Discussion of everything related to the Theory of Evolution.
I apologise to the OP and readers in general for appearing to hijack this thread. It's a fine line one takes when trying to put right a wrong. Does it help or hinder the audience? I don't know, but I don't want to take any chances. I'd suggest if Jevg wants to carry this on we "take it outside" (to another thread).
Maybe the subject could be "handbags at ten paces" or something similarly ludicrous.
This discussion is sadly beginning to degenerate to the level of insults and that is regrettable. I am clearly causing you some distress and I have no wish to do that.
This thread was initiated by a simple question.
Now what I and others have done is to try and answer that question. I have provided details of the LTEE experiment that is demonstrating how difficult it is for random events to effect even a small change in function. I have also directed attention to the Francis Collins paper calling in the research of some 300 or so scientists.
I have argued that this body of accumulating evidence supports my understanding that Random mutations whether gradual or punctuated does not lead to speciation. (commonly referred to as Macroevolution)
I have also argued that the evidence from Francis Collins raises serious doubts about the theory of common decent. (Another fundamental pillar of Darwinian theory classical or modern.)
I was about to move on to the question of natural selection and what part evidence is showing it plays in evolution. Your intervention has interrupted that, however I may be given the opportunity to put that as additional evidence to this original question.
Now you may wish to get into an argument over the finer points of a theory that in my opinion is being rapidly eroded by evidence. I have no desire to try and rearrange the tables on a sinking ship.
It should therefore come as no surprise to you, that I have no wish to trade handbags.
If you feel insulted in any way I sincerely apologise, it was not my intention. Let me take the opportunity to say that personally I don't feel in any way insulted by any of the comments you have made.
Thanks for your concern, however let me reassure you, your views cause me no concern whatsoever. They are your views and clearly you are entitled to hold them and express them. If my views differ, I too have taken the same opportunity.
Feel free to answer the 3 questions I posed to you, and address any points I raised in that post in any thread you choose....
... I would be particularly interested in your views on the points I made about your inaccurate references of the LTEE experiment.
Collins is an authority in his field, I note that when he was appointed to the Pontifract Academy of Sciences by the Pope it raised a few eyebrows particularly because he supports stem cell research. He is also open about his religious views for which he receives criticism from fellow scientists. This is unfair in my view because at least he's being open about it. I mean, if someone is an atheist they don't get criticised from fellow scientists.
I shall have to get hold of a copy of his book, according to USA today...
...hopefully the rest of the forum will forgive my insolence and the delaying of the inevitable.
Thank you for your comments.
As we can now concentrate with questions that deal directly with the question in this thread, I will be very happy to deal with your questions and indeed any others. I have not ignored responding to serious and rational questions in the past and will respond as required in future.
I will however ask for a little patience at the moment as I am going to be away from my computer for about 36 hours or so. I will therefore respond sometime tomorrow evening UK time.
I will try to deal with the issues you raised that are connected to this experiment.
The LTEE experiment is named
Historical Contingency and Evolution of key innovation in an experimental population of Escherichia coli.
I introduced this paper to the forum in my very first post with the appropriate link for all to check against. To suggest that I have not read it and merely relied on someone else’s explanation I find somewhat curious.
To save any further confusion here it is again.
First sentence reads
“The role of historical contingency in evolution has been much debated, but rarely tested. Twelve initially identical populations of Escherichia coli were founded in 1988 to investigate this issue.”
The purpose of the experiment therefore was to determine the validity of the hypothesis of “Historical Contingency”
(Page 1 para 4)
“They have since been propagated by daily 1:100 serial transfer in DM25, a minimal medium containing 25 mg/liter glucose as the limiting resource (2, 22).”
Under Materials and Methods (Page 7)
“The twelve populations have been propagated for almost 20 years by daily serial dilution in DM25, a minimal salts medium that has 139_Mglucose and 1,700_Mcitrate (2).”
“The various DMmedia used to grow cells in different experiments are all based on the same formulation as the DM25 used in the LTEE (1), with only glucose concentration varied. DM25 contains glucose at 25 mg/liter. DM500, DM1000, and DM2000 have 20, 40, and 80 times, respectively, more glucose than DM25, whereas DM0 contains no glucose.”
