Here’s a simple experiment one can actually try. Take a bag of M&M’s, and without peeking reach in and grab one. Eat it. Then grab another and return it to the bag with another one, from a separate bag, of the same colour. Give it a shake. I guarantee (and if you tell me how big your bag is I’ll have a bet on how long it’ll take) that your bag will end up containing only one colour. Every time. I can’t tell you which colour it will be, but fixation will happen.
This models the simple population process of Neutral Drift. Eating is death, duplication is reproduction, and the result is invariably a change in frequencies, right through to extinction of all but one type. You don’t have to alternate death and birth; choose any scheme you like short of peeking in the bag and being influenced by residual frequencies (ie: frequency-dependent Selection), and you will end up with all one colour.
Is Chance a cause here? Well … yes, in a sense it is, in the form of sample error. Survival and reproduction are basically a matter of sampling the genes of the previous generation. More random samples are a distortion of the larger population than aren’t, so, inexorably, your future populations will move away from any prior makeup, increasing some at the expense of others till only one variant remains.
Selection is a consistent bias upon this basic process. If different colours also differed a little in weight, say, more of some would be at the bottom of the bag than others, so you’d be more likely to pick one type than another. In more trials, the type more likely to be picked would be picked more often, to express it somewhat tautologously. You’d get a sampling bias.
Both of these processes are random – or stochastic, to use the preferred term. In reality, they are variations of the same process, with continuously varying degrees of bias from zero upwards. It makes no sense to call selection nonrandom, unless by ‘random’ you mean unbiased. Where there is no bias, all is Drift. But turning up the selective heat does not eliminate drift – sample error – and so does not eliminate stochasticity.
With a source of new variation, these processes render evolution inevitable. Even with a brand new mutation, with no selective advantage whatsoever, 1/Nth of the time (where N is the population size) it will become the sole survivor. That’s the baseline. If there is a selective advantage, it will be more likely and quicker to fix, on the average. If at a selective disadvantage, it will be less likely and slower.
Conversely, without a source of new variation, all existing variation would be squeezed out of the population, and evolution would stop.
Did you hear that, phoodoo? This is the only way to learn.
Are you suggesting appearance-wise it seems like many of these experts are not sure what is correct?
It doesn’t just appear that way. Most people who are supposedly experts are only called this because they talk louder than others. Jerry Coyne and PZ Meyers would be great examples. People tend to think they must know what they are talking about, simply because they talk so dam much. Just variations of different kinds of carnival barkers.
phoodoo,
Inexorably, population sampling should (if populations are finite and individuals are born and die) remove all variation from the population. This has not happened. (Perhaps it has simply not happened yet). If you think that no ‘black’ mutation ever becomes common – ‘black’ being simply a proxy for the first instance of a new mutation, not its selective effect) – then this runs against both mathematical prediction and actual runs of computer models. Not just yesterday, but for the last 50 years or so.
But let’s say you are right. What, therefore, maintains polymorphism in populations, which are finite and have individuals that are born and die?
http://i.imgur.com/mzRBSDK.png
There you go, this nice little graph is from one of the publications from Lenski’s lab. Heck, he even blogged about it recently.
See, the problem is that you don’t actually got the details down very well.
They’re novel(did not exist in the population before, they know this because they sequence the population every 500 generations). They cause a directly measurable increase in fitness (they know this, because they compare descendants with samples from the original population that started the whole experiment and can show that the later descendants outcompete their ancestors) and they’ve now become fixed in the population (which they obviously can document through their contined sequencing of the genomic makeup of the population through generations).
So there, that’s it. Case closed.
phoodoo,
You have a unique chance to interact on this forum with a top expert in mathematical aspects of genetics. His name is Joe Felsenstein. He participates in this very thread.
This is exactly what happens in the Lenski experiment. In fact it’s even worse, there’s only a single mutant arising among billions in the fermentation flask. Yet it outcompetes all the others. Beneficial mutations happens in a single individual and gets fixed through selection in the population.
