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Evolution Basics: From Variation to Speciation, Part 1

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May 16, 2013 Tags: Genetics
Evolution Basics: From Variation to Speciation, Part 1

Today's entry was written by Dennis Venema. You can read more about what we believe here.

Note: This series of posts is intended as a basic introduction to the science of evolution for non-specialists. You can see the introduction to this series here. In this post we examine how variation spreads within a population, and how differences between populations can arise over time.

In the last post in this series, we examined how DNA variation arises as chance events, such as base-pair mismatches, duplications and deletions. In order to understand how this variation may (eventually) contribute to a speciation event, we need to discuss how variation spreads within a population. First, we need a small amount of vocabulary to facilitate the discussion: specifically, we need to explain the distinction between a gene and an allele.

As a geneticist, I pull my hair out at times when reading popular media reports of scientific matters. One of my biggest pet peeves is the use of the word “gene” in the sense of saying that an individual “has the gene” for a specific trait. We have already described genes are a section of DNA sequence on a chromosome that contributes to a function of some kind, usually by coding for a protein product. In this sense, humans all have the same genes (or very nearly so)—the 20,000 or so sequences that make us who we are biologically. What we don’t have, however, are identical genes—there are differences that arise through the copying errors that we have discussed. These differences are called alleles. You can think of an allele as a “version” or “flavor” of a gene. Mutation events don’t usually create new genes (though they can through duplication). Usually, new alleles are created. In a prior post, we used children’s toy bricks to illustrate how a new variant could arise through a DNA base-pairing mistake during chromosome replication:

In this example, we have a sequence that, through a copying error, becomes two slightly different versions of what is (almost) the same sequence.  These differences would be called two distinct alleles, and if they affect the function of a gene, they might have a noticeable effect at the level of the whole organism. When the media talks about the “gene” for this or that trait, what they actually mean is the allele for a given trait—the specific variant of a gene that is correlated with a specific medical condition, for example.

Selection and drift

So, DNA variation is all about the production of new alleles—but what happens to these alleles over time within a population? Obviously, when a new allele arises, it is present in only one individual. If it is to make an impact on the population as a whole, it needs to spread to other individuals by being passed on to offspring. In this way, variation can enter a population and then become more common over time. There are a number of factors that can influence this process. If the population size is small, then chance alone can increase (or decrease) the frequency of an allele in a population—an effect known as genetic drift. Since drift can be a major player in how allele frequencies change over time in a population, it’s worth taking some time to discuss it in some detail.

Drift is essentially a non-representative sampling event. Consider a small population of sexually reproducing organisms that we can represent as rectangles, each containing two alleles (the squares, with the colors representing allele differences). We can represent their “reproduction” as a 50:50 chance of passing on either allele to their offspring in the next generation. (Note: each “passing” event is independent of any other—for example, there is no mechanism to guarantee that any individual would pass down both of their alleles if they reproduced twice.) For the breeding pair on the left, one parent has two yellow alleles, and the other has a blue allele and a yellow allele. When they reproduce, by chance the parent with both alleles passes on only the yellow allele to both offspring. For the breeding pair on the left, the parent with both alleles also passes on the yellow allele twice, and their blue allele not at all. These chance events shift the frequency of the two alleles quite significantly within one generation:

Now imagine that the offspring pair up to mate, and that once again we have, by chance, a slightly non-representative sampling to form the next generation:

The point is that this small population is prone to large fluctuations in the frequencies of the blue or yellow alleles because it is so small. This small size means that chance events within even one breeding pair have a large impact on the population as a whole. In the next generation, for example, the blue allele might be lost completely—and once it has disappeared, it will be absent until it either arises again through a new mutation event, or enters the population through an individual migrating in from a population where it is still present.

For large populations, however, the situation is rather different. Imagine a population with 1000 individuals, with a total of 500 yellow alleles and 500 blue alleles randomly distributed among the individuals. When this population reproduces, it will never vary much from this 50:50 ratio from one generation to the next. In this large population, chance events within one breeding pair are a very small proportion of the population as a whole, and on average, the population will reflect the 50:50 probability of any allele being passed on.

