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Pathogens were the main selective pressure in human evolution?

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In “Signatures of Environmental Genetic Adaptation Pinpoint Pathogens as the Main Selective Pressure through Human Evolution” (PLOS Genetics, November 3, 2011 ) Matteo Fumagalli et al argue,

Previous genome-wide scans of positive natural selection in humans have identified a number of non-neutrally evolving genes that play important roles in skin pigmentation, metabolism, or immune function. Recent studies have also shown that a genome-wide pattern of local adaptation can be detected by identifying correlations between patterns of allele frequencies and environmental variables. Despite these observations, the degree to which natural selection is primarily driven by adaptation to local environments, and the role of pathogens or other ecological factors as selective agents, is still under debate.

To address this issue, we correlated the spatial allele frequency distribution of a large sample of SNPs from 55 distinct human populations to a set of environmental factors that describe local geographical features such as climate, diet regimes, and pathogen loads. In concordance with previous studies, we detected a significant enrichment of genic SNPs, and particularly non-synonymous SNPs associated with local adaptation.

Furthermore, we show that the diversity of the local pathogenic environment is the predominant driver of local adaptation, and that climate, at least as measured here, only plays a relatively minor role. While background demography by far makes the strongest contribution in explaining the genetic variance among populations, we detected about 100 genes which show an unexpectedly strong correlation between allele frequencies and pathogenic environment, after correcting for demography. Conversely, for diet regimes and climatic conditions, no genes show a similar correlation between the environmental factor and allele frequencies.

This result is validated using low-coverage sequencing data for multiple populations. Among the loci targeted by pathogen-driven selection, we found an enrichment of genes associated to autoimmune diseases, such as celiac disease, type 1 diabetes, and multiples sclerosis, which lends credence to the hypothesis that some susceptibility alleles for autoimmune diseases may be maintained in human population due to past selective processes.

Do they mean it wasn’t cooking or shoes or fluid societies or anything? We’ve heard all those and hundreds more … Stay tuned.

18 Replies to “Pathogens were the main selective pressure in human evolution?

  1. 1
    bornagain77 says:

    This clearly sounds like epigenetically driven adaptation to local environments, rather than any ‘random micro-evolution’, despite the mandatory homage paid to Uncle Charley at the beginning and end of the article;

  2. 2
    DrREC says:

    No. It doesn’t. Epigenetics would study the DNA methylation or histone codes that regulate DNA transcription. Epi-genetic means on top of the genome. They studied genes at the sequence level. That is this part: “spatial allele frequency distribution of a large sample of SNPs”

    Nice article News. Should be an interesting read.

    Nothing like a plague wiping out half a population to select for some resistance alleles!

  3. 3
    bornagain77 says:

    DrREC you state:

    No. It doesn’t. Epigenetics would study the DNA methylation or histone codes that regulate DNA transcription. Epi-genetic means on top of the genome.

    Yet I seem to recall Shapiro stating:

    Revisiting the Central Dogma in the 21st Century – James A. Shapiro – 2009
    Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, (Page 14) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112).

    Also of interest from the preceding paper, on page 22, is a simplified list of the ‘epigentic’ information flow in the cell that directly contradicts what was expected from the central dogma (Genetic Reductionism/modern synthesis model) of neo-Darwinism.

  4. 4
    DrREC says:

    Read the list of epigenetic mechanisms. Are any of them mutational? No.

    You’re conflating these epigenetic mechanisms with the notion of “directed genetic engineering” which is a bit more dubious, especially in animals, with a few exceptions like the immune system.

  5. 5
    bornagain77 says:

    DrREC you state:

    Are any of them mutational? No.

    That is exactly the point DrREC!!! And this ‘non-mutational’ process helps you establish ‘random mutations’ for neo-Darwinism how??? Clearly DrREC, this is not helpful to neo-Darwinian presuppositions!

  6. 6
    DrREC says:

    This paper measured coding genetic changes. Coding genetic changes aren’t epigenetic. This paper doesn’t study epigenetics.

    Mutational changes, such as studied in this paper, is the “random variation” of evolution.

    Epigenetics marks aren’t, and aren’t thought to persist long enough to impact evolution.

  7. 7
    bornagain77 says:

    DrREC you state:

    Coding genetic changes aren’t epigenetic.

