Evolution Information Intelligent Design

Are developmental mistakes essential to evolution?

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From Joanna Masel at Big Questions Online:

With the error rate in this example, that could be enough for natural selection to take notice. To see how, imagine you have a permanent, germline mutation that doesn’t affect how well your protein works in normal cases, when it’s transcribed and translated correctly. But the mutation does change the fraction of error-containing variants that work properly, say from 40 percent to 42 percent. That means slightly less work for your cells’ garbage-disposal system and more fitness for you — making you healthier and more likely to survive and reproduce. In other words, this mutation benefits you, evolutionarily speaking. Natural selection doesn’t just judge how well a gene works when its proteins are produced correctly, but also how well all the error-containing versions of the gene’s proteins work.

Because the same protein variants can be produced either by mutation or by gene expression error, evolution under constant pressure from developmental errors leads to improvements not only in developmental robustness, but also in what biologists call “evolvability” — the capacity to produce genetic variants that help adaptation. For evolution by natural selection to work, a reasonable fraction of genetic mutations has to be not just harmless but also helpful. This seems like a tall order. Aren’t random changes to any highly complex thing likely to break it, rather than improve it? Yes, but they are much less likely to break it, and hence more likely to improve it, if those mutations have already been prescreened.

One of the “incorrect” protein variants your body produces in error today could be the new “normal” tomorrow, if the right permanent germline mutation comes along.

Without errors, in other words, evolution’s creativity would be stifled. If we were already perfect biological organisms, evolution would have nowhere to go — no diversity to explore, no fountain of creativity. The takeaway? Embrace the waste, the mess, and the errors — embrace the imperfection. Without it, the diverse wonders of the natural world could not have come to be. More.

Note: “Natural selection doesn’t just judge how well a gene works when its proteins are produced correctly, but also how well all the error-containing versions of the gene’s proteins work. ”

Sure. It’s amazing what Darwin’s followers are willing to believe about how randomness can produce complex, highly specified information.

See also: Darwin will save us from Boltzmann brains

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4 Replies to “Are developmental mistakes essential to evolution?

  1. 1
    mahuna says:

    As much as everybody (including Dembski and Wells) keeps using the flagellum to discuss the impossibility of “random design”, I much prefer Behe’s discussion of Blood Clotting.

    Blood is a tremendously complex biochemical system, if you’re an organism complicated enough to need blood, you REALLY want to have a system that both PREVENTS and INITIATES clotting, each at the right times.

    But the truly amazing part is that the ENTIRE system MUST work on Day 1. If any part of the vastly complicated system is missing, you simply DIE. For example: if you have the “clotter” part but not the “unclotter” part, the blood in your veins simply clots even without a wound. BANG! You’re dead.

    Now how much simpler than THAT can you get? It is “irreducibly complex” while also being vital. And it’s IMPOSSIBLE to start with a partial system and then evolve the missing pieces over the next hundred generations of your offspring because none of your offspring will survive long enough to reproduce. Nor will you.

    So, building up errors as a pathway to success is not going to work because the theory assumes that each and every one of the errors has no negative effects right up to the point where the new error-prone system suddenly demonstrates a new function.

    And people make a living thinking up stuff like that?

  2. 2
    bornagain77 says:

    as to:

    One of the “incorrect” protein variants your body produces in error today could be the new “normal” tomorrow, if the right permanent germline mutation comes along.

    And exactly what is the waiting time for just two mutations to fix in a population?

    Evolution And Probabilities: A Response to Jason Rosenhouse – August 2011
    Excerpt: The equations of population genetics predict that – assuming an effective population size of 100,000 individuals per generation, and a generation turnover time of 5 years – according to Richard Sternberg’s calculations and based on equations of population genetics applied in the Durrett and Schmidt paper, that one may reasonably expect two specific co-ordinated mutations to achieve fixation in the timeframe of around 43.3 million years. When one considers the magnitude of the engineering fete, such a scenario is found to be devoid of credibility.
    http://www.uncommondescent.com.....osenhouse/

    Whale Evolution vs. Population Genetics – Richard Sternberg and Paul Nelson – (excerpted from ‘Living Waters’ video) (2015)
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1161131450566453/?type=2&theater

