Note: The information in italics is taken from:
http://www.talkorigins.org/faqs/faq-speciation.html#part5
Emphasis is placed by me, and my comments follow each segment.
The most compelling (to me) arguments made on this talkorigins page are listed here, with my comments. First a discussion of the definition of speciation reveals that the definition is more than malleable, it is flexible beyond being useful as a tautological tool. It is frequently tailored to be specific to the particular event. Moreover speciation is presumed (by many) fixed and settled feature of biology.
Definition of Speciation
“What a biologist will consider as a speciation event is, in part, dependent on which species definition that biologist accepts. The biological species concept has been very successful as a theoretical model for explaining species differences among vertebrates and some groups of arthropods. This can lead us to glibly assert its universal applicability, despite its irrelevance to many groups. When we examine putative speciation events, we need to ask the question, which species definition is the most reasonable for this group of organisms? In many cases it will be the biological definition. In many other cases some other definition will be more appropriate.”
…
“The literature on observed speciations events is not well organized. I found only a few papers that had an observation of a speciation event as the author's main point (e.g. Weinberg, et al. 1992). In addition, I found only one review that was specifically on this topic (Callaghan 1987). This review cited only four examples of speciation events. Why is there such a seeming lack of interest in reporting observations of speciation events?
In my humble opinion, four things account for this lack of interest. First, it appears that the biological community considers this a settled question. Many researchers feel that there are already ample reports in the literature. Few of these folks have actually looked closely. To test this idea, I asked about two dozen graduate students and faculty members in the department where I'm a student whether there were examples where speciation had been observed in the literature. Everyone said that they were sure that there were. Next I asked them for citings or descriptions. Only eight of the people I talked to could give an example, only three could give more than one. But everyone was sure that there were papers in the literature”.
“Second, most biologists accept the idea that speciation takes a long time (relative to human life spans). Because of this we would not expect to see many speciation events actually occur. The literature has many more examples where a speciation event has been inferred from evidence than it has examples where the event is seen. This is what we would expect if speciation takes a long time.”
“Third, the literature contains many instances where a speciation event has been inferred. The number and quality of these cases may be evidence enough to convince most workers that speciation does occur.”
“Finally, most of the current interest in speciation concerns theoretical issues. Most biologists are convinced that speciation occurs. What they want to know is how it occurs. One recent book on speciation (Otte and Endler 1989) has few example of observed speciation, but a lot of discussion of theory and mechanisms.”“Most of the reports, especially the recent reports, can be found in papers that describe experimental tests of hypotheses related to speciation. Usually these experiments focus on questions related to mechanisms of speciation. Examples of these questions include:
Does speciation precede or follow adaptation to local ecological conditions?”
“Is speciation a by-product of genetic divergence among populations or does it occur
directly by natural selection through lower fitness of hybrids?”
“How quickly does speciation occur?”
“What roles do bottlenecks and genetic drift play in speciation?”
“Can speciation occur sympatrically (i.e. can two or more lineages diverge while they are intermingled in the same place) or must the populations be separated in space or time?”
“What roles do pleiotropy and genetic hitchhiking play in speciation?”
“It is important to note that a common theme running through these questions is that they all attempt to address the issue of how speciation occurs.”
“5.3.5 Sympatric Speciation in Drosophila melanogaster
In a series of papers (Rice 1985, Rice and Salt 1988 and Rice and Salt 1990) Rice and Salt presented experimental evidence for the possibility of sympatric speciation. They started from the premise that whenever organisms sort themselves into the environment first and then mate locally, individuals with the same habitat preferences will necessarily mate assortatively. They established a stock population of D. melanogaster with flies collected in an orchard near Davis, California. Pupae from the culture were placed into a habitat maze. Newly emerged flies had to negotiate the maze to find food. The maze simulated several environmental gradients simultaneously. The flies had to make three choices of which way to go. The first was between light and dark (phototaxis). The second was between up and down (geotaxis). The last was between the scent of acetaldehyde and the scent of ethanol (chemotaxis). This divided the flies among eight habitats. The flies were further divided by the time of day of emergence. In total the flies were divided among 24 spatio-temporal habitats.”
“They next cultured two strains of flies that had chosen opposite habitats. One strain emerged early, flew upward and was attracted to dark and acetaldehyde. The other emerged late, flew downward and was attracted to light and ethanol. Pupae from these two strains were placed together in the maze. They were allowed to mate at the food site and were collected. Eye color differences between the strains allowed Rice and Salt to distinguish between the two strains. A selective penalty was imposed on flies that switched habitats. Females that switched habitats were destroyed. None of their gametes passed into the next generation. Males that switched habitats received no penalty. After 25 generations of this mating tests showed reproductive isolation between the two strains. Habitat specialization was also produced.”