    Yet I have reason to believe that they are:

    Cells Defend Themselves from Viruses, Bacteria With Armor of Protein Errors – Nov. 2009
    Excerpt: These “regulated errors” comprise a novel non-genetic mechanism by which cells can rapidly make important proteins more resistant to attack when stressed,

    Synonymous Codons: Another Gene Expression Regulation Mechanism – September 2010
    Excerpt: There are 64 possible triplet codons in the DNA code, but only 20 amino acids they produce. As one can see, some amino acids can be coded by up to six “synonyms” of triplet codons: e.g., the codes AGA, AGG, CGA, CGC, CGG, and CGU will all yield arginine when translated by the ribosome. If the same amino acid results, what difference could the synonymous codons make? The researchers found that alternate spellings might affect the timing of translation in the ribosome tunnel, and slight delays could influence how the polypeptide begins its folding. This, in turn, might affect what chemical tags get put onto the polypeptide in the post-translational process. In the case of actin, the protein that forms transport highways for muscle and other things, the researchers found that synonymous codons produced very different functional roles for the “isoform” proteins that resulted in non-muscle cells,,, In their conclusion, they repeated, “Whatever the exact mechanism, the discovery of Zhang et al. that synonymous codon changes can so profoundly change the role of a protein adds a new level of complexity to how we interpret the genetic code.”,,,

    i.e. Giving the staggering level of information processing in the cell DrREC, I simply find it a stretch, to put it mildly, to claim randomness for the process when you yourself admitted “This paper doesn’t study epigenetics”;

  8. 8
    bornagain77 says:

    Of related interest:

    Pulsating Response to Stress in Bacteria Discovered – (Nov. 3, 2011)
    Excerpt: The bacterial gene circuit amplifies these molecular fluctuations, also called noise, to generate discrete pulses of ?B activation. The stress also activates another key protein that modulates the pulse frequencies.
    By turning a steady input (the stress) into an oscillating output (the activation of ?B) the genetic circuit is analogous to an electrical inverter, a device that converts direct current (DC) into alternating current (AC), explains Michael Elowitz, professor of biology and bioengineering at Caltech, Howard Hughes Medical Institute investigator, and coauthor of the paper. “You might think you need some kind of elaborate circuitry to implement that, but the cell can do it with just a few proteins, and by taking advantage of noise.”,,, “With this work and recent work in other systems, we’re starting to get a glimpse of just how dynamic cellular control systems really are,” Elowitz adds. “That’s something that was very difficult to see in the past.”

  9. 9
    DrREC says:

    “DrREC you state:

    Coding genetic changes aren’t epigenetic.

    Yet I have reason to believe that they are:”

    This is just a simple definition. Genetic vs. EPIgenetic. See the “EPI” It has meaning. Increased mutation rate in bacteria in stress conditions (where the paper is taking about the human genome) is interesting, but irrelevant.

  10. 10
    tragic mishap says:



    We have no problem admitting that selective pressures exist and do affect allele frequencies. Read The Edge of Evolution. Behe’s entire thesis is based on the demonstration that Darwinian processes not only exist, but that they can be measured.

  11. 11
    bornagain77 says:

    tragic, I didn’t say otherwise, I just disagreed with the a priori conviction that the change in alleles was caused by purely random processes as is required for a neo-Darwinian interpretation in the first place!

  12. 12
    bornagain77 says:

    correction: I just disagreed with the a priori conviction that the change in alleles, in this particular instance cited by the OP, was caused by purely random processes.

    In fact, considering the stunning level of information processing going on in the cell, which we have just the barest glimpse of so far, I would have to say that, aside from induced mutations, it would be extremely difficult for a atheist to find examples of ‘purely’ random mutations, in these ‘local adaptations, so as to make his case with.

  13. 13
    tragic mishap says:

    You do realize that SNP means “Single Nucleotide Polymorphism,” placing these mutations within Behe’s limit, right?

  14. 14
    bornagain77 says:

    tragic, I’m not even questioning that (indeed would not a priori expect Behe’s limit to be violated even with the epigentic programming of the cell adjusting the nucleotide sequences), I am just pointing out that the atheists have not established that the changes were truly random. That is all! It is a simple point, yet it is still crushing to neo-Darwinism since neo-Darwinism is required, scientifically, to establish that the changes are truly random!

  15. 15
    bornagain77 says:

    tragic, of humorous note; here is a experiment, I posted a while back, that would satisfy the empirical requirement, on neo-Darwinism, to establish that purely random processes can create all life:

    Blackholes- The neo-Darwinians ultimate ‘god of randomness’ which can create all things

    Being the helpful guy I am, always trying to help atheists out when I get a chance, I’ve been trying to piece together a experiment that would prove once and for all, for everyone to see, that RANDOM variation plus undirected natural selection can produce functional proteins just as atheists adamantly claim (even though no one has ever seen RANDOM processes do this). Now I just about got the RANDOM part of the experiment down for the atheists! I’ve searched for the maximum source of RANDOMNESS that I could find in the universe, (since the ‘god of randomness’ is who atheists claim for their creator), and I think I’ve found it for them;


    Thermodynamics – 3.1 Entropy
    Entropy – A measure of the amount of randomness
    or disorder in a system.

