I disagree with Travis,

evolution is clearly not the change in allele frequencies. There are even microevolutionary processes that does not produce changes in allele frequencies (e.g. balancing selection). The reason why that definition is still on the books is the same reason why some consider that macroevolution is the accumulation of microevolution: history. Evolutionary synthesis is the result of the condensing of Mendelian work, Neo-Darwinism and frequentist statistics into population genetics. So the reductionist view of population genetics was what dominated the evolutionary theory during the entire the 20th century. In addition there is no mathematical background for any widespread macroevolutionary theory. So all the development came from bottom to top.

There are many types of studies in which microevolution is different to macroevolution. in addition, many new areas (e.g. evo-devo) are opening the door to completely new interpretations of evolution at other scales than population genetics. Even in the genomics realm there are processes that occur in different ways at micro and macro scales, for instance nucleotide substitutions (micro) versus gene duplications (macro). Another example is the mutation rate. When calculated in a micro scale (

Hello Li

Evolution is the change of allele frequencies in a population. Some of these changes are associated with phenotypes, others are not. Some changes are neutral (subject to genetic drift, etc), others are positive (and spread or are maintained), and others are negative (and usually removed). I think the terms micro and macroevolution are misleading, and you can more coherently explain evolutionary change without them! These terms really describe the same process, just over different scales of time. Moreover, the misuse of these terms by creationists has, in my opinion, removed what little explanatory power these terms ever had. As such, I think it is far better to explain our points without them.

All the best

Travis

Changes in environment, gene flow, climate and etc will cause some modifications on different plant charactristics. These characters can be either morphological or anatomical. If these alterations accumulate, it may cause a tremensous occurance lead to macroevolution.

I am also under the impression that very basically, micro evolution eventually leads to macro evolution given enough time and changes in a population/specie.

Macroveolution is often defined as: evolution on a scale of separated gene pools, of evolution which occurs at or above the species level. Microevolution is often defined as evolution which occurs within a population. (Note: There are MANY definitions)

However, Evolution is defined as changes in allele frequency. Therefore, the definition of macroevolution is not really different than the definition of microevolution. The only thing which varies is the taxonomic and temporal scales.

I also worry about the studies which define macroevolution as evolution at or above the level of the species. Evolution acts upon the individual (or more accurately their genes). Most definitions of macroevolution I see are dangerously close to "group selection." If we compound this with the artificial nature of how we group most "species" the term macroevolution becomes almost meaningless.

Using the terms macro and microevolution is a false dichotomy. It is over-complicating the issue. Evolution is the change an allele frequency. Sure, lots of small changes can accumulate into large changes. But at the end of the day, macro and microevolution are the same process. Macroevolution is really only microevolution which has occurred over a longer period of time.

Macroevolution is used very often, even in the scientific literature. However, I posit that separating micro and macro is a false dichotomy. Both are the same process, changes in allele frequency with time. The only thing which varies is the taxonomic and temporal scales. In my opinion we can more accurately and coherently express our evolutionary ideas without these terms.

Travis

I disagree with Travis,

evolution is clearly not the change in allele frequencies. There are even microevolutionary processes that does not produce changes in allele frequencies (e.g. balancing selection). The reason why that definition is still on the books is the same reason why some consider that macroevolution is the accumulation of microevolution: history. Evolutionary synthesis is the result of the condensing of Mendelian work, Neo-Darwinism and frequentist statistics into population genetics. So the reductionist view of population genetics was what dominated the evolutionary theory during the entire the 20th century. In addition there is no mathematical background for any widespread macroevolutionary theory. So all the development came from bottom to top.

There are many types of studies in which microevolution is different to macroevolution. in addition, many new areas (e.g. evo-devo) are opening the door to completely new interpretations of evolution at other scales than population genetics. Even in the genomics realm there are processes that occur in different ways at micro and macro scales, for instance nucleotide substitutions (micro) versus gene duplications (macro). Another example is the mutation rate. When calculated in a micro scale (

Hello Edson

Thank you for your great response! It has really gotten me thinking, but I have a few questions!

If evolution is not a change in allele frequency, what is your working definition of evolution? From how I understand it, Evolution is change over time, whatever that change may be. So population geneticists may talk about evolution as changes in allele (or genotype) frequency, while Ecologists may talk about evolution as changes in fur color. In fact, I have found that most fields have slightly different working definitions of evolution , which makes conversations like these a little frustrating. Perhaps we should have defined our terms before starting! :)

But as most phenotypes are associated with genotypes, the genes are still very important. You could easily substitute allele in my answer with gene, genotype, gene complex, or even chunks of DNA associated with different traits. It does not matter if the change is the result of a single nucleotide difference, a gene duplication or removal, etc different phenotypes are usually associated with different genotypes.