So, how can allele frequencies change in large populations, when drift is largely impotent? We have already seen one mechanism that can accomplish this: natural selection.  Natural selection is simply the effect that individuals who possess a certain allele reproduce more frequently than individuals who do not have that allele. Over time, this skewing of the probability of reproducing increases the frequency of the selected allele in the population. For dogs early in the domestication process, duplication of amylase genes happened as a one-time, chance mutation event. Dogs that carried the duplicated amylase allele reproduced at a slightly greater frequency than dogs without it, since the duplication allele allowed for dogs to derive more nutrition from the food they were receiving from their new environment (i.e. human sources). Over time, the duplicated allele became so frequent in the dog population that the ancestral, non-duplicated allele was lost all together. At this point the new allele was “fixed” in the population: it had a frequency of 100%.

To sum up: in small populations, drift can have a large impact on allele frequencies from one generation to the next. In large populations, natural selection predominates, and drift has little impact. Both of these mechanisms can contribute to changing allele frequencies over time within populations, and as such both can be factors that contribute to speciation events.

Changing allele frequencies and speciation

Speciation is the production of two species from a common ancestral population. (Now, we have already discussed how defining “species” is a fuzzy concept, and it is the fact that they arise slowly and incrementally that makes them challenging to define.)

One way to understand how speciation starts is to consider two populations of the same species, that for whatever reason, stop interbreeding with each other—perhaps through geographic isolation. While a geographic “barrier” has nothing at all to do with genetic differences or reproductive compatibility, if such a barrier is in place, then alleles that arise in one population will not be transferred to the other population. Additionally, if two populations are not exchanging alleles, then allele frequencies in the two populations are now no longer tied to the other and averaged between them. This means that drift and selection will now act independently on the two populations. Once uncoupled, the two populations may then follow different trajectories—one population may start out small, and be dominated by drift until it increases in size. The other population may remain large, and be subject to natural selection in ways the other population is not. Over a long period of time, the two populations may become genetically different enough that they form two distinct species. The key, of course, is the nature of the barrier preventing exchange of alleles between populations. In the next post in this series, we’ll examine how such barriers can form between populations. 


Dennis Venema is professor of biology at Trinity Western University in Langley, British Columbia. He holds a B.Sc. (with Honors) from the University of British Columbia (1996), and received his Ph.D. from the University of British Columbia in 2003. His research is focused on the genetics of pattern formation and signaling using the common fruit fly Drosophila melanogaster as a model organism. Dennis is a gifted thinker and writer on matters of science and faith, but also an award-winning biology teacher—he won the 2008 College Biology Teaching Award from the National Association of Biology Teachers. He and his family enjoy numerous outdoor activities that the Canadian Pacific coast region has to offer. Dennis writes regularly for the BioLogos Forum about the biological evidence for evolution.

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beaglelady - #80176

May 16th 2013

Excellent as ever, Dennis!  

Over a long period of time, the two populations may become genetically different enough that they form two distinct species. The key, of course, is the nature of the barrier preventing exchange of alleles between populations.

A timely and fascinating example would be the periodical cicadas, because the 17-year ones  are emerging from underground about now, looking for a sweetheart.   Not much chance of their meeting the 13-year cidadas!

Lou Jost - #80178

May 16th 2013

The speciation process is fascinating. One of my main topics of research is to discover how complete the barrier must be in order to make the populations diverge (or how leaky it has to be to keep the populations locked together). I look forward to seeing the next installment on the subject.

Dennis Venema - #80183

May 16th 2013

Thanks! Always nice to know I have the BeagleLady seal of approval. Hope you’re doing well.

Dennis Venema - #80184

May 16th 2013

Hi Lou,

Yes, it is a fascinating question. Tomorrow’s post deals with geographic isolation, which is an effective barrier even before any biological differences separate populations.

Lou Jost - #80185

May 16th 2013

I look forward to it.

beaglelady - #80186

May 16th 2013

Same here!

GJDS - #80188

May 16th 2013

I guess I will spoil the endless congratulations .....

“So, how can allele frequencies change in large populations, when drift is largely impotent? We have already seen one mechanism that can accomplish this: natural selection.  Natural selection is simply the effect that individuals who possess a certain allele reproduce more frequently than individuals who do not have that allele. Over time, this skewing of the probability of reproducing increases the frequency of the selected allele in the population.”

