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is evolution sufficient?

posted by Aziz Poonawalla

Partly because I just went to Africa and flew over (but did not have a chance to actually visit) the Great Rift Valley (also known as the Cradle of Mankind), I’ve been thinking a bit about evolutionary theory of late. I am a scientist, but not a biologist – my field is medical physics. Still, my background makes me biased towards the scientific establishment and I am an ardent believer in the scientific method. While technically as a deeply religious person I do believe in “intelligent design” (in the abstract) I don’t believe in Intelligent Design as promoted by the various evolution-denialists in the political arena. I am quite strictly against introducing religious theories such as ID into the science curriculum.

All that said, I still am unable to accept the blind assertion that genetic mutation is the sole source of speciation. Note that I am not talking about the origins of life, but rather the evolution of life afterwards from species to species. It strikes me that the evolutionary dogma can be reduced to the idea that DNA is “read-only”. Contrast this with the (discredited) ideas of Lamarck who argued that the environment can introduce changes to an organism that are then heritable by its progeny; given that DNA is indisputably the mechanism by which species reproduce, that implies that DNA is “read/write”.

From an engineering and aesthetic perspective, I have trouble with the idea that a system so complex as DNA and gene expression can be so rigid. My intuition is that DNA does not posess enough degrees of freedom to “encode” life as we know it. But how can I test that intuition without getting a PhD in genetics? I think I’ve come up with a way, though of course it is crude and rife with bland layman assumptions. Still, bear with me (and I hope to attract some attention to this from experts so we can refine it).

Let’s take some basic numbers. There are about 20,000 genes in the human genome, with an average size of 50 kilobases (ie, 50,000 base pairs. Remember DNA is a double-helix, unlike RNA). Also, we are often told that humans and chimpanzees differ in their genomes by only 1%. Actually, that figure is only for genes where humans and chimps totally differm but there are some genes where the variation between teh species might not be so absolute. I’ll use 5% instead. Finally, we know that according to best estimates, humand and chimpanzees diverged from their common ancestor about 5 million years ago.

Taking these bits of data, we can actually estimate the required rate of evolution in terms of point mutations in DNA needed to turn a chimp into an ape. Of course, humans did not evolve from chimps, so we would then halve the rate we calculate to get the change from the common ancestor of both to humans (or chimps). So, let’s do the math.

20,000 genes x 50,000 base pairs = 1 billion base pairs
5% difference between humans and chimps = 50 million base pairs
rate of change = 1/2 * 50 million base pairs / 5 million years = 5 base pairs per year

So, to go from the common ancestor of humans and chimps, to modern humans, the average rate of mutation required would be 5 base pairs per year. This seems like a very high rate to me; if we discretize into generations of 25 years each, then we are talking about 125 base pairs every generation.

It seems that this is a number that can be tested over time. You’d need to collect DNA data from thousands of people, over a few centuries, to get an idea of the actual rate of change. But it is definitely something that can be tested (and the exact number of people you’d need to test, and how many generations to test, is something that can be estimated by statistical theory to ensure that the results have statistical significance).

I am sure there are many objections to the methodology above – one that is immediate is that humankind has historically had very small populations, unlike other species like insects or rodents etc. That means that other species have a lot more raw genome floating around. But that kind of supports the contention that human evolution must be very rapid indeed to support the observed evolution over the past few million years, given our far smaller gene pool.

The implication of such rapid evolution is that we should actually notice it on human timescales. And that there is actually is some mechanism of action that is actually driving the mutations themselves – cosmic rays? transcription errors? normal statistical variance?

It seems that if we aren’t mutating at a rate comparable to above, then some sort of alternative mechanism must also be operating to accelerate the changes in DNA required to evolve from one species to another. There’s certainly some evidence that there are such “neo-Lamarckian” processes at work, The case of the humble water-flea certainly is not explicable by normal Darwinian processes.

