Evolution Basics: From Variation to Speciation, Part 3

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May 30, 2013 Tags: Genetics, History of Life

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

Evolution Basics: From Variation to Speciation, Part 3

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 the fuzzy line between species and sub-species using so-called “ring species”, and discuss speciation based on resource partitioning.

In the last post in this series, we examined the relatively simple case of geographic separation of populations (such as a new population being founded on an island). Geographic separation is an effective barrier to what biologists call “gene flow” between populations – an effect more properly described as “allele flow”. As new alleles arise in separate populations, lack of interbreeding keeps each allele in the population where it arises. These new alleles may contribute to speciation over time if they affect the characteristics of the organism.  If, on the other extreme, new alleles can pass freely between two populations, then they will not contribute to a speciation event, since they will not make the two populations become more different over time.

What goes around, comes around

While these two extremes (geographically separated populations and fully continuous populations) are straightforward to understand, it is possible to find situations that are shades of gray between them. For example, consider two populations (we’ll call them “A” and “B”) that are members of the same species. They are able to exchange alleles between them, but at a reduced rate compared to sharing within each population. This effect can arise due to the geographic shape of their habitat – if it is long and narrow, then the two populations may abut each other only along a small portion of their range. This means that, on average, an individual from population A is more likely to find a mate within population A than to mate with a member of population B in their small area of overlap. We can represent this with boxes representing the two populations, abutting each other along one of their narrow sides:

This arrangement thus restricts, but does not completely abolish, allele flow between the two populations. In effect, this is a partial barrier to allele flow. Populations A and B are members of the same species, but the two populations are not genetically identical. As new alleles arise in population A, they are not shared across to population B as often as they are shared within population A, and vice versa. As such, populations A and B may have different frequencies of any given allele, and may even have some alleles that the other population lacks all together. It is also possible that the two populations may experience differences in natural selection (since their environments are not identical), and/or differences in genetic drift, depending on the population size for each. The net result is a balance of forces acting on the two populations – some favoring differences (selection and/or drift) and another favoring similarities (limited flow of alleles through interbreeding).

In nature, this effect can extend to multiple populations in a “string” spread out across a ribbon of suitable habitat. Let’s add three more populations (C, D and E) to the above example to illustrate:

Once populations become spread out over a wide geographic area, the differences between the populations at the extremities (populations A and E in our diagram) can become quite significant.  In some cases, interestingly enough, the populations on the ends of the string can be different enough that they do not recognize each other as members of the same species, despite the fact that they are genetically connected through a series of intermediate populations. In some cases, scientists need to bring members of the extreme populations together to see if they are able to interbreed (i.e. employing the biological species concept as a definition of species). In other cases, the topography of the habitat brings them together in nature, allowing the populations at the extremes of the string to meet each other around a ring, but with a natural barrier in the middle (such as a mountain or a valley of unsuitable habitat). The result is what are known as “ring species”:

You can see the inherent difficulty for defining which populations are separate species, (if indeed any are at all). There is allele flow between all populations, but only around the ring. The two populations at the (overlapping) ends, despite encountering each other in the same habitat, are different enough that they do not interbreed. Defining these populations as separate species (or not) is a fruitless attempt to draw a line of demarcation on a gradient. For those interested in a real-life example of a ring species, the subspecies of the salamander Ensatina eschscholtzii on the west coast of North America are both a textbook case and a subject of ongoing research.

Now, if we encountered the populations at the extremities in the wild without the intermediate, “bridging” populations, we would not hesitate to classify them as distinct species. It is also easy to see what would follow if any of the bridging populations were lost, or if changes in habitat severed the connection between any of them – the result would be a break in the chain of allele flow, cutting the terminal populations off from one another. What ring species illustrate is that though speciation is a slow process of accumulating differences between populations, it is possible even without a full barrier to allele flow.