“Throughout the duration of the LTEE, there has existed an ecological opportunity in the form of an abundant, but unused, resource. DM25 medium contains not only glucose, but also citrate at a high concentration.” (page 2 para1)
Was the concentration of glucose deliberately chosen? --- Yes
Why? --- To provide selection pressure.(an ecological opportunity)
Are there variants of E coli that have the ability to utilize citrate?
Yes, they have been detected in the wild. Ref 44 and 45 in the paper provides the sources. It is found in pigeons, pigs, cattle and horses.
“Other findings suggest that E. coli has the potential to evolve a Cit+ phenotype.
Hall (41) reported the only documented case of a spontaneous Cit_ mutant in E. coli.” (page 2 para2)
Did the evolution of Cit+ come as a surprise? (as you have suggested)
“The long-delayed and unique evolution of the Cit+phenotype might indicate that it required some unusually rare mutation……” (page 2 para 4)
If an event is long delayed, it suggests to me that the event was anticipated or at least hoped for. Why you feel they were surprised is beyond me, especially when the ability of E.coli to use citrate already exists in other variants.
The experiment was designed to test the validity of Historical Contingency.
The populations were propagated (fed) in DM25 (a mixture of glucose and citrate) the ratio deliberately chosen for this experiment to provide selection pressure.
After 31500 generations the long delayed evolution of Cit+ arrived in one of the 12 populations. That is after a total of about 360,000 generations of “random mutations.”
It is now up to around 500,000 generations.
Remember this “new” trait only involved gaining the ability to transport the citrate through the cell wall. The ability to digest the citrate was already there.
It is with good reason that Lenski states:- (page 2 para3)
“Despite this potential, none of the 12 LTEE populations evolved the capacity to use the citrate that was present in their environment for over 30,000 generations. During that time, each population experienced billions of mutations (22), far more than the number of possible point mutations in the 4.6-million-bp genome. This ratio implies, to a first approximation, that each population tried every typical one-step mutation many times. It must be difficult, therefore, to evolve the Cit+ phenotype, despite the ecological opportunity.”
It is also with good reason I posted the rather cryptic question.
How many generations would it take to develop a whole digestive tract from teeth to anus.? ( Let alone the whole organism)
The question is not whether evolution is a fact or not. It is a fact.
The question is.
Does evolution progress to the point of producing new species and is the driving force “random mutations”? Remember the mutations have to occur before natural selection can begin to operate.
After some now, 50,000 generations has a new species arrived?
Quite clearly no. It is still E.coli.
In summary this experiment has revealed that
1. Bacteria become fitter and get larger/
2. Most of the gain is in the first 2000 generations
3. Most of the gain comes from five different genes that have mutated.
4. After 20,000 generations, his group sequenced 918,700 bases from 50 isolates- they found 10 changes, all in ones with a “mutator” phenotype.
“It is clearly very difficult for E. coli to evolve this function. In fact, the mutation rate of the
ancestral strain from Cit- to Cit+ is immeasurably low; even the upper bound is 3.6 _ 10_13 per cell generation, which is three orders of magnitude below the typical base pair mutation rate.” (page 6 para. 2)
In English “immeasurably low” means – incapable of being measured.
“Nevertheless, one population eventually evolved the Cit+ function, whereas all of the others remain Cit_ after more than 40,000 generations. We demonstrated that the evolution of this new function was contingent on the history of the population in which it arose. ”
To establish their contention that historical contingency was the cause of the evolution they ran three replay experiments from the potentiated clones.
“Statistical Analysis of the Replay Experiments.
All three experiments show the same tendency for Cit+ variants to evolve more often from clones sampled in later than earlier generations of population Ara-3 “
I did unintentionally overstate the replay experiments results as described above when I stated that the replays “resulted in identical citrate-feeding populations, all of which emerged after the same total number of generations.”
Let me conclude with the question Lenski poses.
“Will the Cit_ and Cit+ lineages eventually become distinct species?
According to the biological species concept widely used for animals and plants, species are recognized by reproductive continuity within species and reproductive barriers leading to
genetic isolation between species (67) Although the bacteria in the LTEE are strictly asexual, we can nonetheless imagine testing this criterion by producing recombinant genotypes.….”
Why is the question left hanging?
Because the evidence simply is not there.