A typical rational:

“Natural selection works by weeding less fit variants out of a population. We would expect natural selection to remove alleles with negative effects from a population—and yet many populations include individuals carrying such alleles. Human populations, for example, generally carry some disease-causing alleles that affect reproduction. So why are these deleterious alleles still around anyway? What keeps natural selection from getting rid of them?” 

This is usually followed by at least 5 reasons why the magic of natural selection may or may not operate, and in any event, since populations are what they are, it must work!

From: J. K. Pickrell, J. K. Pritchard, “Inference of Population Splits and Mixtures from Genome-Wide Allele Frequency Data”, PLOS Genetics, 2012, Vol 8, Issue 11, p.

“We applied this method to a set of 55 human populations and a set of 82 dog breeds and wild canids. In both species, we show that a simple bifurcating tree does not fully describe the data; in contrast, we infer many migration events.”


“However, these methods are not directly informative about history; indeed, the relationship between the major components of genetic variation and true underlying demography is not always intuitive.”....... and   “when modeling the history of populations as a tree is that gene flow violates the assumptions of the model”

Now from reading this “BioLogos introduction” one would be left with the impression that it is all ‘done and dusted’ ...

I am sure there will be numerous (and perhaps weird) response, but can we believe this ‘introduction’ after we compare the views provided by the most advanced methods available to this area?

And how many ‘may be this and may be that’ does it take to get your thinking to June? (rhetorical stuff ... do not get too excited).

melanogaster - #80201

May 17th 2013

Sorry, GJDS, I don’t see anything in your quote mining that negates anything in Dennis’s fine post.

Have you considered the novel idea of stating things in your own words instead of disjointed quoting? That would more clearly describe your concerns and allow others to address them.

For example, Dennis wrote:
“If the population size is small, then chance alone can increase (or decrease) the frequency of an allele in a population—an effect known as genetic drift.”

But you quote mined:
“So, how can allele frequencies change in large populations…”

Doesn’t Dennis’s qualification (the use of “if” is a tipoff) make your mined quote irrelevant?

beaglelady - #80206

May 17th 2013

Many disease-causing mutations are recessive, so they tend to stick around longer.  And some disease-causing mutations are actually advantageous if you are heterozygous for them—an example is the sickle-cell gene.   The “founder effect” can cause bad mutations to be common in a small population.   What about deleterious mutations that kill you by age 10—if you have such a mutation will you mature to adulthood and pass that mutation on to your children? I don’t think so.

PNG - #80217

May 17th 2013

You seem to think there is some connection between the paper you quote mined and what Dennis is talking about. The paper isn’t about whether natural selection or drift occurred. It’s about a new method for estimating past population divergences and subsequent migrations between the populations using mathematical models and large scale allele frequency data from different current populations. As they state in the paper, “it is now feasible to collect genome-wide genetic data in any species; to a large extent it is no longer the data collection, but rather the statistical models used for analysis, that limit the historical insight possible.” Their new method is supposed to allow them to detect gene flow from migrations that occur after the original separation of populations, as if for example, after the Galapagos finches arrived on the islands and differentiated into a separate population, there had been an arrival of more individuals from the mainland who then interbred. 

The first quote just means that they found evidence that dogs continued to interbreed with wolves on occasion for quite some time, something that other studies support as well. The second quote isn’t about the method in the paper - it’s a statement about an approach that other groups have used, and the criticism is one reason for their developing a new method.

Your quote mining seems to follow a pattern that is common among lay anti-evolutionists. Find a paper (that they don’t understand) and find quotes that seem to express some kind of uncertainty about a current research problem, and then use that to assert that the whole field is worthless. (obvious non sequitur) It’s not what I would expect from someone who is a scientist.

I don’t know near enough to evaluate the method described in this paper, but I can say that there is nothing about this paper that should lead anyone to dismiss what Dennis is saying.

GJDS - #80229

May 17th 2013

Your comments are correct as far as they relate to the purpose of this paper. I have looked throuhg it (and am continuing to do so) to get a feel for the methodology and how this may bring certainty or uncertainty to ths subject. I am also looking at a 1993 paper which appears to adopt a somewhat different approach, but have not included it in this post on the assumption this paper may be more advanced.

