The Evolutionary Origins of Irreducible Complexity, Part 6

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June 28, 2012 Tags: Genetics

Today's entry was written by Dennis Venema. You can read more about what we believe here.

The Evolutionary Origins of Irreducible Complexity, Part 6

Note: One of the challenges for discussing evolution within evangelical Christian circles is that there is widespread confusion about how evolution actually works. In this series, I discuss aspects of evolution that are commonly misunderstood in the Christian community. In this post, we continue to examine evidence that proteins in irreducibly complex (IC) systems can form and refine new interactions through gradual mechanisms.

"So nat'ralists observe, a flea
Hath smaller fleas that on him prey,
And these have smaller fleas that bite 'em,
And so proceed ad infinitum."
–Jonathan Swift

Has λ phage evolved a new IC system?

In the last post in this series, we discussed the results of an experiment done by the Lenski group on λ phage evolution, and some of its implications for the argument from irreducible complexity (IC). We now turn our attention to the question of whether the new function observed to arise in this experiment constitutes a new IC system. Recall that in Darwin’s Black Box, Behe (a) introduces IC systems as something beyond the abilities of evolution to produce gradually, and (b) defines them as follows:

What type of biological system could not be formed by “numerous, successive, slight modifications”? Well, for starters, a system that is irreducibly complex. By irreducibly complex I mean a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning. (pg. 39)

For λ phage, the original system of protein J binding to LamB on the outer membrane of E. coli is one interaction out of several that are essential for its replication. These interactions are a single system that requires well-matched parts (for precise protein binding) that contribute to the basic function (replication of the phage). If either LamB or protein J are disrupted, the system ceases to function (the phage loses the ability to replicate). By Behe’s definition, this is an IC system.

The new system is similarly IC: protein J now binds to OmpF on the outer membrane, and this interaction requires well-matched, interacting parts. The other steps in the phage replication cycle are the same, and use the interactions present in the previous IC system. As before, removal of either protein J or its binding partner (now OmpF) causes the system to cease functioning (since at this point in the experiment LamB is already missing). The new system is also IC according to Behe’s criteria.

But here’s the rub: in this experiment, the researchers observed the new IC system form step by step through “numerous, successive, slight modifications” to the previous IC system. At no point did those modifications remove the function of the original system, but in fact improved it (the modified protein J binds to its original partner, LamB, even more effectively than before).

Has λ phage jumped the Edge?

Beyond its troubling ability to generate new IC complexes by modifying old ones, λ phage evolution, as we have seen, is similarly troubling for the probability argument Behe lays out in his book Edge of Evolution. The key section (that we have discussed previously) is as follows:

Although two or three missing steps doesn’t sound like much, that’s one or two more Darwinian jumps than were required to get chloroquine resistance in malaria. In chapter 3 I dubbed that level a “CCC”, a “chloroquine complexity cluster,” and showed that its odds were 1 in 1020 births… Now suppose that, in order to acquire some new, useful property, not just one but two new protein-binding sites had to develop. A CCC requires, on average, 1020, a hundred billion billion, organisms – more than the number of mammals that has ever existed on earth. So if other things were equal, the likelihood of getting two new binding sites would be what we called in Chapter 3 a “double CCC”- the square of a CCC, or one in ten to the fortieth power. Since that’s more cells than likely have ever existed on earth, such an event would not be expected to have happened by Darwinian processes in the history of the world.

Admittedly, statistics are all about averages, so some freak event like this might happen – it’s not ruled out by force of logic. But it is not biologically reasonable to expect it, or less likely events that occurred in the common descent of life on earth. In short, complexes of just three or more different proteins are beyond the edge of evolution… And the great majority of proteins in the cell work in complexes of six or more. Far beyond that edge. (pp. 134-135)

The key point being that mutations, in Behe’s model, are simultaneous mutations, not sequential ones.