So you question me when you state
“so how do you explain ignoring the approx 3.5 million single step genetic mutations that lead to benefitial improvements in the Lenski experiment up to the 20,000th generation.”
I am not able to explain your assertion because I am unaware of the evidence you seem confident you have.
My question therefore is
What is the evidence you call on to support that statement? ( forget the 20,000 bit)
When I asserted that "You really haven't actually read Lenski have you? " you must forgive my generality. I was not suggesting that you hadn't read that particular paper that you were citing. I was inferring that you hadn't read any of the Lenski's papers in which he outlined his reasons for the experiment and the way the experiment was carried out. I believe that if you had read any of these papers, understood them and didn't doubt Lenski's credentials then you wouldn't have said the following
Those statements are misleading. In many papers Lenski has outlined his goals for the experiment; providing data on historical contingency and establishing his own fossil record were two of his main goals but nowhere does he state his intention to force E coli to evolve Citrate digestion. As I have already pointed out, and again this comes from Lenski himself, they provided glucose as the sole source of carbon and energy.
People can look at your words and judge for themselves why you make such statements about the Lenski experiment. I personally try to see the best in people which is why I suggested that you had been seriously misled. If you wish to understand the LTEE more I suggest you visit their own website. There is a huge amount of data, if you are seriously interested in the experiment then you will be rewarded for your time and effort with a greater understanding of historical contingency and the benefits of having a more complete fossil record.
For your info the website is:
I know I open myself to the accusation of being lazy when I say this, but again I prefer to read what Lesnki says, and take his word for it when he states that when citrate using E coli evolved it came as a surprise. Again, you can infer what you wish if it suits your purpose but coupled with the fact that he never stated breeding citrate using E Coli as one of his goals and stating that it was a surprise to him and his team when it happened, I'm happy to say your statement is misleading.
I'd go even further than that and say not only do they have to occur but also they have to take hold in the population before natural selection can do it's thing.
Not according to Lensky et al;
"Although adaptation decelerated sharply, genomic evolution was nearly constant for 20,000 generations. Such clock-like regularity is usually viewed as the signature of neutral evolution, but several lines of evidence indicate that almost all of these mutations were beneficial"
Genome evolution and adaptation in a long-term experiment with Escherichia coli
Jeffrey E. Barrick1,7, Dong Su Yu2,3,7, Sung Ho Yoon2, Haeyoung Jeong2, Tae Kwang Oh2,4, Dominique Schneider5, Richard E. Lenski1 & Jihyun F. Kim2,6
Glad to hear it, hopefully you will acknowledge the same regard towards your other misleading comments on the LTEE regarding their goals and use of Citrate. How you interpret the results of the data is your own business but I hope you agree you haven't represented the LTEE correctly in your assertions of their running of the experiment.
The way I read it Lenski is posing a possible hypothesisc for future testing, I don't think anyone is arguing that the evidence is there. It obviously isn't until experiments can be run to test it.
I looked at the data back when the 20,000th generation was new and since then we have now passed 50,000 generations. Zachary Blount is responsible for co-ordinating testing to establish benefitial single genetic mutations, last I knew he had personally tested 40 trillion e coli cells, then there are others either in the LTEE team or in labs around the world who support their work.
The data to support my statement is contained in the research published on the LTEE website and in fact is more likely to be even greater than this number now which is why I added "approx", in hindsight I should probably have chosen "at least".
The following papers are those that I know cover benefitial single genetic mutations: 122, 140, 155, 166, and 178
What the LTEE has shown is that there have been at least 3.5m instances of e coli cells mutating in a single gene and this mutation leading to improved fitness.
So apart from the rhetoric on the periphery of this question
We are agreed, random mutations and natural selection can make an organism fitter and larger (bacteria in this case) and more adaptive in an existing environment that in more general parlance is referred to as micro evolution.
So lets return to the question that initiated this thread.
Can we also agree then that this 22 year long experiment by Lenski (which as I have stated before is what good science is all about and whose website I have been following for some time now) has not produced evidence that supports a hypothesis that new species emerge as a result of this “Darwinian mechanism”.
The term the macro-evolution is used in the question and again is general parlance for speciation.
In other words there is no empirical evidence that provides support for a continuum between micro-evolution and macro-evolution.
