devils were released and returned to their native environment they would not survive. Their environment has directly effected their evolution.
The paper doesn't say anything about this.  It may be true that captive animals don't do well in the wild, but that may be nothing to do with their genes.
Quote
6. As I believe, if the ones in the zoos continue to reproduce together without bringing in the new genes from their wild counterparts then 2 distinct species of Tassie Devils may occur over time. One group unable to live/reproduce/survive in it's natural habitat.
Survival of the fittest!
Spot on.  This is why captive breeding programmes often swap males (or sperm) to try to keep variation high.


My analysis of the paper (based only on the abstract) is that DFTD leads to population and distribution changes, that can lead to genetic changes over a few generations.  This doesn't necessarily mean mutations, it means variability - different proportions of different alleles etc.
 

Offline BenV

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Re: How big a role does the epigenome play in evolution?
« Reply #60 on: 03/04/2010 10:29:57 »
If epigenomic markers actually allow life to direct mutation to any extent whatsoever, would that qualify as "intelligent design"?

If any process (epigentics)is involved rather than 'random change', you would think there is some 'intelligents'about it?

I think so.

I don't think so.

Intelligence requires consciousness and forethought.  Epigenetic changes do not.
 

Offline JP

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Re: How big a role does the epigenome play in evolution?
« Reply #61 on: 03/04/2010 10:33:19 »
Here is a few more examples which I feel indicate epigenetics causing mutation. . .

Cool.  Thanks for the links.  I'll take a look over them when I have a chance.
 

Offline norcalclimber

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Re: How big a role does the epigenome play in evolution?
« Reply #62 on: 06/04/2010 06:15:01 »
I just came across this, and I'm not sure if I am understanding or interpreting it correctly:

http://www.ncbi.nlm.nih.gov/pubmed/10690404?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=3&log$=relatedreviews&logdbfrom=pubmed

Quote
A decade of research on adaptive mutation has revealed a plethora of mutagenic mechanisms that may be important in evolution. The DNA synthesis associated with recombination could be an important source of spontaneous mutation in cells that are not proliferating. The movement of insertion elements can be responsive to environmental conditions. Insertion elements not only activate and inactivate genes, they also provide sequence homology that allows large-scale genomic rearrangements. Some conjugative plasmids can recombine with their host's chromosome, and may acquire chromosomal genes that could then spread through the population and even to other species. Finally, a subpopulation of transient hypermutators could be a source of multiple variant alleles, providing a mechanism for rapid evolution under adverse conditions.

The first part of the underlined section seems to be referring to epigenomic markers.  "Insertion elements not only activate and inactivate genes, they also provide sequence homology that allows large-scale genomic rearrangements." seems to be saying epigenomic markers are responsible for the mechanism which allows an organism to make a large mutation?

"Some conjugative plasmids can recombine with their host's chromosome, and may acquire chromosomal genes that could then spread through the population and even to other species."  This seems to be saying that certain plasmids may be able to "carry" beneficial mutations throughout a population?  If this occurs, mustn't it have evolved at some point?  The only reason I can think of as to why a mutation like that would be beneficial is because it allows beneficial mutations to be transmitted without direct mating.  If that is true, it seems to be just another element which is starting to show us just how advanced life is, and how much it seems to recognize(consciously or not) the need to evolve into a fitter organism is paramount to survival of future generations.

To be honest, I'm not precisely sure what transient hypermutators are specifically, but I'm guessing from the name that they are theoretical cellular "machines" capable of increasing the rate of mutation under adverse conditions.  I'm also guessing that the reason they are theorizing the mutators might exist is because we consistently see in experiment after experiment that beneficial mutations tend to happen very rapidly when they are really needed, but almost not at all when the organism is not under stress.  Even if the mutations afterward were indeed random, doesn't this still represent the ability of an organism to control mutation, and evolution to some extent?

If I have misunderstood anything I apologize, it is surely not my wish to put forth a misinterpretation of science.
 

Offline echochartruse

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Re: How big a role does the epigenome play in evolution?
« Reply #63 on: 06/04/2010 23:52:00 »

1.Cancer is an epigentic disease characterised by the break down of DNA.

No it's not.  And in particular, DTFD is a contagious cancer - tumour cells from one individual can cause tumours in another.

Cancer is a disease that can be caused by DNA damage - not the other way around.


Quote
http://webcache.googleusercontent.com/search?q=cache:-deFKSjLe1sJ:assets0.pubget.com/pdf/17458893.pdf+Cancer+is+an+epigentic+disease+characterised+by+the+break+down+of+DNA.&cd=49&hl=en&ct=clnk&gl=au

Epigenetic alterations, such as modifications in DNA methylation patterns and post-translational modifications of histone tails, behave extremely
different from genetic modifications,

see also
www.epidna.com/showabstract.php?pmid=15881895

www.epidna.com/showabstract.php?pmid=16210093

www.ncbi.nlm.nih.gov/pubmed/19069364

www.docstoc.com/docs/20476934/02-Cancer-Epigenetics-Group/

http://atlasgeneticsoncology.org/.../GenetInstabilityCancerID20056.html

informahealthcare.com/doi/full/10.1517/17530059.1.1.17?select23...

www.pebc.cat/grupodetalle.php?idg=7

http://ajp.amjpathol.org/cgi/content/full/164/6/1883

 

Offline Geezer

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Re: How big a role does the epigenome play in evolution?
« Reply #64 on: 07/04/2010 06:13:41 »
I must admit to being totally confused (Yea, yeah. Save the cheap shots till later.)