Speciation without geographic separation

While ring species illustrate how species can form by partitioning variation out over a wide geographic area, it is also possible for barriers to allele flow to arise within a population in a more geographically compact location. All that is needed is a bias that promotes allele exchange within a subgroup of the population at the expense of exchange with the wider population – and as we have seen with ring species, this barrier need not be absolute to allow two subpopulations to accumulate differences and diverge from one another over time. One way for this to occur is for subpopulations to begin to exploit resources within a common geographic area differently – an effect known as resource partitioning.  As subpopulations begin to specialize into slightly different “manners of life”, as Darwin put it, they become more likely to interbreed within their subpopulation than with the population as a whole. Since preferential breeding is a (partial) barrier to allele flow, this can place the two subpopulations on a genetic trajectory that reinforces their differences and leads to a speciation event. Resource partitioning is the likely mechanism that drives multiple, rapid speciation events that occur when a founding population reaches a new habitat where competitors are largely absent. The colonization of volcanic islands, a topic we have discussed previously, can lead to adaptive radiation. One example is the numerous species of Darwin’s finches on the Galapagos Islands that descend from one species of finch that originally colonized the archipelago, and subsequently diversified into numerous species that specialize in different food sources. In the absence of other birds on the islands, many “manners of life” (what we would now call niches) were available for different subpopulations of birds to occupy.

Summing up – speciation starts as barriers to allele flow

Full geographic separation, the partial geographic separation seen with ring species, and resource partitioning of subpopulations are all barriers to allele flow between (what starts as) members of the same species. This provides the opportunity for new alleles to arise that are not shared between two populations, and shift the average characteristics of the two groups away from each other.  In the next post in this series, we’ll examine some of the traits that such alleles contribute to – traits that improve barriers to allele flow and thus promote speciation events. 

 


Dennis Venema is Fellow of Biology for The BioLogos Foundation and associate professor of biology at Trinity Western University in Langley, British Columbia. His research is focused on the genetics of pattern formation and signalling.

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Ed Babinski - #80570

May 30th 2013

Great job Dennis! Let me add two quotations from Christians: 

1) Stephen Schaffner, statistical geneticist at the Whitehead/MIT Center for Genome Research—points out why he finds the evidence for evolution compelling. Schaffner (who is a Christian) asks: 

Where is the creationist or I.D.ist model that explains the following types of observed genetic data? Such a model should produce estimates of the following measurable genetic data for modern humans:

a) The minor allele frequency spectrum.

b) The relationship between minor allele frequency and probability that the minor allele is the same as the chimpanzee base at that site.

c) The ratio of transition (purine<->purine or pyrimidine<->pyrimidine) polymorphisms to transversion (purine<->pyrimidine) polymmorphisms.

d) The ratio of polymorphisms at CpG sites to the overall polymorphism rate.

e) The distance over which significant linkage disequilibrium extends in a chromosome.

f) The genetic distance (difference in allele frequencies) between African and non-African populations.

g) The difference between African and non-African populations in the extent of linkage disequilibrium.

h) The distance over which significant autocorrelation in heterozygosity extends in a chromosome.

i) The ratio of fixed transition to transversion differences between humans and chimpanzees.

j) Same as (9), but for CpG sites.

There are other possible questions, but these are a reasonable starting point, since the quantities in question are all ones that I routinely use evolution to predict or intrepret. If the claim is true that creationists/I.D.ists look at the same data and just interpret it differently, there should be no difficulty in providing the creationist interpretation of these data.(Note that the answers should be derivable by anyone using the same model.)

I’m happy to answer questions about my list (which is deliberately terse—I didn’t feel like writing a survey of population genetics). Young-earth creationists should have the most trouble meeting my challenge. As you allow more and more time, and more and more evolution, it becomes harder to distinguish special creation from evolution. In the extreme case where all God does is cause a small number of critical mutations in the development of humans, the results will look exactly like evolution (provided the mutations occur in a fairly large population). In that case, of course, you have to wonder why those mutations also couldn’t have happened on their own, since every other mutation can.