You could go even further and compute the total information content of the human genome, and then try and see whether that is sufficient to describe a human being. But that is a task I’ll leave for later, or someone else. I think I’ve ventured far enough out on this limb for now :)

  • Curt Cameron

    Your error is assuming that in that one percent of different genes, all 50,000 base pairs will be different in that gene. I’m not a geneticist either, but it seems more reasonable that a different gene has a few base pairs different – that would throw off your calculation by a factor of 1,000 or 10,000.
    If you’re saying that you doubt that the information in the genome is not sufficient to describe the final creature, what else is there? Do you instead think that some supernatural force guides the development of every creature, from yeast to mammals, every time one grows into an adult? That’s one busy god.

  • Paul Burnett

    Thank you, Aziz, for understanding that intelligent design creationism isn’t science. The evolution denialists are dealing with pseudoscience, not science.
    Lamarckism or neo-Lamarckism is not real. What is observable is natural selection of random mutations. The environment “chooses” traits and decides which are more successful, but the environment does not drive the change of random mutations. There is drift – noise – in any signal, and RNA/DNA is no different. After all, although all of us get genetic material from our parents, none of us can be completely identical to either of our parents (think about it). Those slight differences, spread over entire populations / species, lead to changes that over large spans of time / location, lead to different species.

  • abb3w

    The base-pair method of calculation is a bit sloppy, since some relatively simple mutations can cause mutliple base-pair changes. While I’m not a biologist, I understand that the “simple” variants include
    1) Point replacement, where one base “letter” is replaced by another
    2) Point insertion/deletion, where one base “letter” is inserted/deleted in the sequence
    3) “amplification”, where extra copies of a subsequence get inserted
    4) Translocations, where a sequence moves from region to another
    5) Inversion, where a subsequence gets reversed within the longer string
    6) Full duplication of a chromosome to provide an additional copy
    7) Fusion of two chromosomes into a single chromosome
    There’s also some more exotic variants, such as lateral gene transfer between species via viral infection. (I believe these are relatively rare).
    Each of these mutation types have been observed in the lab. Most involve multiple base-pair shifts. At least one of these (fusion associated with Chromosome 2) is readily observable in the human/chimp chromosome banding patterns, even without full sequencing (which confirms it). Modern computers have sufficient power to identify sequence overlap, and allow calculation of the probable change-paths based on identifying how the overlaps correspond between genomes, and reconstruction of probable “common ancestor” maps for particular chromosomes, such as the “Y” sex chromosome (doi:10.1038/ng1729).
    Mutation rates (even of a particular type) do seem to vary across species, but I’ve not heard much indication humans rates are extraordinary when compared to other species. Based on divergence studies within the human genome, there’s some evidence packing into cities increased it a bit, due in part to more exciting viruses. However, there are plenty of species with both higher and lower rates.

  • Peter Sandwall

    I’m glad you began your argument with a hedge related to your incomplete education in the theory of evolution. While your logic may be sound, the foundations are flawed. Rather than go on diatribe about what mistakes or false assumptions you’ve made, I’d like to direct you to a resource that might enlighten you. Please read, ‘The Beak of the Finch’ by Jonathan Weiner. He won a Pulitzer Prize for the book, it’s quite a good read. I suspect many of your gaps regarding evolution will be filled.

  • Your Name

    Even if we ignore some of the objections of the other commenters, the rate you calculate is quite compatible with our current estimates of mutation rates in humans.
    For example, Giannelli et al. estimated an overall mutation rate of 2.14 x 10-8 per base per generation, equivalent to 128 mutations per human zygote.
    What you’re really asking at is not how many mutations occur in each generation. It’s how many mutations get fixed in the population per generation. However, considering that every newborn human has about 100 new mutations, it’s pretty clear that the observed genetic differences between chimps and humans are easily explainable by spontaneous, undirected mutations.