My interest has been (from the first time I posted on this site) to get some type of overall outlook on the notion that natural selection can be considered a ‘law of science’ as I understand the phrase. Even though I find some of the assumptions difficult to rationalise in the paper I quoted (and many others), I am not interested in criticising or commenting on the quality of other peoples work - my main interest is to see if I can tie up data, its treatment, with the statements made by some people on this site regarding ‘the law of natural selection’ (as equivalent to say, the theory of chemical bonding).

While I have admitted from the start that this area is not my field, and I have little (if any) professional interest in whatever area of evolution you people get excited about regarding the Christian faith, I consider myself sufficiently competent to distinguish between a genuine law of science and a ‘bunch’ of semantics that purport to be such. So far I have not seen anything on this series (or this blog site) that would indicate you evolutionists understand the distinction between semantics and established laws of science. I would be glad if you can prove this statement is wrong.

In any event, (and in spite of the odd comments people on this site make about my abilities as a scientist) I am at least impressed that one person has bothered to look up one of the many references I have brought up in these posts. Perhaps you may set a novel trend. 

Lou Jost - #80246

May 18th 2013

Yes, but you don’t seem to learn anything from what we tell you when we look up these papers. You did exactly the same thing with a paper about karyotypes on a previous thread: quote-mining parts of the paper completely out of context, making the paper sound critical of common descent, when in fact the paper provided beautiful independent evidence for common descent, and its conclusions were the opposite of yours. I pointed this out and you obfuscated, and now you do the same thing again.

If you think population genetics is semantics, you have never looked at a pop gen textbook. If you think the evidence for common descent is just semantic, you haven’t even read the posts on this website.

GJDS - #80250

May 18th 2013

Can it be Lou the atheist again - are you determijed to become my shadow? Since you are such an world renounded expert, why not comment on the maths that are used in this model and also the assumptions - and then (joy oh joy) tell the world how it is consistent/based on/emerging/ from your blessed ‘law of natural selection’. After all, it does seem to be a tenent of this post by this Dennis fellow.

GJDS - #80252

May 18th 2013

Oh I forgot to add a joke our science teacher used to tell us during my college days (so long ago):

Figures don’t lie, but liers can figure.

The entire class laughed (even the atheists and perhaps even US evangelists, although I will not swear if the latter were amongst us).

PNG - #80289

May 19th 2013

Lou, being not much more than a dilettante on population genetics, I’d be interested to hear what kind of observational evidence can be gathered to support the basic aspects of the theory. I’ve seen things like fitting observations of allele frequency distributions for mutations (transposon insertions) to a neutral model, but I’m curious what other sorts of things are done.

Lou Jost - #80314

May 19th 2013

PNG, that is a very broad question. Maybe it would be useful to first say a word about what population genetics is. Population genetics studies how gene frequencies change over time in a population, and how subdivided populations diverge genetically, among other things. The approach to these questions is analogous to the approach that physicists use in statistical mechanics, and the two fields even share much of the same math. We start with an idealized system, analogous to the “ideal gas” of physicists. The idealizations we make depend on the subject of interest, but often include 1) random mating within a population, 2) fixed mutation rate, and 3) unlinked loci. To establish a baseline for the action of natural selection, we also often look at what happens when natural selection does not affect the locus of interest. As in statistical mechanics, we also often assume that the system has reached equilibrium (though unlike ideal gasses, biological systems reach equilibrium very slowly, so this assumption has to be carefully justified in an application).

For a given set of assumptions, population geneticists derive mathematical laws that have the same force as the laws of statistical mechanics derived for ideal gasses. These derivations are often complex and often involve approximations, just as in statistical mechanics. We first test them by computer simulations because we can ensure that the assumptions are valid. Once they prove robust in the computer, we can try them out in the real world. The paper that GJDS cites is an example of this. The authors show that their population genetics model correctly and accurately identifies known historic migration events between human populations, but the authors also caution that when the model assumptions are badly violated, their model fails.