    Thus, the more entropy a system has the more randomness it will generate for our experiment to find a RANDOM functional protein. And if we ask, ‘what is the maximum source of entropy, i.e. RANDOMNESS, in the universe?’, we find this:

    Entropy of the Universe – Hugh Ross – May 2010
    Excerpt: Egan and Lineweaver found that supermassive black holes are the largest contributor to the observable universe’s entropy. They showed that these supermassive black holes contribute about 30 times more entropy than what the previous research teams estimated.

    “But why was the big bang so precisely organized, whereas the big crunch (or the singularities in black holes) would be expected to be totally chaotic? It would appear that this question can be phrased in terms of the behaviour of the WEYL part of the space-time curvature at space-time singularities. What we appear to find is that there is a constraint WEYL = 0 (or something very like this) at initial space-time singularities-but not at final singularities-and this seems to be what confines the Creator’s choice to this very tiny region of phase space.”
    Roger Penrose – How Special Was The Big Bang?

    Plus for a added bonus for atheists, being the helpful guy that I am, I found that if we find a really supermassive blackhole we might just start to overcome the homochirality problem, which is a huge problem against finding functional proteins, as well:

    Homochirality and Darwin: part 2 – Robert Sheldon – May 2010
    Excerpt: With regard to the deniers who think homochirality is not much of a problem, I only ask whether a solution requiring multiple massive magnetized black-hole supernovae doesn’t imply there is at least a small difficulty to overcome? A difficulty, perhaps, that points to the non-random nature of life in the cosmos?

    But of course there is the problem with actually getting the atheists to the super-massive blackholes to actually do the experiments, so that they may try to RANDOMLY generate a functional protein. Not to mention the problem of someone trying to survive being stretched into as a piece of spaghetti, by the extreme warping of space-time, near the blackhole. But what the hey, it is just a little sacrifice for ‘science’ right!?! At least atheists will have a maximum source of randomness to work with in their experiments!!! But there is another problem I probably need to tell atheists about before they pack up and go off to the super-massive blackholes in order to prove to the world that their ‘god of randomness’ can create all things,

    “Gain in entropy always means loss of information, and nothing more.”
    Gilbert Newton Lewis – Eminent Chemist

    “Is there a real connection between entropy in physics and the entropy of information? ….The equations of information theory and the second law are the same, suggesting that the idea of entropy is something fundamental…”
    Tom Siegfried, Dallas Morning News, 5/14/90 – Quotes attributed to Robert W. Lucky, Ex. Director of Research, AT&T, Bell Laboratories & John A. Wheeler, of Princeton & Univ. of TX, Austin in the article

    But what the hey, atheists haven’t needed any stinking equations to prove their theory so far have they!?!

    Oxford University Admits Darwinism’s Shaky Math Foundation – May 2011
    Excerpt: However, mathematical population geneticists mainly deny that natural selection leads to optimization of any useful kind. This fifty-year old schism is intellectually damaging in itself, and has prevented improvements in our concept of what fitness is. – On a 2011 Job Description for a Mathematician, at Oxford, to ‘fix’ the persistent mathematical problems with neo-Darwinism within two years.

    I even have a inspirational quote for their future experiment;

    “I have attempted to give you a glimpse…of what there may be of soul in chemistry. But it may have been in vain. Perchance the chemist is already damned and the guardian the blackest. But if the chemist has lost his soul, he will not have lost his courage and as he descends into the inferno, sees the rows of glowing furnaces and sniffs the homey fumes of brimstone, he will call out-: ‘Asmodeus, hand me a test-tube.’”(1) Gilbert Newton Lewis

    And even a song for their experiment;

    Creed – Six Feet

  16. 16
    tragic mishap says:


  17. 17
    tragic mishap says:

    Anyway, randomness cannot be proven as a cause, and neither can God for that matter. There is only faith in one or the other.

    I have no particular problem granting that some things can be random, including certain random SNPs happening to provide some advantage relative to the environment, such as disabling most of the production of melanin in the first Europeans. There’s no need to be defensive. We are winning. 😉

  18. 18
    bornagain77 says:

    Tragic Well,,, actually I disagree with you and think it is very important to hold Darwinists strictly accountable to their theoretical presuppositions!,,, and I disagree with you on your other statement of deducing sufficient warrant of ‘proof’ as to source of causality.

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