Drawing the argument together from both Darwin’s Black Box and Edge of Evolution, we can summarize Behe’s argument with three statements:

  1. Evolution of protein-protein binding sites cannot proceed by multiple, simultaneous mutations because the probability of such events is too rare to be expected to happen during the history of life on earth.
  2. Evolution must proceed only by multiple, simultaneous mutations to create new protein-protein binding sites. Gradual modifications to produce new IC systems are not possible.
  3. Thus when we observe complexes with more than three protein-protein binding partners, we can infer that they were not produced by evolution.

The difficulty with this argument is that Behe has not established the second point, but merely asserted it: that evolution must proceed only by multiple, simultaneous mutations to create new protein-protein binding sites. Indeed, Darwin’s original prediction was that “new” systems would not really be “new” at all, but rather gradually modified from previously existing systems through accumulation of small changes. If protein-protein complexes (including IC ones) can be built up over time by gradual addition of new components, then Behe cannot claim statement 3, even if statement 1 remains uncontroversial.

The evidence we have seen from λ phage is doubly problematic for the argument from IC: not only has a new IC system been formed, but its stepwise formation, one amino acid substitution at a time, was repeatedly documented in detail.

λ phage, that tiniest of fleas, has inflicted quite a bite on the argument from IC.

What about other lines of evidence?

As compelling as the evidence from this detailed experiment is, it is not the only evidence that points to the conclusion that new protein-protein interactions, functions and systems can arise gradually. Other lines of evidence we have examined include:

The similarities between whole genomes that speak to gradual change at the nucleotide and amino acid levels over large evolutionary times: the sequence differences between the human and chimpanzee genomes, for example, are tiny. Yet despite these minute differences at the genomic level, we (obviously) exhibit many traits that chimpanzees do not. The obvious conclusion is that the accumulation of small genetic changes to complex systems can have dramatic effects on function.

The gradual emergence of anaerobic citrate metabolism in an experimental population of E. coli bacteria: As we saw when we examined this system, a new, advantageous trait arose piecemeal, eventually cobbling together a new function from mutations that occurred tens of thousands of generations apart in some cases. This evidence further undermines the contention that evolution requires simultaneous mutations.

The recently duplicated p24-2 gene in Drosophila: Whatever p24-2 and Éclair are doing, exactly, there is good evidence to suggest they are not merely duplicates of each other, but have distinct functions. It’s highly likely that p24-2 has developed new protein-protein interactions of some kind (unless we wish to posit that p24-2 does its job without interacting with any other proteins at all, which is highly unlikely). We do not yet know if these genes are involved in IC systems, though the fact that they are required for survival suggests that they have important roles. Interestingly, Behe’s reply to my argument (via comment #70322) in part discusses how existing IC systems might add components:

Now what we have here is an already-intact transport system. At best, the amino acid changes in p24-2 would be analogous to re-arranging the magnets at the end of the oval-shaped object, so that it could transport a different object than before. But that is just taking advantage of an already-existing IC system; it is not a new one.

 

I would argue that observing new components adding themselves to already complex systems, and then becoming essential, is just the type of gradualism that evolutionary theory predicts. Behe continues:

A final point is that there are five specific amino acid differences between Eclair and p24-2. Professor Venema seems not to comprehend that they may not have arisen by random mutation. Once one gets beyond one or two random mutations, one can’t assume that multiple further mutations arose by chance. In other words, as far as anyone knows, those five point mutations may have required guidance or design in their appearance.

But as we have seen, the (repeated) accumulation of five or more amino acid substitutions in protein J of λ phage was no problem at all, despite the astronomical odds of all the needed mutations happening at once (note too that Behe’s argument depends on simultaneous mutations, as we have seen). There is no need to assume that the differences between p24-2 and Éclair arose by chance, but rather cite the evidence that multiple amino acid changes have been observed to accumulate over time in other systems. While we cannot recreate the last 3 million years of Drosophila evolution, it seems strained to argue that this time span is insufficient to generate the same amount of change that we observe in the laboratory in a matter of weeks in other, more tractable systems.

In the next installment of this series, we’ll examine some recent ID arguments from biochemistry that purport to have found a limit to evolutionary mechanisms.

