delcoder wrote:nursebenjamin wrote:Your argument seems to be that the probability of a double or triple mutation is mathematically so low that evolution by natural selection is unlikely. This is pure hogwash.
According to Lenski, whose work you seem to admire,
E. coli is a very common bacterium. Theres some hundred billion billion (10^20) of them in the world. A billion
E. coli cells currently live in your own bowels. Mutations are rare events; however, [e]ven if [
E. coli cells] divide just once per day, and given a typical mutation rate of 10^-9 or 10^-10 per base-pair per generation, then pretty much every possible double mutation would occur every day or so [to each gene]
[1]. Lenskis
E. coli in the lab typically divide 6-7 times per day. Thats a lot of opportunity for evolution.[Ibid.] Periodic evolutionary innovations are not surprising if you actually do the math.
Your claim (not mine) is that the odds of a triple mutation in
E. coli is 1 in 262 billion. Well, considering that there are 100 billion billion
E. coli in the world, and
E. coli divides 6-7 times per day, then those are pretty likely odds, wouldn't you say? What makes you think that evolution by means of natural selection is mathematically unlikely?
Unless you are advancing the probability of more than one source (individual E Coli) in the population your comments make no sense. If you are advancing this possibility the odds become even more ridiculous. The number of E Coli in the population is irrelevant. We still have to end up with a single subject that experiences random and spontaneous mutations in three loci that work together for natural selection to begin to work.
That aside the formula for figuring the odds of three gene mutations which work in concert to produce a specific variation in an individual E Coli subject is (ng * ne) * ((ng-1) * ne) * ((ng-2) * ne) / 1 * 2 * 3. I now find E Coli have over 5000 genes rather than 3200 so I will use 5000 as ng (number of genes). I will use 2 for ne (number of expressions for each gene). (5000*2) * (4999*2) * 4998 *2) / 1 * 2 *3 = one in 167 billion. Then you have to consider the possibility the subject would die before all three mutations occur. You also should consider the fact that a single gene can code for as many as 100 proteins. When you are done 1 in 262 billion is very charitable.
If you wish to carry the probabilities on to the possibility of one E Coli with a fitter trait taking over a population over a reasonable time you end up with 1 in the trillions.
When talking about the probability of random mutations, then the number of individuals does matter. Think of it this way: if the odds of winning a lottery is 1 in 262 billion, and you only buy one ticket, then the probability of you winning are quite low. If you buy 10 billion billion (10 x 10^20) randomly generated lottery tickets, then the probability of you winning is much higher. Reproduction rate also matters; theres going to be more mutations if a population produces 6-7 new generations per day as opposed to one new generation every twenty years.
If you are talking about one lowly
E. coli, then the probability that it was born with a gene mutation would be quite low, given a typical mutation rate of 10^-9 or 10^-10 per base-pair per generation in
E. coli. But when considering 10 billion billion individuals, then the chance for a gene mutation somewhere in the genome in one of those individuals is huge.
Richard Lenski states that in
E. coli populations, pretty much every possible double mutation would occur every day or so.[Sourced in previous post] A double mutation would be a gene that experiences two different mutations. This would also mean that triple mutations could also be possible, quadruple mutations would be less likely, and so forth.
By the way, mutation rates differ between species and even between different regions of the genome of a single species.
[4] Estimates for mutations in the human genome vary, but one researcher has estimated that each human is born with an average of 175 new mutation in their genome.
[5]
delcoder wrote: a single subject that experiences random and spontaneous mutations in three loci you have to consider the possibility the subject would die before all three mutations occur
Sorry, but because of these comments, it is clear that you dont know much about
Lenski's long term evolution experiment. I will explain this experiment to you, even though the probability of this explanation going in one ear and right out the other is high. I will do this because Im a nice guy, the conversation cant continue unless you know what you are talking about, and for the benefit of others.
In 1998, Lenski took nearly* genetically identical (strain Bc251)
E. coli and inoculated 12 identical flasks, thus creating 12
E. coli tribes.
[2][6]
[7][8] Lenski chose an
E. coli strain that reproduces only asexually; this limits the study to evolution by natural selection based only on new mutations.
Each flask contains the same amount of nutrient-rich broth; this broth contains glucose, which would be the bacterias main food source. The flasks are kept in a shaking incubator in order to evenly distribute the bacteria through the broth and to keep the bacteria warm, which promotes cell growth and division.