Some of the most basic predictions of population genetics involve the distribution of allele and haplotype frequencies in a randomly mating population, and the accuracy of these predictions is very well confirmed. These predictions were derived by the famous mathematician Hardy and independently by the biologist Weinberg a hundred years ago. They are fairly trivial results. Much more complex predictions based on things like the Ewens sampling formula are also confirmed in humans and other organisms.

More interesting predictions can be made when we can measure the fitness of a set of alleles (perhaps by breeding experiments, or by multi-generation observations in the field). Then we can predict the action of natural selection: we can tell what the equilibrium allele frequencies will be, and how long it will take the population to reach that equilibrium. These predictions are also broadly confirmed.

Population genetics also predicts that genetic drift will occur under certain specific conditions, and it predicts the average magnitude of the drift. These predictions have been confirmed in experiments with fruitflies and other organisms. The prediction of random genetic drift does not mean that “anything can happen”, as some people like to say. The exact conditions for drift, and its mean magnitude, are mathematically determined by an equation involving population size, strength of natural selection at the locus, and (if we are considering long time scales) mutation rate.

While much of pop gen is based on idealized models, there is also a constant effort made to extend the models to include more and more layers of complexity and realism. The math gets hairy, sometimes computer simulations can implement algorithms that have no simple mathematical solution. Pop geneticists love computers!!!!

There is a lot more; check out any good pop gen text like Hartl and Clark, “Principles of Population Genetics” or for a more basic one, Hedrick’s text.

Pop gen is not perfect: much of my own work consists of trying to correct a fundamental mistake that has been around since the 1930s….

Lou Jost - #80320

May 19th 2013

PNG, this was probably too basic for you…but may help some of the other commenters who don’t have much background in what population genetics is.

GJDS - #80325

May 19th 2013

This is consistent with what I have read in this paper - however my question remains - how does this work show a ‘natural selection’? By this I am trying to see a similar basis that I would expect (without question) when I apply any modelling and simulations involving, say molecular bonding and structure - e.g. valence bonding theory involves hybridisation of s and p orbitals to give the familiar structure of methane, and we go on the model bond lengths, angles, electron densities, and show how physical (measureable) properties can be derived from all of this.

The previous paper PNG had commented on (a previous post) showed how the entire population of humans could be modelled based on a host of measured and historical data (migtation, deaths, births, etc etc), on the assumption that it began with one male and one female, and they gave a resonable time span, without including these genetic matters discussed in the present paper. Surely if the basis for such simulations is a law of science (natural selection) the latter simulation would have to have failed (and in anticipation of an aggressive response, the latter example does not mention Adam and Eve or any religious matter).


GJDS - #80278

May 18th 2013

I will respond to you on the assumption you value your credibility as a worker in your field and are not interested in the argy bargy that is typical of this series - I direct your attention to the statement that in this post in this series natural selection is given as either one of the mechanisms (whatever that may mean) or the means by which this thesis is supported. The paper I refered to simply shows that natural selection is not evoked, referred to, relied on etc. This stikes me as strange when one considers the centrality of this notion to the entire subject discussed.

It is also appropriate to point out that another simulation package discussed in this cyber-place has simulated the entire population on earth, based on the premise that it commenced with one male and one female, in a time span (I cannot recollect the number) of between 5,000 and 10,000 years.

Surely only a fanatic would make claims for any ‘law of nature’ based on these type of treatments of the data - yet the way your collaborators ‘scream’ about data and how all others are blind to it, would suggest such extreme outlooks.

These models are a way of using a data base. the paper I have to referred to also shows that it MUST use some type of tree model to get any results - again you should appreciate that this is embedded in the treatment methid, and not support for any mechanism(s) based on a ‘law of nature’. It is not evidence in the correct use of the term - it simply shows the treatment method is just that type of method.

I am going through the last stages of examining this paper and if you wish for further comment you should make it and I will consider it when I go through the paper for the last time.

You should understand the difference between the banality of the ‘quote mining’ term used by Lou and others, and my examination of published work, to examine if any fundamental laws and the associated certainty that accompanies such, may be detected in the research. 