  • Aziz Poonawalla

    So, really the calculation is reasonable in terms of order of magnitude, but my intuition about that being “fast” is wrong? That makes more sense.
    I can intuit everything about evolutionary dogma above the level of gene expression. But it’s teh specificity of those mutations leading to such “large” changes that throws me off. It seems that we dont see incremental changes in nature at a organ or functional scale (I am aware that there are “transitional fossils” but thats a level above what I am talking about).
    This is probably a hackneyed example but let’s take as an example the blood clotting system. its pretty awesome thta one day an organism ended up with extra functionality like that, but was that the result of one point mutation? Or did the blood clotting system slowly take shape over millenia, and if so, then what were the intermediate stages of functionality? and were each of those a single point mutation? how would a point mutation that leads to partial functionality for something new be selected for, if the full functionality that would confer survival advantage isnt yet manifest?

  • Larry Moran

    Here’s a calculation that I did in 2007: Mutation rates.
    The bottom line is that there will be about 130 new mutations in every human baby. If you think about the entire human population there will be 7 x 10^11 new mutations every generation. Isn’t that enough? :-)

  • Anton Mates

    Or did the blood clotting system slowly take shape over millenia, and if so, then what were the intermediate stages of functionality?
    It did slowly take shape…over the entire history of the chordates, which is, I dunno, upwards of 600 million years. We can get some idea of the intermediate stages from looking at more distantly-related critters…in particular, lampreys and sea squirts. (Keeping in mind that these aren’t really true intermediates, since they and all other modern organisms have been evolving along their own paths just as long as we have.)
    and were each of those a single point mutation?
    Almost certainly not. Many of the clotting factors, and the genes that produce them, are closely related to other ones. These are the result of gene duplications, when a DNA copying error produced two copies of a preexsting gene. (This happens much more often than you’d think!)
    Once you have two copies of the same gene, one copy can often mutate without harming the organism, because the other copy is still pumping out whatever important protein it’s supposed to produce.
    Ken Miller has a very nice article outlining this process
    how would a point mutation that leads to partial functionality for something new be selected for, if the full functionality that would confer survival advantage isnt yet manifest?
    A gene which is only “partially functional” for one purpose may already be fully functional for another. If you look at the sea squirt example I linked to, it turns out that even though they don’t (and can’t) use various clotting factors for clotting, they already use them for other very important purposes. Thus these partially functional factors are already selected for on the basis of what they can do. Further mutations to add them to a clotting cascade only make them more useful!
    Also, a given mutation doesn’t have to be selected for to stick around…it simply shouldn’t be strongly selected against. The majority of mutations appear to be neutral, and many of them survive or even spread in the population due to genetic drift; thus they’re already in place to be combined with future mutations and produce some new “functionality.”

  • Mike Haubrich, FCD

    To piggyback on what Larry said, evolution spreads through populations. The exercise you created is interesting, but the important point is that evolution doesn’t work through a straight generation-to-generation lineage. Genes and their mutations “swarm” and “flow” into and through populations. Natural selection, chance, biogeographical isolation and catastrophe ensure the survival of genetic mutations and not others.
    Further, gene expression is not guaranteed by a gene’s presence. Genes interact and suppress expression, further complicating matters.

  • genemachine

    It might be more informative to calculate the required base pair change rate per birth. If we assume a population of 1 000 000, maybe 40 000 people will be born per year, we would need 130 base pair changes per 40 000 births.
    If we change the population a bit then we get figures spanning quite a broad range:
    1000 -> 130/40 = 3
    10000 -> 130/400 = 0.3
    100000 -> 130/4000 = 0.03
    1000000 -> 130/40000 = 0.003
    Mutations often involve more than one base pair so maybe we can divide these figures by the average number of basepairs changed in a mutation.
    If these mutations per birth figures still dont seem capable of creating enough genetic variety to replace 130 base pairs per year then what rate of mutations per birth do you think would be required?

  • abb3w

    Aziz Poonawalla asks “how would a point mutation that leads to partial functionality for something new be selected for, if the full functionality that would confer survival advantage isnt yet manifest?”
    “Partial functionality” may provide a lesser advantage even in partial form (and thus selected for), may be useful for some other purpose (and thus selected for), or may merely not provide significant benefit OR detriment (and thus, not be strongly selected, but spread via genetic drift).
    For an example of the last, search out Lenski’s technical papers (doi:10.1073/pnas.0803151105) on the evolution of citrate metabolism in his lab, and note that the final beneficial mutation was contingent on two neutral mutations earlier.