Are we, or are are we not, debating about the existence of an intelligent designer? (which is usually what is strongly implied by the term "intelligent design".)

or;

are we debating the complexity of the process of evolution and how factors other than random mutation can play an important role in the process?

If it's the former, fine, then we are debating about the existence of an intelligent designer.
If it's the latter, does anyone mind if we change the title of this topic, because it is very confusing?
 

Offline norcalclimber

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Re: How big a role does the epigenome play in evolution?
« Reply #65 on: 07/04/2010 18:31:32 »
My intent when I started the topic was to debate the evidence and logic in support of organisms choosing mutation, rather than merely random chance mutations resulting in the diversity of life we have.  I posted it the way I did, because if life has a way to influence and choose mutation then life would in a sense be "intelligently designed" but not by some god figure, rather by the organisms themselves.

A lot of people seem to be stuck on me using "intelligent design" in the title, I suppose I can see how with as many replies as there are it could be awfully confusing as to whether I am talking about a higher power or not.  I am most definitely not talking about "god", so if the title is just too confusing for people it should probably be changed.  Actually, it could even probably be merged with "Is evolution really down to random mutation?", since that is a very similar topic I posted before I had learned a little more on the subject.
 

Offline Geezer

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Re: How big a role does the epigenome play in evolution?
« Reply #66 on: 07/04/2010 19:17:26 »
Thanks for the clarification. That should do the trick. It's probably best not to change the topic title, as that might lead to even more confusion.  :D
 

Offline echochartruse

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Re: How big a role does the epigenome play in evolution?
« Reply #67 on: 07/04/2010 23:29:12 »
Just a few interesting links for those who are not bias.

Quote from: http://www.abc.net.au/catalyst/stories/s1486827.htm
Intelligent Design or ID, is being put forward as a serious scientific theory. It's even found it's way into some high schools.


Quote from: http://internationalstem.com/
Intenational Institute of Stem Cell Research and Regenerative Medician
Introduction:  California is currently becoming the main international hub of stem cell research.   Our staff is fully committed to creating this international center for stem Cell Research and clinical applications.  Dr. Schafer has been a twenty year pioneer in adipose tissue harvesting and fat transfer.  He is currently involved in the harvesting and preservation of “Intelligent” Stem cells which are naturally occurring in our bodies and not from fetuses or evoke religious taboos.   These Adult stem cells are extremely valuable and have great potential for future therapies.  It is important to note that these cells do not induce any type of immune reaction in the body.  Our Institute is at the forefront of this emerging technology.  Many of the pharmacological protocols as well as cosmetic proceedures  of  the twentieth century are being replaced by the utilization of stem cells for a cosmetic procedure.  This Institute provides world leading innovations in fat grafting with stem cells and regenerative medicine.  Dr. Schafer provides the vision and scientific guidance to advance the Institute to it’s potential of scientific excellence.

Quote from: http://en.wikipedia.org/wiki/Microbial_intelligence
Microbial intelligence (popularly known as bacterial intelligence) is the intelligence  shown by microorganisms. The concept encompasses complex adaptive behaviour shown by single cells, and altruistic and/or cooperative behavior in populations of like or unlike cells mediated by chemical signalling that induces physiological or behavioral changes in cells and influences colony structures.

Quote from: http://www.world-science.net/exclusives/exclusives-nfrm/050418_bact.htm
Yet the humble microbes may have a rudimentary form of intelligence, some researchers have found.

Quote from: http://www.astrobio.net/interview/2111/bacterial-intelligence
If you look up consciousness in the dictionary, it says, "awareness of the world around you," and that's because you lose it somehow when you become unconscious, right? Well, you can show that microorganisms, or bacteria, are certainly conscious. They will orient themselves, they will work together to make structures. They'll do a lot of things. This ability to respond specifically to the environment and to act creatively, in the sense that that precise action has never been taken before, is a property of life. Of course, it has to be moving life, or you can't tell. You can't tell if a plant is thinking, but in organisms that move, you can tell their intelligence.

So yes I think life itself is intelligent and there is a degree of design about it which we have not yet been able to understand
 

Offline Geezer

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Re: How big a role does the epigenome play in evolution?
« Reply #68 on: 07/04/2010 23:52:06 »
Intelligent Design, otherwise known as ID, has nothing to do with science. It is creationism wrapped up in pseudoscience and mumbo-jumbo. The fact that George W. Bush fell for it should tell you something, both about ID and GWB.