Absolutely agreed, I only wish you had said this at the beginning. I would be pretty certain that if an experiment could be conceived that would breed a new species in an extremely short amount of time (and I mean that in the same sense that Gould and Darwin both used it) it would receive both praise and criticism in equal measure. It would certainly be headline news.
As it stands all we have to satisfy ourselves are clues such as the existence of ring species, an extremely incomplete fossil record and multiple experiments to push the boundaries of micro evolution.
What we have is a smoking gun, some empty bullet cases, lots of blood but unfortunately no body. Again thats just my view of it.
This is what I wrote on June 25 Page 2 of this thread.
Anyhow at least there is some measure of agreement now.
I did say I would go on to the question of natural selection but that will have to wait till the
weekend as I am rather busy with other matters till then.
You said a heck of a lot more than that. Bygones I suppose.
I'm actually looking forward to seeing how you tie up historic contingency and non randomness, which is I think where your heading?
I'd say this is different enough from the OP's question to be in it's own thread by now. Otherwise your going to find people discussing the OP popping up in the middle of some discussions over what you postulate.
Apologies for the delay. I was away longer than anticipated.
The experimental evidence to date does not show random mutation/variation as a driving mechanism that leads to the formation new species. That is now fairly clear.
What variation that does occur does so within species.
The Darwinian hypothesis majors on (environmental) Natural selection as being the main driving mechanism causing speciation.
The question therefore is whether this fundamental pillar of the hypothesis is borne out in experimental evidence.
A 30 year project carried out by K.Gartner is reviewed in his 1990 paper found here
Part of the summary reads
“Utilizing methods established in twin research, only 20-30% of the range of the body weight in inbred mice were directly estimated to be of environmental origin. The remaining 70-80% were due to a third component creating biological random variability, in addition to the genetic and environmental influences. This third component is effective at or before fertilization and may originate from ooplasmic differences. It is the most important component of the phenotypic random variability, fixing its range and dominating the genetic and the environmental component.” ( my emphasis)
These finding are endorsed by D.L.Lajus & V.R. Alekseev in their 2004 paper
This is how they introduce their paper
“It is commonly thought that phenotypic variation in the wild population of most bisexual species is determined by two factors. The first is the genotypic difference between the individuals. The second is caused by diversity of environmental conditions during the formation of the phenotypic trait and manifests itself as phenotypic plasticity. Therefore different environments may result in different phenotypes even if genotypes are the same.
Most studies focus on genotypic variation because this kind of variation provides the basis for population's adaptive response to change in environmental factors by
means of selection. Much less attention is usually paid to the non-genotypic component. But some experiments have shown that even when both genetic and environmental causes of phenotypic variation have been accounted for, variation still exists.”( my emphasis)
In 2005 Albert H.C. Wong et al confirmed the above.
http://hmg.oxfordjournals.org/cgi/conte ... uppl_1/R11
They write (under PHENOTYPIC VARIATION IN GENETICALLY IDENTICAL ANIMALS: ‘THE THIRD COMPONENT’)
“In an elegant series of experiments designed to explore the relative contributions of genes, environment and other factors to laboratory animal phenotype, Gartner (17 ) was able to demonstrate that the majority of random non-genetic variability was not due to the environment. Genetic sources of variation were minimized by using inbred animals, but reduction of genetic variation did not substantially reduce the amount of observed variation in phenotypes such as body weight or kidney size. Strict standardization of the environment within a laboratory did not have a major effect on inter-individual variability when compared with tremendous environmental variability in a natural setting.
Only 20–30% of the variability could be attributed to environmental factors, with the remaining 70–80% of non-genetic variation due to a ‘third component...effective at or before fertilization’” (17 ).(my emphasis)
There are clearly built in mechanisms that cause probably most of the variation we see within species.
So what the experimental evidence and genetic research is showing is fairly clear.
The Darwinian mechanisms for speciation, so often touted as fact, are really not supported by experimental/empirical evidence.
Research in Developmental biology is probably causing the greatest stress to these hypothetical mechanisms.
So returning to the original question
Yes there is empirical evidence and NO it does not support “macroevolution”.
In fact all the available evidence is serving to falsify this Darwinian (neo or classical) hypothesis.
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