    The waiting time problem in a model hominin population – 2015 Sep 17
    John Sanford, Wesley Brewer, Franzine Smith, and John Baumgardner
    Excerpt: The program Mendel’s Accountant realistically simulates the mutation/selection process,,,
    Given optimal settings, what is the longest nucleotide string that can arise within a reasonable waiting time within a hominin population of 10,000? Arguably, the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer), for a single point mutation is not timely adaptation in the face of any type of pressing evolutionary challenge. This is especially problematic when we consider that it is estimated that it only took six million years for the chimp and human genomes to diverge by over 5 % [1]. This represents at least 75 million nucleotide changes in the human lineage, many of which must encode new information.
    While fixing one point mutation is problematic, our simulations show that the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years (Table 2). This is ten-fold longer than the estimated time required for ape-to-man evolution. In this light, we suggest that a string of two specific mutations is a reasonable upper limit, in terms of the longest string length that is likely to evolve within a hominin population (at least in a way that is either timely or meaningful). Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect), in terms of the evolution of modern man.
    It is widely thought that a larger population size can eliminate the waiting time problem. If that were true, then the waiting time problem would only be meaningful within small populations. While our simulations show that larger populations do help reduce waiting time, we see that the benefit of larger population size produces rapidly diminishing returns (Table 4 and Fig. 4). When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years.
    http://www.ncbi.nlm.nih.gov/pm.....MC4573302/

    Human Evolution: A Facebook Dialog – By Ann Gauger – Nov. 12, 2012
    Excerpt: PM:Is it also possible that the mechanism that you refer to in your video clip is not the only/main one at play?
    Biologic: The mechanism I refer to is based on the standard Darwinian model for evolution. Published population genetics estimates for how long it would take to make *and fix* a single base change to a DNA binding site in a 1 kb segment of DNA are prohibitively long—six million years. To get a second mutation in the same DNA binding site would take in excess of 200 million years.
    Now to go from hominid to human requires many changes, most of them to gene expression patterns. It is much easier to change the DNA binding site than to change the transcription factor’s specificity. And all these mutations must work together and be beneficial to the evolving organism. The window of time available according to the fossil record and phylogenetic estimates is too short for known mechanisms to be sufficient. So do I think there are are other things at play?
    Yes.
    http://www.biologicinstitute.o.....ialog?og=1

    Moreover, negative epistasis, between even supposedly beneficial mutations, is the rule rather than the exception:

    Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations)
    Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
    http://www2.cnrs.fr/en/1867.htm?theme1=7

    New Research on Epistatic Interactions Shows “Overwhelmingly Negative” Fitness Costs and Limits to Evolution – Casey Luskin June 8, 2011
    Excerpt: In essence, these studies found that there is a fitness cost to becoming more fit. As mutations increase, bacteria faced barriers to the amount they could continue to evolve. If this kind of evidence doesn’t run counter to claims that neo-Darwinian evolution can evolve fundamentally new types of organisms and produce the astonishing diversity we observe in life, what does?
    http://www.evolutionnews.org/2.....47151.html

    As well, although there is a little tolerance for mutations to proteins that may be beneficial in one environmental context, mutations to developmental gene regulatory networks (dGRNs), which control the when and how much of gene expression, are almost ‘always catastrophically bad’.

    A Listener’s Guide to the Meyer-Marshall Debate: Focus on the Origin of Information Question -Casey Luskin – December 4, 2013
    Excerpt: “There is always an observable consequence if a dGRN (developmental gene regulatory network) subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.” –
    Eric Davidson – developmental biologist
    http://www.evolutionnews.org/2.....79811.html

    When Theory Trumps Observation: Responding to Charles Marshall’s Review of Darwin’s Doubt – Stephen C. Meyer – October 2, 2013
    Excerpt: Developmental gene regulatory networks (dGRN) are control systems. A labile (flexible) dGRN would generate (uncontrolled) variable outputs, precisely the opposite of what a functional control system does. It is telling that although many evolutionary theorists (like Marshall) have speculated about early labile dGRNs, no one has ever described such a network in any functional detail — and for good reason. No developing animal that biologists have observed exhibits the kind of labile developmental gene regulatory network that the evolution of new body plans requires. Indeed, Eric Davidson, when discussing hypothetical labile dGRNs, acknowledges that we are speculating “where no modern dGRN provides a model” since they “must have differed in fundamental respects from those now being unraveled in our laboratories.”8
    By ignoring this evidence, Marshall and other defenders of evolutionary theory reverse the epistemological priority of the historical scientific method as pioneered by Charles Lyell, Charles Darwin and others.9 Rather than treating our present experimentally based knowledge as the key to evaluating the plausibility of theories about the past, Marshall uses an evolutionary assumption about what must have happened in the past (transmutation) to justify disregarding experimental observations of what does, and does not, occur in biological systems. The requirements of evolutionary doctrine thus trump our observations about how nature and living organisms actually behave. What we know best from observation takes a back seat to prior beliefs about how life must have arisen.
    http://www.evolutionnews.org/2.....77391.html

  3. 3
    bornagain77 says:

    This almost ‘always catastrophically bad’ result for developmental mutations is especially true during early embryological development, which is precisely the place in an organism’s development where Darwinists most need plasticity in the organism in order for their theory to be viable.