For further reading:

Behe, M.J. Darwin’s Black Box: the Biochemical Challenge to Evolution. Free Press, New York, 1996.
Behe, M.J. The Edge of Evolution: the Search for the Limits of Darwinism. Free Press, New York, 2007.
Meyer, J.R., Dobias, D.T., Weitz, J.S., Barrick, J.E., Quick, R.T., and Lenski, R.E. (2012). Repeatability and contingency in the evolution of a key innovation in phage lambda. Science 335; 428-432. http://www.sciencemag.org/content/335/6067/428.abstract


Dennis Venema is Fellow of Biology for The BioLogos Foundation and associate professor of biology at Trinity Western University in Langley, British Columbia. His research is focused on the genetics of pattern formation and signalling.

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Gregory - #70915

July 7th 2012

Hi Folks, a quick semantic question coming from a non-biologist. It is noted that Dennis places the term ‘edge’ in scare quotes, while ‘Bilbo’ does not. And that both sometimes capitalise ‘Edge’ and at other times do not.  

My question is rather simple: is a legitimate ‘edge of evolution’ even possibly allowed in this discussion? Can there be an ‘edge of evolution’?

For Bilbo, do you believe Behe has successfully established the/a ‘biological edge’ of evolution?

For Dennis, what could possibly count as a legitimate ‘biological edge,’ or if not an ‘edge’ then what barrier or constraint (or your own preferred term) stops ‘biological evolution’ from turning into a universal theory, such as what Ard Louis has cautioned against at BioLogos?

Thanks,

Gregory

p.s. please attempt non-technical answers for non-biologists if possible


melanogaster - #70939

July 7th 2012

Gregory:
“My question is rather simple: is a legitimate ‘edge of evolution’ even possibly allowed in this discussion?”

Absolutely, Gregory!

The silly thing about Behe’s thesis is that he claims to have mathematically defined the edge, but he pathologically avoids mathematically defining the underlying terms. The prime one is “new binding site,” which any biochemist would define as a decrease in a single number, the dissociation constant (Kd).

“Can there be an ‘edge of evolution’?”

There is! It’s just orders of magnitude away from where Behe has placed it.

Don’t you realize that the limitations on evolution are the most obvious reason that ID by an omnipotent designer is so unlikely?


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Eddie - #70916

July 7th 2012

Dennis:

You said above:

“Behe defines his “edge” as the probability of multiple, simultaneous mutations to produce a new protein-protein interaction (squared) to produce two new interactions simultaneously. This assumes that all pairs of interactions arose together, that all triple interactions arose together, and so on.”

I’m a rookie in this area, and may well have misunderstood Behe’s argument, so can you help me out with some references?  

I thought that Behe had said that empirical evidence indicated that the mutations had to be simultaneous in the specific case of chloroquine resistance, but I don’t recall that he ever claimed that this was a general rule for Darwinian evolution—at least, not for neutral mutations.  (For mutations that are deleterious when they occur alone, the case would be different—simultaneous mutations would then be necessary.)  

You probably know Behe’s writings better than I do, so can you point me to the passages where he argues that, where two or more neutral mutations are necessary for an evolutionary change, those two or more mutations must be simultaneous?


GJDS - #70959

July 8th 2012

Irreducible complexity – debate: I want to make it perfectly clear that I am not for or against ID; my terse response to mega-blusterer however may have given the wrong impression. I also state emphatically that I will not involve myself in any exchange with this person, or anyone with such boorish manners, whatever their views.

My understanding of the debate is based on ‘cramming’ information in the short time I can give to this topic, and I do not present an expert opinion. I am showing that I seek information within severe time constraints, which I am sure we are all under.

The idea of ID, as I understand it, is based on analogous reasoning, in that any complex mechanism or device can only function in its intended way if all sub-systems are also functional, and its functionality is due to combination of such units. If one unit is removed or rendered inoperable, than the entire unit would cease to function. This has been illustrated by considering engines such as a steam engine, and bio-organisms such as the bacterial flagellum. Since evolution is believed to operate through gradual and sequential changes to a given entity, it is extremely improbable that a combination of all of the functional units in a complex mechanism could have been put together in this manner, thus the appeal to Intelligent Design.