Interestingly recent research has indeed shown that very different phenotypes can result from environmental activation and suppression of the same set of genes during development, and even later on in life. However, offspring will still inherit that genotype AND the ability to express the different phenotypes depending on environmental inputs. I would not use evolution to define a generation of smaller than average rodents, whose small size is a result of poor nutrition. This change is not a result of heritable DNA, but of environmental factors. Although sustained malnutrition may indeed result in selection which influences DNA. To me, it always comes back to the DNA. Even if the environment alters how the DNA is expressed, or even what chunks of that DNA are expressed, it all comes back what alleles (genotypes, chunks of DNA) are present in the first place.

I also think we may be talking past each other as a result of definitions. For instance, when you say that a gene duplication is an example of a macro change, I am not sure I would define it that way. I think this has a lot to do with the difficulty of defining "Macroevolution." In fact, I think we may actually be saying mostly the same thing, just in very different ways!

I agree that we are radically altering the way we think about evolution! Just last year research was published which showed that stress in a mother's life can alter the DNA of her gametes, and thus influence her offspring. However, even in this example it all does come back to the genes, gene complexes, DNA, alleles, or chunks of DNA coding for a trait. As everything seems to come back to DNA. I continue to define evolution as changes in allele frequency with time. With the caveat that allele can be defined many ways!

Thank you again for your response, and I am looking forward to communicating with you further. However, I think we have hijacked this thread away from its original purpose! I would love to continue this via email to continue this discussion. If you are so inclined email me at [email protected]

All the best

Travis

Yes, it can. Even clade selection can ultimately be explained by changes in gene frequencies, the dynamics of gene-duplication and deletion, and changes in regulatory elements (which are themselves changes in gene frequencies).

Hi Travis,

I agree with you that microevolution and macroevolution are the same process but different scales. But I think these two terms are still useful in science because they define a range for study. Microevolution is usually studied in inner-species and can be analyzed directly as mutation, selection, migration and drift, while macroevolution is usually studied in species level and need to be speculated by fossils or morphology/molecule evidences.

Best wish,

Hao-Sen

Hi Atena,

I agree with you. I think macroevolution is comprised by ever-change microevolution. But it is quite hard for us to understand how ever-change environment shapes microevolution.

Best wish,

Hao-Sen

Hi Eugene ,

I think the critical problem of understanding the relationship of their two is how to reconstruct the macroevolution history from the limited evidences.

Best wish,

Hao-Sen

Hi Travis and Edson,

Thank you for your interesting and meanful discuss! Edson's idea is quite against my origin thinking. I am a beginner of phylogenetics and evolution study. I hope we can have further communication in this interesting field.

Best wish,

Hao-Sen

For me, it all comes down to the benefits of using a term. When macroevolution is used, it is often used incorrectly - the media, creationists, even scientists. Some definitions of macroevolution actually suggest group selection, ie selection between groups, species, etc.

At the end of the day, macro and micrevolution are the same process. Evolutionary change, and the only change that matters is that which occurs to the heritable DNA. As scientists we love to have terms for everything, but often they just complicate the matter.

So to answer the question of the original post, Yes macroevolution is likely just the accumulation of microevolution (in my opinion). But if at the fundamental level they are the same process, I posit we abandon the terms. They are adding a needless layer of complication to a process which is, at its core, very simple.

If the terms are to be used, however, we need to make sure that we define how and why we are using them. This won't help with confusion in the media, or misuse by creationists. But perhaps if we clarify how we communicate with each other, other confusions will be cleared up in time.

Edson, I would still very much like to hear from you about how you define evolution. At the end of the day, the only change that matters is changes to the heritable DNA. We may define alleles broadly (genotypes) or narrowly (Single nucleotide differences), but only changes to the germ line DNA are passed on. The environment may alter expression of that DNA, or even change the DNA, but again it is only the DNA which is passed on. Thus evolution, at its finest level is changes in allele (or genotype) frequencies. Sure, we may measure proxies of phentoyptes like fur color of beak depth, but it all comes back to the DNA!

All the best

Travis

Coming back to the original question, "Can macroevolution be explained by the accumulation of microevolution?" we need to first make sure we are talking about the same phenomenon. The short answer is: sometimes.

As I see it, microevolution occurs through the process of heredity (change in allele frequency) and drift (nucleotide mutation with subsequent fixation). The net accumulation of these changes affect the phenotype over centuries and thousands of years, with the environment at large as final arbiter if any confer selective advantage or disadvantage. These also encompass regulatory gene changes, epigenetics and the like. Some nucleotide changes have far-reaching effects, though, so of course if we are attempting to pin down these terms, we need to expand our vocabulary.