    Darwin or Design? – Paul Nelson at Saddleback Church – Nov. 2012 – ontogenetic depth – video
    Text from one of the Saddleback slides:
    1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows.
    2. Thus, to change — that is, to evolve — any body plan, mutations expressed early in development must occur, be viable, and be stably transmitted to offspring.
    3. But such early-acting mutations of global effect are those least likely to be tolerated by the embryo.
    Losses of structures are the only exception to this otherwise universal generalization about animal development and evolution. Many species will tolerate phenotypic losses if their local (environmental) circumstances are favorable. Hence island or cave fauna often lose (for instance) wings or eyes.
    http://www.saddleback.com/mc/m/7ece8/

    Thus, where Darwinists most need plasticity in the genome to be viable as a theory, (i.e. developmental Gene Regulatory Networks), is the place where mutations are found to be almost ‘always catastrophically bad’. Yet, it is exactly in this area of the genome (i.e. regulatory networks) where ‘striking differences’ are found between even the supposedly closely related species of chimps and humans (R. Sternberg).

    On Human Origins: Is Our Genome Full of Junk DNA? Pt 2. – Richard Sternberg PhD. Evolutionary Biology – podcast
    Excerpt: “when you get to the folder and the super-folder and the higher order level, that’s when you find these striking differences (between organisms).”
    http://www.discovery.org/multi.....-dna-pt-2/

    Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012
    Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,,
    A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species.
    On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,,
    http://www.the-scientist.com/?.....plicing%2F

    Gene Regulation Differences Between Humans, Chimpanzees Very Complex – Oct. 17, 2013
    Excerpt: Although humans and chimpanzees share,, similar genomes (conservatively 88% per J. Tomkins), previous studies have shown that the species evolved major differences in mRNA expression levels.,,,
    http://www.sciencedaily.com/re.....144632.htm

    Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing – 2016
    In Brief
    Alternatively spliced isoforms of proteins exhibit strikingly different interaction profiles and thus, in the context of global interactome networks, appear to behave as if encoded by distinct genes rather than as minor variants of each other.,,,
    Page 806 excerpt: As many as 100,000 distinct isoform transcripts could be produced from the 20,000 human protein-coding genes (Pan et al., 2008), collectively leading to perhaps over a million distinct polypeptides obtained by post-translational modification of products of all possible transcript isoforms (Smith and Kelleher, 2013).
    http://iakouchevalab.ucsd.edu/.....M_2016.pdf

    as to the strikingly different interaction profiles for proteins generated by alternative splicing, Behe’s limit for just 2 new protein-protein binding sites evolving by Darwinian processes is,,,

    Kenneth Miller Steps on Darwin’s Achilles Heel – Michael Behe – January 17, 2015
    Excerpt: Enter Achilles and his heel. It turns out that the odds are much better for atovaquone resistance because only one particular malaria mutation is required for resistance. The odds are astronomical for chloroquine because a minimum of two particular malaria mutations are required for resistance. Just one mutation won’t do it. For Darwinism, that is the troublesome significance of Summers et al.: “The findings presented here reveal that the minimum requirement for (low) CQ transport activity … is two mutations.”
    Darwinism is hounded relentlessly by an unshakeable limitation: if it has to skip even a single tiny step — that is, if an evolutionary pathway includes a deleterious or even neutral mutation — then the probability of finding the pathway by random mutation decreases exponentially. If even a few more unselected mutations are needed, the likelihood rapidly fades away.,,,
    So what should we conclude from all this? Miller grants for purposes of discussion that the likelihood of developing a new protein binding site is 1 in 10^20. Now, suppose that, in order to acquire some new, useful property, not just one but two new protein-binding sites had to develop. In that case the odds would be the multiple of the two separate events — about 1 in 10^40, which is somewhat more than the number of cells that have existed on earth in the history of life. That seems like a reasonable place to set the likely limit to Darwinism, to draw the edge of evolution.
    http://www.evolutionnews.org/2.....92771.html

    Michael Behe – Observed (1 in 10^20) Edge of Evolution – video – Lecture delivered in April 2015 at Colorado School of Mines
    25:56 minute quote – “This is not an argument anymore that Darwinism cannot make complex functional systems; it is an observation that it does not.”
    https://www.youtube.com/watch?v=9svV8wNUqvA

    Needless to say, since Darwinian evolution presupposes the unlimited plasticity of organisms, the finding of inflexible, yet radically different, alternative splicing patterns (developmental gene regulatory networks) between even supposedly closely related species is exactly the opposite finding for what would have been predicted for what should have been found in the genome by Darwinists.

    If Darwinian evolution were a normal science that was subject to rigorous testing like other sciences, instead of the pseudo-science that it is, this finding, by itself, should have been more than enough to falsify neo-Darwinian claims and consign it to the trash heap of failed scientific theories.

  4. 4
    Robert Byers says:

    The fable of evolution being behind the complexity and diversity in nature is founded on mutationism. without , errors or mutations, they couldn’t turn a fish into a giraffe.

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