  • Bad

    I think you are poorly served by your idea of what evolutionary “dogma” is and isn’t. You sort of make up the “read only” off the top of your head. But this is a general idea about DNA: it isn’t a central tenet of the basic variation/selection scheme that constitutes the core of evolutionary change. We’ve known for a long time that there are other inheritable features other than nuclear DNA. I think journalists generally do a sloppy job of describing the context and scope of various debates, and generally when they try to speak about “Darwin” in general, this is a big red flag that we’re about to get some rather sloppy stuff rather than a real picture of what the current debates in a field are.

  • JE

    To Aziz Poonawalla. I don’t want to come off as patronizing, as this response is in good faith. But without being straight to you, it is hard to do so via a blog comment. Anyway, please take this as well-intentioned. Here goes:
    You would be well served by reading up a bit on the basics of both evolution and genetics, both theoretical and empirical. Many of your intuitive objections (insufficient mutation rate and too few “degrees of freedom”, for example) aren’t generally considered to be problems in the field, despite considerable amounts of thought about those very topics. In fact, some of these issues (in slightly revised form) are active topics of research.
    For starters, the mutation rates of eukaryotes fall consistently above your back-of-the-envelope calculation of 125 mutations per year. Moreover, not all mutations are basepair substitutions, and some of them can both create and destroy considerable amounts of hereditary information (duplication and deletion for example). Also, you might want to learn a bit about basic concepts like the pleitropy and epistasis, as it may speak to your comment on “degrees of freedom”. Also, the growing field of developmental biology may also make the current evolutionary framework seem less implausible.
    Additionally, your thought experiment has been conducted empirically in many contexts for decades (eg mutation accumulation experiments and sperm typing experiments as well as genealogical studies like for hapmap).
    It isn’t that your questions are unreasonable ones. On the contrary, a lot of research is conducted about rates of mutation, proportions of good/bad/neutral mutations, evolutionary potential, developmental plasticity, epigenetics, etc. However, these questions are asked with a lot more background, context, and subtlety, not to mention decades of active research. Also, you might want to steer clear of some language that seems a bit teleological. On a second reading, your description of non-Mendelian sources of variation isn’t teleological, but biologists are usually much more careful about their language to ensure that an interpretation of teleology isn’t even possible.
    Here are a few references that can get you off to a good start:
    Molecular Evolution, Li, ISBN: 978-0878934805
    Somewhat dated, but an excellent review of the field of molecular evolution and population genetics. It predates the genomics era, unfortunately.
    Principles of Population Genetics, Fourth Edition (Hardcover), Hartl & Clark, ISBN: 978-0878933082
    A thorough introduction to population genetics appropriate for advanced undergraduates with moderate quantitative skills or 1st year graduate students in evolutionary biology.
    Coalescent Theory: An Introduction (Paperback), Wakeley, ISBN: 978-0974707754
    An excellent theoretical introduction to population genetics from a coalescent perspective.
    Progress and Prospects in Evolutionary Biology: The Drosophila Model (Oxford Series in Ecology & Evolution) (Hardcover), Powell, ISBN: 978-0195076912
    Another dated text, but it summarizes a good swath of all of the relevant issues in the model system where the most thorough work has been done, Drosophila.
    I would also recommend picking up a basic text on genetics (sophomore or junior level undergrad) and developmental biology (junior or senior level undergraduate).

  • Your Name

    And another point to further your arguement…
    After that first mutation you have now reduced your available sample size to those that have undergone the assumed positive genetic mutation. The probability that generation after generation one can string together succesive positive genetic mutations is definately not non-zero, but is quickly approaching it.