Macroevolution could be thought of as microevolution occurring over geologic time scales, as you ask, or more rapidly through high-risk genomic events such as chromosomal reorganization, gene duplication, developmental change and the like. These confer raw material for microevolutionary forces to work upon. One might think of these as significant alteration of the phenotypic, such as the wholesale suppression of multiple characters, or the addition of characters.

Warm Regards,

Nick

I agree that there is a confusion about definitions and personally find the micro-/macro- distinction to be largely artificial and potentially dangerous. Like "populations" and "species", any attempts to make discrete categories of a continuum is ultimately doomed to fail if done too dogmatically: context is key.

Evolution over long timescales is dependent on (and cannot cheat) "microevolution" over short timescales but most lineages ultimately go extinct and so there are likely to be some additional factors at play in determining long-term success. This is true at all scales, though, whatever you define as "long" and "short" term. (Just think of a cancer or bacterial biofilm.)

In practice, I think that "macroevolution" tends to have more of a historical component and feature more rare random events, such as environmental catastrophes. Ultimately, though, it is still a matter of differential survival of genetic variants through time. Mutations with larger phenotypic consequences, whether classed as "macro" or "micro", are governed by the same rules that determine the future of lesser mutations - they are simply more likely to be nearer the ends of the fitness distribution.

Richard,

I cannot see the continuum (you mentioned), when I look in the microscope.

Chromosomes have been found to differ in almost all cases between species. For any chromosomal rearrangement to replace the original throughout a population, the new rearrangement must increase in frequency, despite its deleterious effect on fertility, and produce new homozygotic carriers that are better adapted than the original homozygotes. Yet, the frequency of such replacement episodes seems to be extremely low, otherwise groups of individuals within a population would frequently be found to differ in chromosome complements, which is clearly not the case.

However, differing chromosome complements, with identical sets of two homologous autosomal chromosomes each, are the hallmarks of diploid species and any thoughtful speciation theory has to provide a mechanical explanation, independent of considering mutations or structural chromosomal rearrangements as being the cause of speciation.

(passages from my paper)

Attached figure: How many bottlenecks are required to generate this kind of karyotypical mess between closely related species?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3935097/figure/Fig2/

@Reinhard, that’s an interesting question. We know the answer to this (to some extent) in yeast, where 73 inversions and 66 reciprocal translocations in the last 100 million years can account for the current Saccharomyces cerevisiae organisation (see attached paper). Clearly primates are more complex, being obligate sexual organisms but also harbouring many repetitive elements etc.

I am not sure how this invalidates the concept of evolution and mutation being continua, though. Genetic rearrangements vary in both scale (from small indels to whole genome duplications) and fitness impact. For balanced translocations, the impact might not be huge. Clearly any translocations that are large enough to impact fertility will require a counterbalancing force to reach high frequency. This could be a selective advantage of the new arrangement that exceeds the initial fertility cost (or a linked beneficial allele that the rearrangement hitch-hikes), or it could be a chance event. Whilst the latter is going to be more common in a small population, I am not sure that a bottleneck is always required. Population size will affect the probability, for sure. Nevertheless, unlikely events do happen, just more rarely than likely ones, and 40 million years is plenty of time for many rare unlikely events to occur. (And once the translocation reaches a frequency of 50%, the fertility cost disappears and starts to negatively impact the ancestral arrangement instead, accelerating fixation.)

Being predominantly non-neutral, I would expect any changes in chromosome structure to be quickly fixed or, more commonly, quickly lost, so we would not expect to see variation very often in populations but if the sampling was sufficient we would expect to see some. (Smaller structural variants such as CNVs, on the other hand, should be - and are - much more common.) I’ve not read your paper and must confess to a naivety regarding the depth of karyotyping that has been done across wild populations of different organisms. Is there much?

http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1000485

Evolution has no relation to what is called microevolution. See my article here.

V. Chupov

Evolution has no relation to what is called microevolution. See my article here.

Article Dynamics of Chromosome Number in Long Structured Phylogeneti...

Richard,

Thanks for your interesting reply, however I do not agree! The impact of a heterozygous balanced translocation is huge, not for the individual, but for the survival of the offspring. Actually, a balanced translocation in one of the parents is a common cause, why a childless couple asks for genetic counseling.

You have to keep in mind that a balanced translocation only stays balanced in the offspring, if both rearranged chromosomes make it into the haploid gamete (>meiosis). Otherwise you get an unbalanced translocation in the zygote! So, a sporadic chromosomal translocation in an individual always (significantly) reduces fertility.

That was one of the reasons why evolutionary biologists switched to the gene mutation business, because nobody could explain how these chromosomal aberrations can spread in a large population. Yet, they exist…

Chimps and humans differ in one fusion of two chromosomes and nine large pericentric inversions. Yet, in none of the inversion breakpoints has any interrupted or newly created gene been found and therefore the reasons underlying the homozygous fixation of these inversions remain an enigma to molecular genetics (Kehrer-Sawatzki and Cooper 2007, 2008).