GJDS - #80327

May 19th 2013

I am having trouble with the reply button again ... I repost this:

This is consistent with what I have read in this paper - however my question remains - how is this work based on the scientific law termed ‘natural selection’? By this I am seeking the basis you claim is similar to molecular bonding and structure. When I apply any molecular modelling and simulations, the theory of molecular bonding and structure is always the basis and it is directly linked to the maths and reasoning - e.g. valence bonding theory involves hybridisation of s and p orbitals to give the familiar structure of methane; modelling provides bond lengths, angles, electron densities, and we than provide various properties from all of this (e.g. NMR spectra) which can then be directly compared with the measurements.

The previous paper PNG had commented on (another post) showed how the entire population of humans could be modelled based on a host of measured and historical data (migration, deaths, births, etc etc), on the assumption that it began with one male and one female, and a reasonable, historically measured time span, without including these genetic matters discussed in the present paper. Surely if the basis for such simulations is a law of science (natural selection) the latter simulation would have to have failed (and in anticipation of an aggressive response, the latter example does not mention Adam and Eve or any religious matter).

Again I ask, where does the treatment provided in this paper show a direct link to a law of science termed natural selection, and then rationalise the results of the simulation with the workings of this law? I for one cannot find anything that would even resemble the mundane example of the treatment of methane that I have given.

Lou Jost - #80330

May 19th 2013

I am still unsure about what you are asking, but I will give it a shot. First, I said that population genetics is analogous to statistical mechanics, not bonding chemistry. Its laws are like the laws of statistical mechanics for ideal gases; they apply exactly to idealized systems, and become less realistic as departures from the idealizations become large.

Natural selection over the short periods of time involvd in this study will have noticeable effects on only a very few loci of the genome; most of the genetic code will be neutral, or nearly so, with respect to natural selection. So in the paper you cited (which is not very relevant to Dennis’ post), they work with an idealized model that ignores natural selection. Since they are working with such a large portion of the genome, the tiny number of loci which are affected by natural selection in these short time periods has little effect on the results.

The laws that they are using (as far as I can tell after a cursory reading) are the laws about how migration affects genetic diversity and differentiation in the absence of natural selection. These laws are not really discussed in the paper.  If you want to learn about the basic laws governing genetic systems, you need to look at a basic textbook, not an applied research paper. The Hartl and Clark one is a good start, and is available in any university library. You will find some laws that include natural selection, and others that are valid only for neutral loci.

GJDS - #80332

May 19th 2013

I have responded to the statment in this post:

“So, how can allele frequencies change in large populations, when drift is largely impotent? We have already seen one mechanism that can accomplish this: natural selection.”

I have given additional examples to show you how the ‘laws of science’ are employed in everyday research - if your research differs, it is inapropriate to constantly use sentences such as ‘evolution is a theory such as that of chemical bonding and quantum mechanics’.

The example below shows that how gas phase chemistry may be treated (I cannot understand why you refer to a theory of gases that you assume uses little balls bouncing around a container).

If your approach somehow seeks to use statistics and then may refer to some sort of natural selection, it should be part of any research paper. I have shown by simple textual analysis of some papers that the meaning of the research remains unaffected if one simply ignores any referenc to Darwin’s thinking. Surely this should be relevant to an authentic scientific research!

Lou Jost - #80338

May 19th 2013

I suggest you look at the text I mentioned if you are sincere in wanting to know what kind of laws we have in population genetics. I have tried to explain what they are like, but you need to see and study the actual equations and derivations to really understand them.

I told you that natural selection is not involved in the processes studied by the article you cite. If you want to see how natural selection works, I suggest you look at the textbook I mentioned or read a paper that involves natural selection.

GJDS - #80339

May 19th 2013

Are you saying the statement by Dennis (that I have quoted on at least two occasions and can be read by anyone) is untrue?

I also remind you that your pompous rejection of the paper that discussed variation and natural selection (my quote mining?) in fact was entirely on these ideas - if you are sincere, you would have examined and commented on the remarkable statements that I interprete as:

A - variation as discussed in Darwinian thinking cannot be shown to be true using current scientific techniques.

B- Natural selection is either a tautology or unnecessary as a species existing must by definition conform to this.

C - However, a combination of variation and natural selection must be true.