  • JE

    @”Your Name”
    The probability of any one outcome (a string of any positive mutations, negative mutations, or no mutation at all all) is vanishingly small, as well. What’s your point? You can make the same argument with dice. The probability of you rolling any particular sequence of 20 6-sided dice is really small, at about one chance in 3,656,158,440,062,976. Consider the following sequence:
    1 6 5 4 3 4 2 1 4 5 3 5 2 4 5 1 5 2 4 1
    Does that seem particularly unusual to you? Well, the probability of obtaining that particular sequence is vanishingly small, but it is no more or less likely than any other sequence, like for instance this one:
    5 6 3 5 6 6 3 4 3 1 2 2 6 2 3 4 2 2 4 4
    Furthermore, your objections apply equally well to genetic algorithms as well as both natural selection and artificial selection. And there are abundant examples of all three. I’m not really sure you appreciate that evolution is huge class of observations. Fact if you will. And natural selection (or genetic drift and/or various demographic and population structure scenarios) are just different forces that may or may not be the best explanation for the observed facts. We see this differences that have accumulated over time, we can see difference as they accumulate generation after generation, and we’ve done the molecular biology to understand the mechanisms of how mutations arise. We also understand the statistics of several mechanisms that can cause mutations to change frequency. Of course, we never necessarily know 100% what the precise forces that controlled the changes in frequency of those mutations, but we can make our best guess. And even the most likely scenario will have vanishingly small probabilities just like the dice example I showed.

  • RBH

    I get the jim-jams when I see these two statements from Aziz Poonawalla :
    I am a scientist, but not a biologist
    I can intuit everything about evolutionary dogma above the level of gene expression.
    Uninformed intuitions are a bad basis for evaluating a scientific theory. Would Aziz think well of me if I were to deploy my uninformed intuitions about his field of expertise as though it were a useful contribution to a discussion in any way except to identify where I need some education?

  • Argon

    Your Name (February 2, 2009 5:21 PM): “After that first mutation you have now reduced your available sample size to those that have undergone the assumed positive genetic mutation.
    The majority of genetic variations between humans and chimps appear to be neutral. As it happens, neutral mutations accumulate in a population at a rate approx. equal to the mutation rate.

  • ChaosEngineer

    So, to go from the common ancestor of humans and chimps, to modern humans, the average rate of mutation required would be 5 base pairs per year. This seems like a very high rate to me; if we discretize into generations of 25 years each, then we are talking about 125 base pairs every generation.
    That doesn’t seem like a very high rate. Remember that a generation has multiple people in it. Suppose there are a million proto-humans in the average generation. To get 125 mutations, we only need a beneficial mutation in one proto-human out of every 8000. (And it doesn’t even need to be a beneficial mutation…it can be a neutral mutation that happens to become widespread through genetic drift.)
    Here’s the first document I could find with solid numbers on the mutation rate. It says that the average person has 3 mutations relative to their parents’ genes:
    So we can get the required 125 mutations per generation, provided one mutation out of every 24,000 (8000 * 3) survives and becomes widespread.
    Your Name: After that first mutation you have now reduced your available sample size to those that have undergone the assumed positive genetic mutation
    No. Suppose that one proto-human gets Beneficial Mutation A, and another proto-human halfway around the world gets Beneficial Mutation B. Because the mutations are beneficial, the populations carrying those genes will expand to larger territories over many generations. Eventually the two populations will meet and some of their offspring will have both A and B. After more generations, those offspring will expand through the old territories, out-competing their A-only and B-only cousins.
    The only time this wouldn’t happen is if Mutations A and B were on the same gene, so that no one would be able to have both. In that case, the less-beneficial mutation would eventually vanish. If they were both equally beneficial then they’d both survive, possibly restricted to different parts of the world.

  • Darek

    Whats so difficult about consulting an expert in the field first before pontificating about something you aren’t completely well-versed in? I mean, come to any conclusion you want and post it on the internet, but at least demonstrate some intellectual honesty by also revealing how this argument stands up to someone whos studied it?
    I don’t know where Aziz lives but it shouldn’t matter – most universities have their academic staff’s email address handy online…
    It would at least make for a more interesting blog post.
    Just saying..

  • Barry

    Here are some comments by a mathematician:
    Summary – Aziz doesn’t know what he’s talking about, and still pretty much demonstrated the feasibility of what he thinks is not possible (or likely.

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