ID was invented in an attempt to require schools in the USA to teach creationism by pretending that it is some sort of science.

Perhaps we will have to change the title of this topic after all.
 

Offline echochartruse

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Re: How big a role does the epigenome play in evolution?
« Reply #69 on: 08/04/2010 03:07:00 »
It is unfortunate for all that "intelligent design" can not be looked at scientifically. That we are all in a bias pot of random selection fighting for survival.
 

Offline Geezer

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Re: How big a role does the epigenome play in evolution?
« Reply #70 on: 08/04/2010 04:26:45 »
It is unfortunate for all that "intelligent design" can not be looked at scientifically. That we are all in a bias pot of random selection fighting for survival.

ID would be looked at scientifically if its proponents presented some scientific evidence. However, proponents of ID are not interested in conducting real science. They are only interested in pursuing their political agenda by deceiving gullible individuals into believing that ID is science.

Personally, I have no problem with religions, but I have a very big problem with religions that masquerade as science in an attempt to trick people.
 

Offline echochartruse

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Re: How big a role does the epigenome play in evolution?
« Reply #71 on: 08/04/2010 05:19:23 »
It is unfortunate that Science can't prove that ID is totally and specifically scientific.
I am not a religous person, yet feel that our earth's evolution and everything in it  has not been entirely random.

Quote from: http://www.livescience.com/strangenews/050923_ID_science.html
Darwin himself admitted that if an example of irreducible complexity were ever found, his theory of natural selection would crumble.
 
"If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down," Darwin wrote.

"complex specified information," or CSI for short.

An example of CSI from nature is DNA, the molecule found in all cells that contains the genetic instructions for life. DNA is made up of four repeating chemical bases arranged into complimentary pairs. The bases can be thought of as "letters" in a four-letter alphabet and can be strung together to form genes, which can be thought of as the "words" that tell the cell what proteins to make.

The human genome is made up of some 3 billion DNA base pairs and contains about 25,000 genes. DNA is obviously complex. The fact that humans always give birth to humans and not chimpanzees or naked mole rats shows that DNA is also specific.

When science takes the god out of 'intelligent design' that will be the day science can go forward. Until then we will continue going in circles trying to prove the theory of evolution by natural selection.
 

Offline Geezer

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Re: How big a role does the epigenome play in evolution?
« Reply #72 on: 08/04/2010 05:51:42 »
It is unfortunate that Science can't prove that ID is totally and specifically scientific.

You don't seem to understand. It's not up to "Science" (whatever that is) to prove that ID is scientific. It's up to ID to prove that it has some legitimate scientific foundation.

Thus far, ID  has done nothing but try to appeal to non-science and religious fundamentalism. (Apparently, in that regard, it has been quite successful.)

We may "wish upon a star" all we want, but, unfortunately, that does not make science.
 

Offline norcalclimber

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Re: How big a role does the epigenome play in evolution?
« Reply #73 on: 10/04/2010 16:59:27 »
It is unfortunate that Science can't prove that ID is totally and specifically scientific.

You don't seem to understand. It's not up to "Science" (whatever that is) to prove that ID is scientific. It's up to ID to prove that it has some legitimate scientific foundation.

Thus far, ID  has done nothing but try to appeal to non-science and religious fundamentalism. (Apparently, in that regard, it has been quite successful.)

We may "wish upon a star" all we want, but, unfortunately, that does not make science.

Ok, but like I said, this topic has nothing to do with creationist intelligent design.

What do you think about the evidence that I posted regarding directed mutation via epigenetics?
 

Offline JP

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Re: How big a role does the epigenome play in evolution?
« Reply #74 on: 12/04/2010 05:10:45 »
Here is a few more examples which I feel indicate epigenetics causing mutation:

http://www.gate.net/~rwms/EvoMutations.html

. . .

Sorry it took me so long, but after reading through all of those sources and watching the last 5 minutes of the Naked Science video, I still have to disagree that there's evidence for epigenetic changes causing genetic mutation.  Those experiments all show that you can "rapidly" develop a lot of genetic diversity, but they don't attribute that to epigenetics.  I still haven't seen any direct evidence of epigenetic change causing genetic mutation. There's also the difference in time scales of "rapidly."  The sources you cite seem to be talking about time scales that are long compared to the life cycle of an individual, 10,000 generations in one study and mutation probability of ~10-8 per cell division in the other.  Epigenetics seems to be a much faster process, allowing single organisms to change (so changes on the scale of 1 generation).  If epigenetics induced mutation, then I would expect it to happen orders of magnitude faster than any of those studies show. 

Again, it's not that I think epigenetics isn't interesting and promising.  It's just that there doesn't seem to be enough evidence to link it to actual genetic mutations.  If that link is made, then it certainly would change things.
 

The Naked Scientists Forum

Re: How big a role does the epigenome play in evolution?
« Reply #74 on: 12/04/2010 05:10:45 »

 

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