What’s the big problem?
Why bother learning when it’s so much easier to blindly attack things one doesn’t understand? I’m only surprised we haven’t heard
“That’s not evolution because the M&Ms are still M&Ms!! I demand to see them turn into a roast beef sandwich!!”
Besides, everyone knows the reason why Jesus doesn’t like M&Ms*
*sorry, you’ll have to look up the punchline yourselves.
Lizzie’s code does (almost) exactly what is described in the OP: at each iteration one random M&M is eaten and replaced with a copy of another random M&M:
Eaten=randsample(1:N,2,true);
Doubled=randsample(1:N,2,true);
Bag(Eaten)=Bag(Doubled);
(The ‘almost’ qualification is due to the fact that there is a chance of an identity transform when Eaten=Doubled.) That’s not what you describe above, is it?
My average time to fixation for a bag of 64 with 5 colors is about 3,500 iterations.
You’re clearly not here to have an open, friendly discussion about the subject of this thread, but just to publish empty and dismissive comments about nasty atheist darwinist materialist boogeymen like PZ Myers and Jerry Coyne.
No no, they’ve got an even better one. It’s just pre-existing variation (all the colours already existed in the population, they didn’t evolve through mutation). Also, a simple change in colour is just microevolution. No new bodyplans.
See, I would make an excellent creationist. Got almost all their non-arguments memorized.
Not only that but it’s empirically observed in the real world too. I’ve mentioned this before but my favorite example is the Apo-a1 Milano mutation that helps reduce HDL cholesterol.
“Discovered by accident, the mutation was found to be present in about 3.5% of the population of Limone sul Garda, a small village in northern Italy. It has been traced to a mutation in a single man, Giovanni Pomarelli, who lived in the village in the 18th century and passed it on to his offspring.”
Furthermore, can an M&M change into a Smartie? No !! This proves that evolution can’t work.
Perhaps, in part, junk DNA with occasional transposition of some of this so that it becomes coding DNA.
I have to say I admire the energy that you and a few others display in arguing (in the Monty Python sense) with so many opponents in this forum.
But I don’t agree with anything in your comments
I simply meant that this discussion seems to me to be a minor example of the fun scientists have doing their work.
Arguing
The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski’s research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT. … In the most open-ended laboratory evolution experiment (Lenski 2004), in which no specific selection pressure was intentionally brought to bear, all of the adaptive mutations that have been so far identified have either been loss-of-FCT or modification-of-function mutations, and there is strong reason to believe that most of the modification-of-function mutations diminished protein activity. – See more at: http://www.evolutionnews.org/2010/12/michael_behes_quarterly_review041221.html#sthash.aqY3n8CJ.dpuf
You have even gotten up to the point that we are discussing neutral drift, not beneficial ones, so I think you have a ways to go.
Great, let’s see if he can run the experiment using one black M&M (to represent a new mutation) into a population of 1000 non-black M&M’s and let’s see how often the whole bag ends up black then.
I am not sure why you all are all arguing with phoodoo. You all admitted in the other thread that both Avida and Mendel’s accountant can’t model evolution, so how can you argue M&M Moran model is anything more than a toy model. It serves the purpose of showing fixation in a constant population with one simultaneous death and birth and that’s fine, but phoodoo’s contention is evolution is far more complex than that – isn’t it true?
Fair enough. But until you are willing to address where you disagree, I won’t take your lack of agreement too seriously.
I updated it to clarify what I meant originally.
But the referenced video provides my thoughts on why further comment would be futile, and probably subject to prosecution by Inspector Thompson’s Gazelle.
Where did anyone claim the simplistic M&M model represented all of ToE?
In my opinion one has to consider almost all arguments from evolutionists online, and particularly ones who also claim to be skeptics, to have a certain basis of theology in their emotional responses. Its not just an argument based on fact, no matter how much they insist it is, it is one of preaching their ideology of fervent atheism.