2) Todd Wood, a Ph.D. prof. of biology at Bryan College (and both a Christian and creationist), admits:

The genome revolution. . . presents significant challenges to creationist theory, particularly in the realm of biological similarity. . . . [creationists] Robinson and Cavanaugh concluded that all extant felids [cats] belong to the same baramin [“kind”] and presumably descended from a single pair of cats on the Ark, but geneticists found distances greater than 5% among felid [cat] Zfy genes and greater than 3% among felid [cat] Zfx genes. Certainly if felid [cat] sequences can vary by that amount, what is to preclude the conclusion that the much lower differences observed between human and chimpanzees genomes indicates that they belong to the same “kind?” . . . . As with the genetic diversity of cats, what is to preclude application of this same argument to chimpanzees and humans with the conclusion that we share a common ancestor with an animal? To put this question another way, how can we maintain that cats share a common ancestor with their genomic differences, and deny that the smaller differences between humans and chimpanzees could not also arise from a common ancestor? . . . . This argument could be significantly amplified from recent findings of genomic studies. For example, geneticists have surveyed 50 olfactory receptor genes [“for smell”] in humans and apes. They found that the open reading frame of 33 of the human genes were interrupted by nonsense codons or deletions, rendering them pseudogenes. Sixteen of these human pseudogenes were also pseudogenes in chimpanzee, and they all shared the exact same substitution or deletion as the human sequence. Eleven of the human pseudogenes were shared by chimpanzee, gorilla, and human and had the exact same substitution or deletion. While common design could be a reasonable first step to explain similarity of functional genes, it is difficult to explain why pseudogenes with the exact same substitutions or deletions would be shared between species that did not share a common ancestor.


See Todd’s paper, The Chimpanzee Genome and the Problem of Biological Similarity

Todd has also stated on his blog

Evolution is not a theory in crisis. It is not teetering on the verge of collapse. It has not failed as a scientific explanation. There is evidence for evolution, gobs and gobs of it. It is not just speculation or a faith choice or an assumption or a religion. It is a productive framework for lots of biological research, and it has amazing explanatory power. There is no conspiracy to hide the truth about the failure of evolution. There has really been no failure of evolution as a scientific theory. It works, and it works well.


Ed Babinski - #80571

May 30th 2013

Great job Dennis!

Let me add two quotations from Christians:

1) Stephen Schaffner, statistical geneticist at the Whitehead/MIT Center for Genome Research—points out why he finds the evidence for evolution compelling. Schaffner (who is a Christian) asks: 

Where is the creationist or I.D.ist model that explains the following types of observed genetic data? Such a model should produce estimates of the following measurable genetic data for modern humans:

a) The minor allele frequency spectrum.

b) The relationship between minor allele frequency and probability that the minor allele is the same as the chimpanzee base at that site.

c) The ratio of transition (purine<->purine or pyrimidine<->pyrimidine) polymorphisms to transversion (purine<->pyrimidine) polymmorphisms.

d) The ratio of polymorphisms at CpG sites to the overall polymorphism rate.

e) The distance over which significant linkage disequilibrium extends in a chromosome.

f) The genetic distance (difference in allele frequencies) between African and non-African populations.

g) The difference between African and non-African populations in the extent of linkage disequilibrium.

h) The distance over which significant autocorrelation in heterozygosity extends in a chromosome.

i) The ratio of fixed transition to transversion differences between humans and chimpanzees.

j) Same as (9), but for CpG sites.

There are other possible questions, but these are a reasonable starting point, since the quantities in question are all ones that I routinely use evolution to predict or intrepret. If the claim is true that creationists/I.D.ists look at the same data and just interpret it differently, there should be no difficulty in providing the creationist interpretation of these data.(Note that the answers should be derivable by anyone using the same model.)

I’m happy to answer questions about my list (which is deliberately terse—I didn’t feel like writing a survey of population genetics). Young-earth creationists should have the most trouble meeting my challenge. As you allow more and more time, and more and more evolution, it becomes harder to distinguish special creation from evolution. In the extreme case where all God does is cause a small number of critical mutations in the development of humans, the results will look exactly like evolution (provided the mutations occur in a fairly large population). In that case, of course, you have to wonder why those mutations also couldn’t have happened on their own, since every other mutation can.