Yes, there is lots of data on differing karyotypes between closely related species. Chromosomal aberrations are also ideal candidates for reproductive barriers between species.

Check the link in my last reply, it does not contain the paper, just one figure.

Once you see the colors…you will understand…there is no continuum…species are real ;-)

This is a continuos debate since the begining of the modern synthesis.

I think the current debate must include biological mechanism whit high impact over evolutionary thought as symbiogeneticism, lateral gene transfer, phenotypic evolution and the study of major evolutionary transitions (where the Reinhard's sentence of the lack of continuum gene-chromosome can be defended)

Hi

it should be noticed that, tremendous changes are as a result of small ones. then, it can be concluded that if several microevolution happen, there is n't any doubt that macroone will possibly occure.

Many factors either natural or artificial elements can cause such modifications. Overtime, all organisms will change morphologically or anatomically.

Hi!

The theory of evolution - the only mechanistic biological theory, the rest is not transformed since the mid 19th century. Even water penetration into the cell, carbon dioxide, oxygen is not provided by diffusion, and hav a special energy-consuming machinery. And only in the theory of evolution "evolutionists" do not want to look for any special mechanisms of transformation of the genome. Modern evolutionary theory - it's a shame of biology. Need to search for intracellular mechanisms of evolution. You can call them intracellular mind.

Hello Vladimir

I am afraid that I do not understand your post.

Are you trying to say that evolutionary theory has not really changed since the mid 19th century? If so I must disagree strongly with you. Evolutionary theory has changed, and changed greatly. Only this year evidence was put forth that suggests that maternal stress can alter DNA, which then influences traits such as anxiety in offspring. Such a theory would have been impossible to even postulate decades ago. If you want even more evidence as to how evolutionary theory has changed in the past few years, read the conversation above, between Reinhard Stindl and Richard J Edwards. What they are discussing is fascinating, has huge implications to evolutionary theory, and is very very new. Just because evolutionary theory maintains a consistent logical core, based upon Darwinian Natural selection, does not mean that the theory has not changed greatly.

Could you expand on what you mean by intracellular mechanisms of evolution? I have said it before, but to me the only change which matters to Evolution is changes to the DNA, which are then heritable. What do you mean by intracellular?

Travis

@Reinhard, I still do not understand your point about there being no continuum. Species may be real (some of them at least) but so is common ancestry and the reality that the chimp and human lineage were once the same ancestral species. Furthermore, a reduction in fitness is not the same as a reproductive barrier, although it will promote one.

Yes, you need opposite segregation of balanced translocations to get a healthy gamete/zygote but that can happen, right? If there is something to counteract that fitness impact, such as its occurrence in a particularly dominant alpha male, carriers might still have more net offspring despite the reproductive issues. (Obviously this would need to happen in a few generations but I think you get the point - rare but possible, and hence rare but observable changes.)

One question: could a translocation be so detrimental if unbalanced that the gametes themselves (i.e. the eggs and sperm) would be inviable? This might actually be less deleterious than a “medium sized” translocation that produced viable gametes but inviable zygotes.

I am also not suggesting that NO translocations have downstream affects, just that those effects will vary dependent on the nature of the translocation. Pericentric inversions do not create big meiotic problems, do they? They will have the effect of making the chromosomes look even more fragmented as in your figure. (Gibbon chromosomes 6 & 14 being prime examples, I think.)

Finally, just because we do not know the cause of a particular rare, unlikely event, it does not make that event impossible or lacking a potential explanation. I think "macroevolution" often suffers from limited data and making potentially untestable hypotheses about specific past events, whereas "microevolution" studies tend to be data-rich and primarily concerned with establishing evolutionary “laws”, such as inclusive fitness, and watching them play out in laboratory and/or wild populations. Perhaps this contributes to the perceived disconnect?

PS. I did look at your figure before, by the way. I must confess that I am little hazy about the exact details of the FISH experiment used - is it also possible that some of the pattern is the results of the FISH markers themselves moving, rather than entire chromosomal chunks translocating?

Richard,

Thanks for your detailed reply!

Regarding your concerns about the reliability of my mFISH experiment:

Already in 1992, Jauch and colleagues published their comparative FISH results using human FISH probes on gibbon chromosomes (Jauch et al. PNAS 1992). However, they could only use two fluorescence colors per experiment, so it required a lot of work.

Ten years later at UC-Berkeley I just hybridized the human multicolor FISH probes (MetaSystems) to gibbon chromosomes in a single hybridization. Using the mFISH-system from MetaSystems it was pretty easy and the results have always been reliable. After all, I had used these probes a lot on human cancer samples. My experiment did not generate any new data, it is just a colored demonstration of chromosomal evolution in action. See the attached file below with the findings of Jauch et al. and the colored version of my hybridization experiment. You will see that the results are pretty identical.