I mean just look at the nonsense spewed by guys like thorton the moment he hears someone question his beloved religion, he practically has foam coming out of his mouth with every reply. The more rabid and spastic their replies, the more obvious the lack of content their arguments contain.
Its amusing, but also telling. Its the same folks who go around trying to censor education in schools, or trying to censor Wikipedia to preach their world views. Its become quite common. They call it “guerrilla skeptics”. Talk about a religion.
I like Monty Python as much as the next guy.
Alas its another link I can’t open unfortunately.
And you start off with all the populations of colors being equal?
You don’t have to. You are free to write your own code, phoodoo. Why not do that?
Join the fun.
LOL! Yeah, double darn those guys who reference the primary scientific literature instead of Genesis.
What were we thinking? 🙂
While many proteins will allow some variation if the rest of protein is unaltered, multiple substitutions will generally lead to a loss of function. So the question is whether the extremely rare beneficial mutation can become fixed in the population before the more common deleterious mutations are allowed to accumulate.
Agreed. And this cuts both ways.
If a constant input of beneficial mutations is required, then It is not sufficient for the proportion to be just non-zero. The proportion must be at least high enough to outweigh the accumulated deleterious mutations that are also becoming fixed.
I like the analogy. And from what I’ve seen, most adaptive changes (i.e. finches beaks) return to normal when the stressor is removed.
Also, Phoodoo, if you could code an ID model we’d all love to play with it!
Thanks in advance.
Yes, he can. However, if Joe does all the work, you, phoodoo, will learn exactly nothing.
So get off your lazy ass and do some numerical experiments. You can’t learn anything by merely looking.
Dop you have any evidence that deleterious mutations accumulate to the point where a population is endangered? Why are bacteria not extinct.
In particular, how do you account for the hundreds of mutations fixed in the Lenski experiment?
Lenski’s population started from a single cell and underwent 58,000 generations. Why didn’t it go extinct.
Dou you have a quantitative model that accounts for this?
That’s a shame. I am not sure whether you are familiar with the show and so know the sketch: it’s the one where someone visits a company that allows you to buy time to engage in a argument with an employee.
But after paying, the customer gets frustrated because he finds the employee simply contradicting whatever he says, rather than engaging in what he thought he paid for, namely a reasoned, considered discussion. Then the customer goes to the complaints department where he has to listen to someone’s complaints. Etc. It ends with Inspector Thomson’s Gazelle arresting everyone, for among other things, ending sketches by having policemen arrest everyone, and so of course he gets arrested…
I just ran a variant on the original simulation, assuming a one-dimensional world and a fixed mixing radius: at each iteration, after an M&M is eaten, it is replaced with a copy of an M&M in its neighborhood defined by the mixing radius. With a population of 64 and 5 alleles, the time to fixation increased in an inverse relationship to the mixing radius, from about 3,400 iterations for a radius that encompasses the entire population to about 5,600 for a mixing radius of 3. Interestingly, at the radius of 2 the number of iterations bounces back to 5,300. It would be interesting to try this in a higher-dimensional world.
Can phoodoo or Piltdown2 please explain why the Apo-a1 Milano mutation is spreading through and becoming fixed in the population?
What is the mechanism for this empirically observed event?
Neil Rickert,
I’d still count that as a mutation, myself.
phoodoo,
He doesn’t really have to. 1 in every 1000 replicates on average. p(fixation) = current frequency. f=1/N therefore p=1/N. N=1000 so p is 1 in 1000.
Suppose one of us wrote some code and announced that they had achieved approximately that result. Would you believe it? Doubtful. Suppose, conversely, that YOU wrote the code. How much more satisfying would that be? This is an experiment anyone can do, with a bit of basic computing. You don’t even need to do the computing, with a bit of basic math.
phoodoo,
Yes, very interesting. Now, back to models of population sampling …
I bet a smart cat like Phoodoo could make excel do it…!
The single color M&M’s would simulate asexual reproduction. I think I see what you’ve done to expand it to 2-color M&M’s to get the same result for a sexual population, just taking longer. Thanks.