This often acerbic debate is countered by an argument that seeks to identify other organisms which are believed to represent previous or less functional examples of the more complex entity, in an effort to show that a sequential development has occurred. It is argued that these were ‘less complex’ entities, and thus are examples of the road to evolving the final more complex entity. Other examples are given to rebut the notion that the ‘final’ entity is the result of a number of fully functioning sub-systems put together intelligently to arrive at the ‘final’ entity.

This summary is obviously brief and could not possibly encompass all the information and argument that is put forward by both sides.

While fully conscious of the risk, I venture this: I think any argument that is based on analogy is faulted. Just because a steam engine is designed by a human being does not prove or disprove anything. The bio-entities used as examples are by definition fully functional, and it is circular reasoning to argue that removing some component would result in loss of function- how can it be otherwise?

The counter-arguments are even weaker. How would these define a lesser function? Is it less adapted, in which case it is unlikely to have survived? If it is fully functional, then they are indulging in spurious reasoning, by supposing it is so prior to another more complex entity which they hope is the ‘next sequence’ in their hypothetical development.

I am looking at a number of other aspects that may be relevant to this debate, and the following references are starters:

M.A.Nooren, J. M.Thornton, “Diversity of protein-protein interactions”, The EMBO Journal Vol. 22 No. 14 pp. 3486-3492, 2003.

T. M. Baetu, “Mechanistic Constraints on Evolutionary Outcomes”, Philosophy of Science, Vol. 79, No. 2 (April 2012), pp. 276-294.

Felicity C. Jones, et al., “The genomic basis of adaptive evolution in threespine sticklebacks,” 5 APRIL 2012 | VOL 484 | NATURE | 55.

von Michael J. Behe, “Irreducible Complexity: Obstacle to Darwinian Evolution,” Professorenforum-Journal 2007, Vol. 8, No. 3.

Chang C. Liu, et al., “Evolution of Proteins with Genetically Encoded “Chemical Warheads”, J. AM. CHEM. SOC. 2009, 131, 9616–9617.


GJDS - #71026

July 11th 2012

Prof. Venema, you provided four key points in the discussion (series 5) of the phage discussion: I am going through the Lenski paper and the key points that I identify in it are:

“This finding suggests a complex interplay between coevolving phage and bacteria, one that depends on the entire community and its diversity. ………. which confirmed the effect of bacterial diversity on the phage’s evolution.

More generally, our study shows some of the challenges that make it difficult to observe and explain the origin of many new functions, including the requirement for multiple mutations, the complex interactions of mutations within and between species, and the resulting historical contingency that can enable or impede the outcome of interest depending on the order in which mutations occur. The “all-or-none” epistasis among the four canonical phage mutations implies that it would have been unlikely for the new function to evolve on the scale of our experiments, except for the lucky fact that some of the mutations were beneficial to the phage in performing their current function, thereby pushing evolution toward the new function.”

I hasten to add that this is not my area of expertise, so my post is to seek clarification from you. On my reading, the authors are suggesting an example of what as a non-expert in this field, appears like symbiosis. The authors also state, “an all-or-none” form of epistasis among the four mutations,” which may be closer to the argument by Behe. I cannot find a comment on sequential addition of protein (point 4) but instead the “all-in-one” statement.  Would you comment.


Eddie - #71088

July 13th 2012

Dennis:

I posted a question about a week ago—70916 above.  You don’t appear to have answered it.

Maybe you are very busy, or on vacation, or maybe you have stopped looking in on this thread.  But if you are checking in, please let me know if you intend to answer the question.

By the way, I report—not to take sides in any way, but just to let people know—that Behe has read your series, and has replied to it recently on Evolution News and Views:

http://www.evolutionnews.org/2012/07/at_biologos_con061851.html

 


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