By the way, Johannes Wienberg showed a similar slide at a cancer meeting in Vienna (it was in 1997, I think), where he demonstrated the “superiority” of the spectral karyotyping system (Israel) and their human SKY FISH probes.

The restructuring of chromosomes is by no means a rare event! It has just been forgotten in the ages of molecular genetics. ;-)

There’s a huge literature on chromosomal change in evolution…but it is old and therefore not sexy anymore.

Here is a “newer” reference:

S. J. O'Brien, M. Menotti-Raymond, W. J. Murphy, W. G. Nash, J. Wienberg, R. Stanyon, N. G. Copeland, N. A. Jenkins, J. E. Womack, J. A. Marshall Graves, The promise of comparative genomics in mammals. Science 286, 458–462, 479–481 (1999); published online EpubOct 15

In this issue of Science (O’Brien 1999) there was a wall chart included, you might have a look at. (Genome maps 10. Comparative genomics. Mammalian radiations. just in the paper version)

You mentioned the special scenario where an alpha male with a sporadic chromosomal translocation will be able to spread it in a population. Yes, I agree! However, his offspring will still have just one copy of the translocation. Yet, a diploid species is defined by two identical copies of autosomal chromosomes. So, to become fixed in a population, every sporadic chromosomal change requires massive inbreeding (= a bottleneck) to become homozygous.

Please just look at the chromosomal changes that have occurred in the gibbon lineage (attached figure just shows the translocations, not the pericentric inversions).

The population sizes of gibbons must have been oscillating like a yo-yo!

References:

A. Jauch, J. Wienberg, R. Stanyon, N. Arnold, S. Tofanelli, T. Ishida, T. Cremer, Reconstruction of genomic rearrangements in great apes and gibbons by chromosome painting. Proc. Natl. Acad. Sci. U. S. A. 89, 8611–8615 (1992); published online EpubSep 15 (10.1073/pnas.89.18.8611).

R. Stindl, The telomeric sync model of speciation: species-wide telomere erosion triggers cycles of transposon-mediated genomic rearrangements, which underlie the saltatory appearance of nonadaptive characters. Naturwissenschaften 101, 163–186 (2014); published online EpubFeb 4 (10.1007/s00114-014-1152-8).

Travis. Good day .

I mean the theory that is taught in universities specialists in the theory of evolution. With her many biologists disagree: paleontologists and immunologists, molecular biologists and taxonomists. But they do not share a common fruitful idea. Also widespread idea that selections can be contrasted only creationism.

Understanding of intracellular intelligence can be a good working hypothesis for future research.

We have no direct evidence of its existence, but it says a lot for this opportunity. 1. Our studies show that evolutionary transformation phenotype is preceded by some of the transformation of the genome. 2. All biological processes are strictly controlled. Strange to assume that evolutionary processes are left to chance coincidence. Such an assumption is made in honor of the 19th century explorer, but not acceptable in 21. 3. All the basic functions of multicellular organisms are presented in unicellular. Permissible to assume that the similarity of intelligence may have a cellula. 4. Genome is not a set of genes. Should be an integrating mechanism, making workable set of genes. 5. Human intellect operates images of objects. In the cell there are "images" of proteins, RNA, and even behavioral reactions in the form of nucleotide sequences. Intracellular Intellect has something to manipulate.

Our working hypothesis: The leading factor in the progressive development is intracellular mechanisms of coordination and upgrade internal cellular processes and communication systems with the environment (Chupov, 2011).

Vladimir,

do you know this new paper?

J. A. Shapiro, Epigenetic control of mobile DNA as an interface between experience and genome change. Frontiers in genetics 5, 87 (2014)10.3389/fgene.2014.00087).

If you don't have access to this specific journal, let me know. I could send you the pdf-file.

It might be of interest to you...

@Reinhard, I'll have a read of your paper as it looks interesting. (Hopefully I will have the time and mental energy to give it the deserved attention.) I did not mean to cast aspersions on the reliability of your FISH. I was just interested in (and ignorant of) the number and size of the probes. Have you cross-validated your Lar gibbon FISH with the Nomascus leucogenys genome? I'm guessing there have been a few extra changes since their divergence but most of the differences will be in common? Having the Jauch et al image for cross-reference is useful for me because I am mildly red-green colour-blind and some the colours look the same to me!

Richard,

these are whole chromosome probes, every piece of DNA is labelled by a (chromosome-)specific combination of 5 fluorescent dyes. The imaging system is using a filter wheel attached to a microscope and takes a series of images of one metaphase. You get wonderful colored pictures of chromosomes. Subsequently, the system combines them into one pseudocolor image. Of course, since 24 different colors are required to visualize all human chromosomes, some of them look similar...