Every day, each tribe is transferred to a new virgin flask. Exactly 1% of old broth is drawn up into a pipette, and transferred into fresh broth. Initially, when introduced to fresh broth, there would be a population explosion, and then a population plateau as starvation set in. Glucose in the flasks is a limited resource. Each flask averages between 6 and 7 new generations per day. Every 75 days (approximately 500 generations) a sample from each tribe is frozen; this allows Lenski to study old
E. coli "fossils" and experiment with ancient populations. The populations are also regularly screened for changes in mean fitness, and supplemental experiments are regularly performed to study interesting developments in the populations.
As of Feburary 2010, the population reached a milestone of 50,000 generations. To put that into perspective, if we were to go back 50,000 human generations, which would be approximately 1.1 million years ago, humans were walking around as
Homo erectus.[6]
page 19
*Above I said that Lenski founding populations began with
nearly genetically identical clones. Lenski actually inoculated six flasks with an Ara+ variant, and six flasks with an Ara- variant. This allowed the tribes to be color-coded (red versus white) if stained. When handling the bacteria populations, they handle the Ara+ and Ara- alternately. This way they would know if the tribes had ever been contaminated with bacteria from another tribe. This genetic marker has since evolved to allow for unique identification of each strain.
In the early years of the experiment, average fitness in all twelve tribes increased as the bacteria got better at surviving in glucose-limited conditions. This is evidenced by the fact that population grew faster in successive flasks and an increasing average bacterial body size:
[center]
[/center]
Many of the tribes increased cell fitness through different mutations, although, at times, evolution was parallel in different tribes.
One of the more interesting results was that one of the tribes developed an ability to metabolize citrate (Cit+ cells). In addition to a limited amount of glucose, the broth in the flasks also contains citrate. E. coli possesses all of the enzymes necessary for citrate metabolism via the Citrate Acid Cycle. However,
E. coli normally cant metabolize citrate under oxic condition because it cannot transport the molecule through the cell membrane under aerobic condition.
The three mutations that you keep referring to did not occur in one
E. coli individual. Experimenting on those frozen samples, Lenski determined that the first mutation, a potentiating mutation, occurred somewhere around the time of generation #20,000. This first mutation primed the population to take advantage of a future mutation. This second mutation occurred shortly after generation #31,000, and allowed the
E. coli cells to transport citrate through their cell membranes. A third mutation enhanced the transportation of citrate and occurred after generation #33,000. With these new mutations, Cit+ bacteria would still be able to grow and reproduce once the limited amount of glucose was exhausted. Thus, natural selection allowed the population of Cit+
E. coli to explode.
The three mutations occurred in different generations, not within the same individual.
delcoder wrote:With epigenetics, however, the possibility of many E Coli responding to the stress in the environment is very good. Every individual E Coli experiences the same stress, hence it is logical that perhaps over 50% would have the same genetic response. One needs only to understand how epigenetics works and works quickly to understand why random and spontaneous mutations if they happened against the odds would be confronted with a population that has already changed. I like to say epigenetics has already got a hit and ran the bases while Neo-Darwinism is still selecting a bat.
The evolution of Cit+
E. coli was the result of three separate
mutations. Again,
mutations are
not epigenetics. I have no idea why you would cite an experiment that seems to confirm evolution by means of random mutations and natural selection to argue that Neo-Darwinism can not be a basis for evolution.
I admit that the exact mutations have not been identified
yet. Lenski actually considers the possibility that the Cit+ population could be the result of the activation of a cryptic transporter. But he concludes that [t]his explanation seems unlikely to us because the Cit- phenotype is characteristic of the entire species, one that is very diverse and therefore very old. We would expect a cryptic gene to be degraded beyond recovery after millions of years of disuse.
[2, page 6]
What do you know that Lenski doesnt? Random and spontaneous mutations do, in fact, happen.
E. coli is typically unable to utilize citric acid. The inability to grow on citrate acid is often used to identify of
E. coli in a clinical setting.
[9] If epigenetics can explain the Cit+ characteristic of one of Lenskis twelve
E. Coli populations, then why is
E. colis inability to grow on citrate so reliable? You said that, [e]very individual E Coli experiences the same stress, hence it is logical that perhaps over 50% would have the same genetic response. So why doesnt 50% of
E. coli cells grow on citrate? I ask this because Im just trying to figure out your logic.
Also, keep in mind that, while some transgenerational epigenetic changes have been observed, most of these multigenerational epigenetic traits are gradually lost over several generations.
[10] Lenskis Cit+ population has been present for nearly 20,000 generations.
P.S. I also asked nicely for you to reveal your sources, but you have failed to do this. I am interested in reading your sources.
Additional sources:
[6] Dawkins, Richard;
The Greatest Show on Earth; pages 116-133.