“They next repeated the experiment without the penalty against habitat switching. The result was the same -- reproductive isolation was produced. They argued that a switching penalty is not necessary to produce reproductive isolation. Their results, they stated, show the possibility of sympatric speciation.”
This initially compelling experiment fails to ask the initial question: why did the flies self-differentiate in the first place? Their eyes, at least the eyes of the progeny, were different colors indicating a prior differentiation of some sort. Perhaps they were not the same strain to start with. Keeping the logic of experiments true to the purpose is difficult, perhaps not really possible in the complexity of living things. In fairness, the report is not the original; keeping logic in reporting is also difficult. Other unanswered questions: control sample behavior; randomness of population sample selection for the experiment; purity of strain initially, and generations of purity (no recessive genetics), etc.
“5.7 Speciation in a Lab Rat Worm, Nereis acuminata
In 1964 five or six individuals of the polychaete worm, Nereis acuminata, were collected in Long Beach Harbor, California. These were allowed to grow into a population of thousands of individuals. Four pairs from this population were transferred to the Woods Hole Oceanographic Institute. For over 20 years these worms were used as test organisms in environmental toxicology. From 1986 to 1991 the Long Beach area was searched for populations of the worm. Two populations, P1 and P2, were found. Weinberg, et al. (1992) performed tests on these two populations and the Woods Hole population (WH) for both postmating and premating isolation. To test for postmating isolation, they looked at whether broods from crosses were successfully reared. The results below give the percentage of successful rearings for each group of crosses.
WH × WH - 75%
P1 × P1 - 95%
P2 × P2 - 80%
P1 × P2 - 77%
WH × P1 - 0%
WH × P2 - 0%
They also found statistically significant premating isolation between the WH population and the field populations. Finally, the Woods Hole population showed slightly different karyotypes from the field populations.”
It would be more compelling if the original population had been split as a control; this shows a presumption of valid control without actually being known to be valid control. It is still somewhat compelling, without being totally validatable. It should be falsifiable, with replication, but replication is not noted. So this is empirically incomplete.
“5.8 Speciation Through Cytoplasmic Incompatability Resulting from the Presence of a Parasite or Symbiont
In some species the presence of intracellular bacterial parasites (or symbionts) is associated with postmating isolation. This results from a cytoplasmic incompatability between gametes from strains that have the parasite (or symbiont) and stains that don't. An example of this is seen in the mosquito Culex pipiens (Yen and Barr 1971). Compared to within strain matings, matings between strains from different geographic regions may may have any of three results: These matings may produce a normal number of offspring, they may produce a reduced number of offspring or they may produce no offspring. Reciprocal crosses may give the same or different results. In an incompatible cross, the egg and sperm nuclei fail to unite during fertilization. The egg dies during embryogenesis. In some of these strains, Yen and Barr (1971) found substantial numbers of Rickettsia-like microbes in adults, eggs and embryos. Compatibility of mosquito strains seems to be correlated with the strain of the microbe present. Mosquitoes that carry different strains of the microbe exhibit cytoplasmic incompatibility; those that carry the same strain of microbe are interfertile.”
So. The mosquito can only breed to an uninfected mate. This relates to speciation how?? (question to self: what is “improper condensation of chromosomes”?)
“5.9.2 Morphological Changes in Bacteria
Shikano, et al. (1990) reported that an unidentified bacterium underwent a major morphological change when grown in the presence of a ciliate predator. This bacterium's normal morphology is a short (1.5 um) rod. After 8 - 10 weeks of growing with the predator it assumed the form of long (20 um) cells. These cells have no cross walls. Filaments of this type have also been produced under circumstances similar to Boraas' induction of multicellularity in Chlorella. Microscopic examination of these filaments is described in Gillott et al. (1993). Multicellularity has also been produced in unicellular bacterial by predation (Nakajima and Kurihara 1994). In this study, growth in the presence of protozoal grazers resulted in the production of chains of bacterial cells.”
OK, they produced the Great Dane of bacteria by eating up the small ones. Then they saw them to stick together, making them presumably harder to predate. Is this valid, replicable, nonreversible, etc and so on. If so what does it mean? Did any cells in the CONTROL population ever stick together? Get bigger? “Unidentified bacterium”? Why are such questions not even asked? Maybe in the actual reports, which I don't have.