No, I did not cross-validate my findings, because others already did. I just hybridized human probes to gibbon chromosomes, to be able to explain to molecular geneticists what the problems of chromosomal evolution are.

Gibbons are an extreme example of chromosomal evolution, of course. Yet, differing chromosome complements are the hallmarks of closely related species (White 1978, Modes of Speciation).

Let me just quote one of the experts, Max King. As King writes: “For the moment it should be stated that there is no longer any room for debate as to whether profoundly negatively heterotic chromosomal rearrangements can reach fixation in derived populations, the fact of their fixation is undeniable. It is up to the opponents of chromosomal speciation to explain how these rearrangements have reached fixation. That is, our concepts of population genetics must be modified to account for the existing phenomena” (King 1993, Species evolution : the role of chromosome change, p. 122).

I did provide an alternative model to the standard explanation of translocations in gibbons. Figure is attached...

@Reinhard, I’m glad that you brought up Fig 6 from your paper as it really speaks to the topic in hand of how macroevolutionary changes can be explained by multiple microevolutionary ones. I totally agree that a fusion-fission cycle with intermediate pericentric inversions is more likely than reciprocal translocations and was actually going to propose something similar myself! It is a great example how something that initially appears to be a single large deleterious evolutionary event can actually be explained by a number of smaller, sequential steps, none of which is particularly improbable or harmful (see: http://pandasthumb.org/archives/2009/02/the-rise-of-hum-1.html for some quoted references regarding these kinds of rearrangements).

In fact, I would argue that this is precisely the kind of explanation that King is asking for in your quote (and does not require numerous population bottlenecks). Whether these events are all macro- or micro- depends on your definition. Personally, I would always class single mutational events as microevolution - even a reciprocal translocation. (Actually, I prefer just “evolution” but if I *had* to choose...)

Richard,

Fusions of acrocentric chromosomes do not change the phenotype of a species, they just reduce the chromosome number and fertility (in some reported cases).

So the reason for their spread in a population is also an enigma. In my model, the reason for the fusion of acrocentric chromosomes is short telomeres near the centromere. Interestingly, the shortest telomeres in humans are located on acrocentric chromosomes, exactly where you expect them to be. In humans a chromosome-specific telomere profile has been found. See attached image...

The observed meiotic drive of newly formed metacentric chromosomes would be a consequence of the fact that after fusion of two acrocentrics the critically short telomeres are gone. (=stable genome, increase in fitness)

In contrast, based on standard models of population genetics, you would still need bottlenecks and massive inbreeding for every chromosomal fusion event you want to see spreading...

That's the reason, why I prefer transgenerational telomere erosion as the cause for chromosomal evolution ;-)

J. Graakjaer, J. A. Londono-Vallejo, K. Christensen, S. Kolvraa, The pattern of chromosome-specific variations in telomere length in humans shows signs of heritability and is maintained through life. Ann. N. Y. Acad. Sci. 1067, 311–316 (2006); published online EpubMay (10.1196/annals.1354.042).

Reinhard, Good day .

I know earlier work of the author. I would very much like to get acquainted with this article. If you can send me the file.

Thank you very much.

Vladimir.

@Reinhard, there is no enigma regarding the spread to fixation of something that does not affect phenotype. It's called random genetic drift. Although drift is more prevalent with smaller population sizes, I am not convinced that multiple bottlenecks are required for the patterns you observe. Do you have a reference that models this and demonstrates the need for bottlenecks?

Although fertility *can* be affected by such rearrangements, it is not always. (See the link I added before. There is also fertile interbreeding between equids of difference chromosome numbers, for example.) Therefore, I do not see the need to invoke new population genetic models at this stage. Personally, I think that external forces, such as environmental change, are more likely to drive clusters of extinction and speciation than synchronised telomere collapse. This could even be quite cyclical, if linked to geological and/or astrophysical cycles.

Presumably, one can partially investigate the role of chromosomal rearrangements in speciation by testing whether rearrangement rates correlate more with speciation rates than extinction rates or evolutionary time? Has this been done? It would not rule out other explanations (correlation is not causation) but it would seem to be a necessary minimum requirement for any theory that posits chromosomal rearrangements as a major driver of speciation. With all of the genome sequences now available, it should also be possible to assess whether rearrangements happen in synchronised bursts, which I must admit to finding highly unlikely.