2) Todd Wood, a Ph.D. prof. of biology at Bryan College (and both a Christian and creationist), admits:

The genome revolution. . . presents significant challenges to creationist theory, particularly in the realm of biological similarity. . . . [creationists] Robinson and Cavanaugh concluded that all extant felids [cats] belong to the same baramin [“kind”] and presumably descended from a single pair of cats on the Ark, but geneticists found distances greater than 5% among felid [cat] Zfy genes and greater than 3% among felid [cat] Zfx genes. Certainly if felid [cat] sequences can vary by that amount, what is to preclude the conclusion that the much lower differences observed between human and chimpanzees genomes indicates that they belong to the same “kind?” . . . . As with the genetic diversity of cats, what is to preclude application of this same argument to chimpanzees and humans with the conclusion that we share a common ancestor with an animal? To put this question another way, how can we maintain that cats share a common ancestor with their genomic differences, and deny that the smaller differences between humans and chimpanzees could not also arise from a common ancestor? . . . . This argument could be significantly amplified from recent findings of genomic studies. For example, geneticists have surveyed 50 olfactory receptor genes [“for smell”] in humans and apes. They found that the open reading frame of 33 of the human genes were interrupted by nonsense codons or deletions, rendering them pseudogenes. Sixteen of these human pseudogenes were also pseudogenes in chimpanzee, and they all shared the exact same substitution or deletion as the human sequence. Eleven of the human pseudogenes were shared by chimpanzee, gorilla, and human and had the exact same substitution or deletion. While common design could be a reasonable first step to explain similarity of functional genes, it is difficult to explain why pseudogenes with the exact same substitutions or deletions would be shared between species that did not share a common ancestor.


See Todd’s paper, The Chimpanzee Genome and the Problem of Biological Similarity

Todd has also stated on his blog

Evolution is not a theory in crisis. It is not teetering on the verge of collapse. It has not failed as a scientific explanation. There is evidence for evolution, gobs and gobs of it. It is not just speculation or a faith choice or an assumption or a religion. It is a productive framework for lots of biological research, and it has amazing explanatory power. There is no conspiracy to hide the truth about the failure of evolution. There has really been no failure of evolution as a scientific theory. It works, and it works well.


beaglelady - #80622

May 31st 2013

Good comments, Ed! If God is pushing evolution along, obviously he wants us to believe that it’s happening naturally.  And if that’s what he apparently wants, why not go along with it?  Kind of like movie magic.  No director wants to be told that his special effects look fake! 


Roger A. Sawtelle - #80575

May 30th 2013

Dennis,

The problem with this view is that it is not true.

Geographic separation does not create genetic change.  Adaption to new ecological niches fosters genetic change.  All life forms need to adapt to their environments.    


Lou Jost - #80676

June 2nd 2013

Roger, no, you are wrong. Any time there is limited gene flow between subpopulations, genetic drift and new mutations will begin to make those subpopulations different, even if their environments are identical. For example, a frog might be red on one island, and blue on another, just because of genetic drift and mutations. As these small, selectively neutral differences accumulate, eventually the two subpopulations can become genetically or behaviorally incompatible, so they could not mate even if the barrier between subpopulations eventually disappears. See the work of Gavrilets for a mathematical analysis of this.


Roger A. Sawtelle - #80599

May 31st 2013

Ed,

Evolution is not in crisis, but Darwinism is.

Denis Noble has finally revealed how hollow and superficial NeoDarwinism really is.

The question now is whether Biologos will go with the new paradigm or stick with Dawkins & Co.


glsi - #80663

June 1st 2013

Roger,

It will be interesting to watch whether we see a slow, gradual evolution away from NeoDarwinism or whether there will be a sudden emergence of a new kind of evolutionary biologist here at BioLogos and everywhere else for that matter.

I suppose some will dig in their heels while others will have sense enough to move on.  Damage control efforts from groups like the NCSE will need to be titanic.  And Eugenie Scott has just naturally selected her retirement!  

Has Denis Noble’s work been discussed much at this website?


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