8 comments:
Stan,
In
5.8 Speciation Through Cytoplasmic Incompatability Resulting from the Presence of a Parasite or Symbiont
I think, from what you have reproduced here, what is meant is that the symbiont "Rickettsia-like microbes" are driving speciation by assuming partial genetic control of the host cells. Its well known that cells of some higher organisms have delegated genes to obligate parasite bacteria. In other words neither can live without the other. So speciation in the mosquito could in fact be controlled by variation in the parasite Rickettsia bac.
That's my theory, anyway.
[Beelz]
“improper condensation of chromosomes”
probably refers to the condensation of chromosomes that happens at metaphase (?) in the mitotic cycle.
First comment: Declaring a speciation event based on which parasite a mosquito carries is an even more suspect claim.
Second comment: "improper condensation of chromosomes" sounds like a mutation to me... something that Scott seems unwilling to accept.
Scott's position that "populations mutate but individuals do not" still has the appearance of word play, in the sense of redefining the meaning of "mutation", and of ignoring the concept that the set is identical to the sum of its members.
Individuals must be mutated between parent - child, and the mutation must be both positive and either a) useful or b) retained until it is useful.
I think perhaps the reason that these premises are so hard to swallow is that they don't fit well with the other evolution stories. Randomness in the process seems hard to admit; redefining things makes it easier.
Why is skepticism applied to the mind, free will and free agency, but not to the endless stories out of historical and unreplicated experimental biology?
First comment: Declaring a speciation event based on which parasite a mosquito carries is an even more suspect claim.
Stan, I think you may be missing the point of this reference. In a sexually-reproducing species, any process or structure that leads to the genetic isolation of a population can potentially promote speciation, since all that is required is that the population be isolated long enough for enough changes to occur, such that gene flow with the ancestral population is no longer possible. The authors of this paper have identified a previously-undescribed isolating mechanism, and it is of special interest since it can promote what is called sympatric speciation, without the temporal or spatial barriers associated with (the more common) parapatry.
Scott's position that "populations mutate but individuals do not" still has the appearance of word play, in the sense of redefining the meaning of "mutation", and of ignoring the concept that the set is identical to the sum of its members.
See, you think you've got some great logical argument here, but your analogy fails because you're ignoring the way populations interact with their environment. You seem to be trying to treat living populations as machines, the products of design, all working together as the sum of the individual parts. This is wrong, for populations are not sets that are reducible to the sum of their individual member's genetic potential. The genes are not the sole source of the interaction that produces evolutionary change, Stan, nor is all the information expressed in a population contained in the genes.
Perhaps an analogy will prove helpful. Consider ice melt runoff in the Sierras. In the sense, the moving column of fluid could be thought of as a population of molecules, and its net movement the sum of the individual particles and forces acting upon it. We treat such systems statistically, of course, because the sheer number of particles defy both our imagination and the limits of computing power available to us.
Now, if that column of fluid was set loose on a uniform surface, we could certainly predict the general motion of the population of molecules, and thus predict the course of icemelt's flow downstream. In such cases, we would say that the pattern of flow and change was simply the sum of the forces involved.
But of course that's not the case, is it? The course of the stream's flow is not determined by it's own internal motion alone. Patterns of flow are complex interactions between the fluid and the environment through which they flow. Most of the information which creates the pattern of flow actually comes from outside the fluid.
In the same way, most of the information in a population of genes actually comes from outside the pool of genes.
Individuals must be mutated between parent - child, and the mutation must be both positive and either a) useful or b) retained until it is useful.
Both of those statements are false. Genetic change at the individual level is not required for the population to evolve; all that is required is that there be genetic variation which is sensitive to environmental change. Nor do mutations need to be positive; at any given moment, most mutations are selectively-neutral. In fact, I maintain you can have speciation without a single beneficial mutation.
OK Scott, you have taken great pains, which I appreciate, to lay this out, yet I still don't understand your idea here:
" Genetic change at the individual level is not required for the population to evolve; all that is required is that there be genetic variation which is sensitive to environmental change"
To me this is saying that environment A requires that dogs be tiny: chihuauas; environment B requires that dogs be huge: great Danes. Why are they different species? They cannot interbreed (without help) but they are still canines, yes? Or are they expected to become something else? If so, why?