This has been an interesting discussion, but for me the best contribution has come from Edson Sandoval-Castellanos. Macroevolution is not simply not microevolution writ large. Goldschmidt, Waddington, Raff, and Gould (and many others; I highly recommend Gould's "The Structure of Evolutionary Theory") understood this and from that thinking emerged the importance of development in understanding evolution of phenotypes and the diversity of life. Can change in allele frequency really explain crawfish, giraffes, and mushrooms, all descended from the same common ancestor? Yes, we can quibble that the production of a novel phenotype (say leglessness in lizards) is simply a change in the frequency of a phenotype, but clearly it is much much more than that. Patterns predicted by punctuated equilibrium theory belie the necessity that evolutionary changes are a continuum and developmental biology seems to be the best place to look (although gene duplication and subsequent co-option of function is also a promising place) to explain these rapid phenotypic changes and differential rates of speciation.

Reinhard Stindl you have great arguments¡

you are reintroducing the neodarwinism's displeasure of Barbara Mcclintock, her works on cytogenetics make her argue in favor of the "lamarckian" response viewed on the rol transposons in the evolution

But im disagree whit this sentence "There’s a huge literature on chromosomal change in evolution…but it is old and therefore not sexy anymore". The rise of the epigenetics as chromosome biology is very exciting and it´s bringing back the chromosome as a important object in the evolution

one example

Brian,

I agree that evo-devo is a promising field, which has shifted the genetic agenda to the search for mutations in developmental genes, capable of producing large and/or many phenotypic changes at once. However, it is hard to imagine how sporadic mutations in these “macromutation” genes would create anything other than lonely monsters, which would hardly ever find a compatible mate, and would again make widespread and ubiquitous organic evolution a mission impossible (Stindl 2014).

Aimer,

You misunderstood me, I find chromosomes very sexy!

However, it is a fact that young ambitious scientists want to do sequencing and prefer to hunt for genes. They think the chromosome business is a girly thing...that it does not require much logical thinking. ;-)

That's a huge mistake!

Richard,

obviously, you believe in the power of computer models. When it comes to evolutionary theory, I think we don't need more computer models. ;-)

Large chromosomal aberrations, like fusions and translocations, usually result in some problems during meiosis. Of course, a fusion of two acrocentric chromosomes at the centromere (=Robertsonian translocation) seems to be less harmful. Still, if e.g. during human meiosis the chromosome fusion product 13-21 and a normal chromosome 21 end up in an oocyte, the fertilized egg will be trisomic for chromosome 21 (= Down syndrome).

That's the daily routine at a department for human genetics. And this is just one example of the many chromosomal effects on human health and fertility. Now, look at the dozens of chromosomal aberrations in gibbons again (see above), and please tell me...how the accumulation of so many sporadic chromosomal aberrations can happen in every individual of a species...without massive chromosomal instability...which again would be deleterious.

Barbara McClintock once wrote: ‘‘Our present knowledge would suggest that these reorganizations originated from some shock that forced the genome to restructure itself in order to overcome a threat to its survival’’ (McClintock, ’84).

Reinhard

There's no doubt some chromossomic changes, just like point mutations are deleterious. But many others are neutral, or even beneficial.

As Richard put above, they don't have to happen in many organisms at once, just spread by drift. Although bottlenecks could have happened, they dont have to. The fact the all gibbons presented it today says nothing about how it apeared, but the population genetic models (those Richards asked you for) explain well how they could have spread.

Barabra McClintock citation refers to transposition in stressfull condition, like when epigenetic reparterning unleash transposition and can enhace evolvability, and have no "necessary" relation to chromossimal changes. Needles to say that processes like these produce all sort of outcomes related to fitness (deleterious to beneficial).

I'm going to bow out of this discussion for a bit after this (unless asked a direct question) out of fear of over-contribution but I would just like to question Edson, Brian and Reinhard for their definitions of "microevolution" and "macroevolution". Evolutionary biology has come a long way since Gould et al and I think that we are in danger of arguing across each other due to differences in definition. I do not, for example, define microevolution as simply changes in allele frequency, unless you explicitly include zero to non-zero frequency changes - it also has to incorporate the generation of novelty by the kinds of mutation we witness occurring. It must also be made clear that the alleles concerned do not need to be coding sequences or even single nucleotides. Presence/absence of a transposable element or translocation would count. There is no direct correlation between the size of a genetic mutation and the scale of its phenotypic outcome - we are not discussing (genetic) micro-mutations versus macro-mutations.

For me, "microevolution" versus "macroevolution" is about whether the evolutionary forces we can witness and measure occurring, and the well-established rules regarding whether certain genetic variants can/will persist in a population, are sufficient (in combination with the Earth's environmental history) to account for the larger differences that we see accumulate over longer timescales. Can single events, large or small but each explicable by itself, add up over time? Or, do multiple events have to occur simultaneously, governed by a separate process that does not act at the individual event level? I think we also need to distinguish between short-term macroevolutionary forces proposed to generate macro-variants, and long-term macroevolutionary forces that simply determine which (microevolutionary) lineages have a long-term future. (Evolution has no foresight and will regularly evolve itself into a corner.)