So, A = false

B = false


But A+B = true

Wild stuff for science Lou. And why is there so much discussion on semantics and terminology in the literature on philosophy of biology, if it so clear, settled and text book perfect?

Just a few remarks Lou - do not get too aggresive on this.

Lou Jost - #80340

May 19th 2013

The statement of Dennis is true, as Melanogaster and PNG also explained.

PNG’s explanation of the paper you cited is also very clear and correct.

Your statement A above is not true; variation is obvious and easy to demonstrate, even just by looking closely at individuals of any species, including people.

Your statement in B that natural selection is a tautalogy is partly right, in the sense that the most fit alleles have to increase relative to the others, in a population of fixed size. This is one reason evolution is undeniable. But there is more to it than that. We can measure fitness of each allele, and then we can use those numbers to predict the future genetic composition of the population at equilibrium, and predict the time it will take to arrive at that equilibrium.

Theoretically we could predict fitness from an allele’s effect on the body, if we know a enough about the organism’s environment and requirements. If there is an achievable optimum in some dimension, we can show that the organism will approach that optimum (without the need to invoke design).

GJDS - #80342

May 19th 2013

I can see that it is pointless having conversations/discussions with you - of course variation is there, it is self-evidnt. You should feel obligated to describe the scientific basis for variation that leads to the formation of new species. You trivialise deep discussions of this point and then speak as if these matters were self evident. I will not continue this pointless exchange, but repeat what I have said it seems too many times - tie in these (or other research papers/results) with the ‘scientific law’ of natural selection - not what you insist must be the case. You and others have done everything. except do that - any scientist could provide an answer to such a question for his field in half a page. You lot seem to look for more argumentation and nonsense.

The end. 

Lou Jost - #80344

May 19th 2013

“You should feel obligated to describe the scientific basis for variation that leads to the formation of new species.”

Why didn’t you say that is what you wanted? All you said was “variation as discussed in Darwinian thinking cannot be shown to be true using current scientific techniques.”

Separated populations will evolve in different directions by genetic drift, even in the absence of selective advantages, as long as there is not too much migration between them. The meaning of “too much” can be precisely quantified. This differential drift between the populations will eventually lead to reproductive isolation as physical and genetic incompatibilites accumulate. Look up articles by Gavrilets on speciation, for math details. In insects, reproductive isolation is often mediated by variation in genitalia structure. In plants, random variations that lead to shifts in pollinators often cause reproductive isolation (see studies of Mimulus for examples). When the populations live in places that have different mixes of pollinators, natural selection will act to shift each population’s characteristics to better fit the local pollinator assemblage, and this can also lead to reproductive isolation. Once isolated reproductively, the populations are separate species even if later their ranges come to overlap each other.

GJDS - #80333

May 19th 2013

A brief comment on Lou’s analogy of gas phase chemical kinetics (theory of gases) – this should (dare I hope) the fundamental error made by people such a low, as they appear to seek the legitimacy that is derived from sound ‘laws of science’ basis.

The treatment of gas phase chemistry/physics is chemical kinetics. I have developed a package that deals with gas phase combustion (the simplest version) and others have also developed similar packages. The treatment of these may readily be performed by setting up a series of chemical reactions which are treated as ordinary differential equations. The system is solved using standard mathematical techniques (not statistics) – if the system includes variable temperature, than the gas law is used in the maths. The results are directly dependent on measured rate constants, and the results are expressed as concentrations of products, which can be compared with measured values for particular systems.

Each and every step of the treatment is identified, and errors be related to the treatment method (number of steps and difference allowed for each iteration), the rate constants used in each equation, and any equations which may be based on different assumptions – each and every reaction is traced back to specific experimental data, and parts of the scheme (as well as the entire scheme) are subjected to critical analysis. Even then, certain assumptions are explicitly stated (e.g. a scheme may assume a perfectly stirred reactor).

These types of treatment can be extended into reactions schemes that seek to identify intermediates and transition state species. I can assure you that ‘laws of scienc’ are explicitly stated and understood in these treatments.

Packages that perform equilibrium calculations for such systems are also used, and these too must be assessed against well established data and ‘laws of science’.

I can discuss statistical approaches (e.g. conformational analysis of structures and those which may be preferred at given conditions).

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