Sometimes analogies only work up to a point. For example, I understand the separation of waterflow into isolated rivulates... up to the point that it all returns together in a coherent river (analogous to a single specie?)
"In the same way, most of the information in a population of genes actually comes from outside the pool of genes."
Isn't this Lamarkianism? If not, what does this mean? To the Grants, it apparently meant hybridization, because they specifically gave the causes of speciation as a) mutation; b) introgression. But hybrids always were seen to be weaker and failed to produce speciation:
"Genetic drift becomes progressively reduced through the process of random drift in small finite populations in the absence of mutation, migration and selection."
"Mutation, migration, and selection must be considered becasue they also influence the amount of genteic variation. Alleles are lost through most forms of selection, and are gained through mutation and selection; migration is used here in the sense of interbreeding with members of another poulation."
Both quotes: Grants, EDNP, p286.
Then the Lande and Barrowclough satement requiring mutation to stabilize the loss of Alleles due to selection.
This is followed with equations and discussion on the balance between mutation and hybridization that is required to stabilize a popluation.
And BTW, there are a boatload of definitions for species, and speciation; what definition are you using?
Time prevents a detailed reply, but a few quick thoughts:
Alleles are lost through most forms of selection, and are gained through mutation and selection;
Selection is non-random and part of the information involved in the interaction between the genome and the environment.
BTW, there are a boatload of definitions for species, and speciation; what definition are you using?
Unless biologists say otherwise, Mayr's 'reproductive species concept' has become the default position for the metazoa. That's the one virtually everyone uses virtually all the time for plants, animals, fungi and most protists; the prokaryotes don't fit. But, when you look into the technical literature on species concepts, you'll find that there is no one species concept that is equally applicable for all life. That's one of the things that makes biology so interesting...SH
Another comment.
Isn't this Lamarkianism? If not, what does this mean? To the Grants, it apparently meant hybridization, because they specifically gave the causes of speciation as a) mutation; b) introgression. But hybrids always were seen to be weaker and failed to produce speciation:
Hmm. First of all, what I'm saying isn't Lamarckian, because I'm not saying that acquired characteristics are inherited. Not only does this fly in the face of the evidence, it would blur the line between evolution and development, a very clear line in my thinking.
Look. What I am saying is that there is a vast amount of genetic variation in healthy sexual populations, the kind of populations that the reproductive species concept describes so well. Some of that variation may be alleles produced through new mutations, some of it isn't. But how that variation is expressed, and which alleles change in frequency, is dependent upon information that the genome does not supply. That information comes from the environment, and the unfolding of that interaction is the development of the individual. How that interaction affects the fitness (reproductive success) of all of the alleles in all of the individuals in that population is evolution.
In the case of the Grants work, I don't recall them claiming that the hybrids were a new species. I think the point was that the main lines hybridized only under considerable stress and that as soon as conditions became more clement assortative mating and prezygotic barriers drove the populations back toward their original fitness peaks....right?
Scott, I understand your time constraints and I appreciate your input here. I will keep checking here from time to time for more input, thanks.
Scott said: "That information comes from the environment, and the unfolding of that interaction is the development of the individual. How that interaction affects the fitness (reproductive success) of all of the alleles in all of the individuals in that population is evolution."
At first I took this to mean that the environment affects the alleles in the sense of modifying them. However, I now take it to be another way of saying "selection" occurs, weeding out the least fit, etc. If this is the proper interpretation, and I don't know that I have got it right, then we still have: a) a group with a self-compatible, yet presumably broad spectrum in its genome (despite the Grant findings quoted earlier pointing to a reduced spectrum); and b)selection due to environmental variables.
This defines the set-up conditions for micro-evolution, i.e., alleles plus selection.
Now, in order to go beyond the group genome, to make a new incompatible specie, how does that happen?
For the Finches, the environment caused populations of birds with beak sizes that fit the available food to source to flourish. This cycle followed the drought / flush cycle, and did not produce permanent changes such as proto-toucans or some such. Sure, selection follows environmental constraints, even to the point of extinction due to non-competitiveness.
But this is not the same as saying that the environment changes alleles. And alleles form the living being.
As before, I grant you that selection exists. But I need a specific mechanism in order to get to the bottom of evolution just by selection alone, no mutation.
BTW, you are correct, the Grants did not claim speciation due to introgression (crossbreeding), because the crossbreeds produced weak and /or noncompetitive offspring. They surmised, however, that without the introgression the genome would have tightened considerably, although I don't think they had data for this.
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