I’m not convinced that only novel mutations can restore diversity. Don’t want to get too far out of my depth, but since the genome contains large amounts of non-coding region, diversity could be maintained by the existing genome. And I do not deny the possibility of new mutations being fixed, I just realize how long it takes, especially in a large sexually-reproducing population.
phoodoo,
Why do you think this matters? If we start with them unequal, we’d be accused of weighting the game in favour of the majority colour (since p(fixation) equals … ). So starting with them all equal is … ummm … ‘fair’.
In fact the best way to think of all runs is in terms of N different colours. Then, they must all start at the same frequency – 1/N. Number them; it makes life easier. Alternatively, make 500 the same and 500 all different. Or … or do what you like. In all cases, an ‘ancestor’ will fix, drawn from a pool of whatever size you delimit by common character.
What do you mean by novel mutation? How is that different from a non-novel mutation?
SophistiCat,
Interesting – how many runs did you do to establish the time to fixation? It’s pretty variable, as you can see from staring at Lizzie’s grid, so would need quite a few runs at each parameter to get a realistic distribution.
Not only do the finches beaks simply fluctuate and return to the norm, this phenomenon stretches across every living thing. Bacteria always return to the original form, dogs do, plants do, …what we see is that for every extreme phenotype which deviates from the more common population, they always have some fitness disadvantage which takes them too far down the road, and they either die, or are forced to return to the mean.
Its why no matter how much plant breeding or dog breeding or fly breeding we do, the organisms hit dead ends and can never become something else. Every dog breed is a testament to the fact that evolution doesn’t work. To achieve these extreme phenotype expressions, they suffer too many health affects which make them much less adept at surviving, not more. Make a dog too big they suffer health problems and premature death, make a dog too small, they suffer health effects and premature death. Once the pressures are removed from lenski’s citrus eating bacteria, they can’t compete against the non-mutated forms, there is too high a cost in fitness.
But you won’t ever get anyone here to acknowledge that, because their rationalizations know no bounds.
Why do I think this matters? You really need to ask this?
We are trying to make a model of how a NOVEL mutation, which is not deleterious, can drift through the population and become the norm. So we have to start with it being novel don’t we? Why weight the game so that the novel function has already spread equally throughout the population? Isn’t that obvious.
Start with one, see where it goes. It will die every time. I can tell you that even without a little computer program. You have to begin the game being smarter than the machine or the machine is useless.
How do you know that, phoodoo? Have you checked?
I suggest that you write some simple code and run it many times to see whether you are right. Several commentators on this blog have said that the probability of fixation in this case is nonzero. In fact, they have estimated what it is. It shouldn’t be hard to check.
Maybe you’ll learn something that way.
Well, the average lifespan of a wolf is about 7 years, and they can breed at two, give or take a bit. I don’t know of any domestic dog breed with a shorter lifespan.
Most of the health problems occur due to population bottlenecks and inbreeding.
I’m not sure how biblical literalists get around the problem of inbreeding after the flood. Ken Ham seems to teach that there was an explosion of evolution, producing new species from “kinds.”
That’s is exactly right. Science is never able to establish the fact that these adaptive novel functions that we view in nature are not already existing genomes in the organism, which just get turned on or off.
The is not reasonable explanation in science for how an epigenetic network came about through random mutations.
The more we learn, the less likely Darwinism becomes. The only people who can deny this are the “skeptics”; who quite profoundly possess zero skepticism.
How is a NOVEL mutation different from a mutation?
In captivity wolves can live up to 20 years. Its rare for a Great Dane to live more than 10. But don’t let that upset your worldview.
And a Chihuahua in the wild will live to about a week, assuming someone helps it find water.
Feral dogs certainly undergo some weeding out, but they do not go extinct and they do not revert to wolves.
Lots of species — the overwhelming majority of known species — have gone extinct. Environments change.
At the moment, poodles live an an environment that favors poodleness. Wolves, on the other hand, have gone extinct over most of their range.