Gould's "punctuated equilibria" is both nonsense (from a purely genetic point of view) and utterly expected (from a phenotypic adaptation point of view). The only thing it argues against is pure gradualism, i.e. a constant gradual rate of evolutionary change at all levels, which no one in my life-time has seriously proposed. Such gradualism is not something that microevolution (i.e. general molecular evolutionary theory) predicts. Ever. Not even in "simple" microevolution experiments, such as Lenski's bacterial evolution. Adaptation is always predicted to have a quick initial burst and then taper off.

So, a request please. If you are going to make a case for some kind of special macroevolutionary force (and perhaps there is one), please start by giving a *contemporary* definition of what you understand macroevolution and microevolution to be, rather than relying on those with a pre-genomics understanding of genetics.

Daniel,

you misunderstood me. The chromosomal aberrations in the gibbons, cannot be neutral, even if generated by fusions and inversions and not by translocations (as I suggested in my model).

Translocations and fusions always lead to a (slight) decrease in fertility, because of the problems in meiosis, I pointed out previously. So, sporadic chromosomal changes like fusions and translocations always have to provide some benefit to the phenotype, otherwise they cannot spread in a population.

Or you need some kind of meiotic drive, which has been described for Robertsonian translocations.

See:

M. King, Species evolution : the role of chromosome change. (Cambridge University Press, Cambridge, New York, 1993), pp. xxi, 336.

And yes, Barbara McClintock focused on both, transposons and broken chromosome ends which result in breakage-fusion-bridge cycles and chromosomal change. In her paper, she also cites the Indian Muntjac deer with 7 chromosomes and its closest relative the Chinese muntjac with 46 chromosomes. The 7 chromosomes (6 chromosomes in females) are the result of the fusion of 46 chromosomes. This has been shown by FISH.

Richard,

I never used the terms macroevolution and microevolution in this discussion. Of course, I know the definition of these terms.

Chromosomal change is by no means "macroevolution". I just wanted to point out that chromosomal change is a bit more complicated than the gene stuff. For example, you can easily duplicate a gene...but you should not duplicate a chromosome! Proof comes from human population studies: there are no human populations with different karyotypes (at least, haven't been found yet), but there are 100000s of genetic variants. Yet, chromosomes have changed a lot during evolution and almost all species have a different chromosome complement.

So, either chromosomal change happened suddenly or it is nonrandom and directed. (short telomeres on certain chromosomes)

To make any progress in evolutionary theory, I think we have to switch to a lower magnification ;-)

To summarize, the currently favored molecular mechanisms (in micro- and macroevolution) do not comply with the chromosomal evidence!

"...relying on those with a pre-genomics understanding of genetics."

Last but not least, I think that there is no evolution in scientific thinking either. The older literature definitely is of higher quality, because scientists spent much more time on each project. I do not see the great benefits of modern genomics...except for the industries ;-)

Dear Sirs!

It's not that "is no evolution in scientific thinking either". The fact that the scientific community does not accept new thoughts. It has always been so. But the current system of financing science aggravates the situation. Scientists have to seek not the truth, but grants. These are two different things. In a basis of outdated views on evolution as a struggle for existence. But the struggle for existence does not develop, and to stasis. What we observe.

Richard and Reinhard this debate is exciting. I want introduce a middle position:

1.There´s an obvious relation between macro-mutation and micro-mutation with the evolutionary process, but.. is this relation enough to differentiate two kinds of evolution, non-translatable with each other?: In this point. I think we can get a common position: If we differentiate the evolutionary process by this criteria, this process would be something like macroevolution of short term (or the classic name punctuated equilibria).

The nature and consequence of this macro-changes, that we can found to be normal in the chromosome level, is too strong that can accomplish the successful sympatric speciation, e.g duplications at the genome scale (polyploidy) in plants abbolish the decrease in fertility of a hybrid of two populations with different karyotypes.

In other words, this change just doesnt make happen things much faster than microevolutionary change, also it open the door to new qualitative evolutionary possibilities

2. The strategy of translate p or q in other things like chomosome translocation or duplication its very intresting for study the spread of this changes and other phenomens, for that reason i´m disagree whit Reinhard when he say "I think we don't need more computer models". However this changes are so big, that we need something like population genomics, one recen field include the study of pattern and degree of genome-wide heterogeneity as chromosomal/positional differences...reconmbination rates and etc.. (Luikart G. et al 2003)

Aimer,

I meant, we don't need more of these computer models, which are not based on "real world evolution".

If the computer does not know of the problems of chromosomal rearrangements during meiosis, it will always give you wonderful data regarding the spread of chromosomal rearrangements in a population.

So, the computer is always limited by the biological knowledge of the programmer.