Last week, science unexpectedly revealed an unpublished evaluation by Richard Lenski and two authors of my e-book Darwin Devolves. I have already sent a brief reply, noticing two of their most necessary near-perfect response to the guide's argument, however I was going to say extra. This longer message offers with the points they make, grouped into 4 topics: the supposed counter-examples to which they refer; they convey out obsolete arguments; Lenski's personal improvement work;
For readers who should not have time to daybreak at all, listed here are the take-off lessons:
- the gene-level counter-examples mentioned by the evaluators are shamefully asked in begging; Evaluators simply lived with genes and assumed that they have been produced and / or built-in into dwelling methods by random processes, however not even by evaluators or anybody else making an attempt to show that that is potential,
- body-level counter-examples to which evaluators produced by comparable processes are Equally, query questions,
- criticism from previous books by critics have been additionally begging questions and / or confident obscure, imaginative tales
- . Many of my detailed solutions to earlier criticisms and paperwork mentioned by the evaluators
- as said in the previous letter, do not even try to grasp an important argument within the ebook that useful decaying mutations come shortly, relentlessly inevitably competing for useful constructive mutations each time and on a inhabitants scale  Anticipated Examples
The evaluators point out two ways through which they assume that evolution can construct novelties – exaptation and gene overlap. I’ll focus first on taking. Evaluators write:
The absence of a Behe dialogue is a sign that nature retrovides buildings for a brand new perform…. The feathers of birds, fish crevices and mammalian species are comparable.
Quite the opposite, in Chapter 3, "Synthesizing Evolution", which summarizes and criticizes both Darwin's unique concept and neo-Darwinism, I’m immediately discussing the calling of revolution (referred to as "action change") by Ernst Mayr. I write: three
But how do such trendy new biological features come about? The two broad methods by which evolutionary modifications are deliberate to happen, Mayr, are "enhancing action" and "action change." In the change of features, the structure used for one function has been tailored to serve another. ; For example, lungs might have changed to swim [gas] fish. This is an instance of what has been referred to as [by Mayr] as the “tinkering principle”.
Later, the casserole Mayria was steaming in a wavy hand. (In reality, "the principle of tinkering"! Not the identical epistatic place as to say, in Newton's regulation.) Nevertheless, like Mayr, critics don’t even attempt to present – or mention anyone else who has tried to point out that any body they point out might be produced even from present organs by the Darwin mechanism or by any uncovered involuntary mechanism. Although Mayr has expressly been responsible of it, the evaluators themselves take pleasure in the same obscure hand waving.
And the non-reflective hand ripple quickly descends into opaque convulsions. In Darwin Devolves, I write that "the most difficult problem in biology – how to explain the origin of the special, sophisticated and functional structures of life" 4 is invisible to most evolutionary biologists. Inspectors themselves illustrate my point with pleasure:
Exaptation also challenges Behe's concept of "decentralization" by displaying that the loss of one perform can result in another's victory. Whale evolutionary ancestors misplaced their capability to walk on the bottom, as their forelegs, for example, developed into covers, but the covers turned out to be favorable over the long term.
In different phrases, the evaluators seem to be "guilty", the whales had their ft, but the whales now have ft, so the change should have led to random mutation and natural selection. Have they ever heard the word non sequitur? As strange because it might sound to individuals outdoors the circle of love, many Darwinian biologists discover it troublesome to differentiate the question of what occurred in biology about how it happened. Inspectors are unaware of the fact that the legs, ft, or transitions between them have by no means been defined non-trivially. The central query of the ebook – whether or not modifications in life history have occurred by probability or design – is comprehensible to them
Overlapping of the 2nd gene
Now for gene overlap. Lenski and companions acknowledge that I am very skeptical that the overlap of genes and random mutation resulting in vital evoluutiovälitteisiin – in different phrases, anything aside from a small change within the unique perform of the mother or father gene. Nevertheless, they do not mention that I did not all the time assume so. Particularly, I observed my guide, that I’ve changed my thoughts on whether Darwin's evolutionary path resulting in the overlapping gene easy myoglobin-like precursor to the subtle oxygen supply system, which is hemoglobiini.5 In 1996, I wrote Darwin's Black Field that I assumed it might be. In 1996, I imagined that gene overlaps and random mutations / natural decisions might actually explain the rise within the complexity of this degree. Why did I modify my thoughts? Inspectors don't consider readers need to listen to anything about this.
Then again, that I ought to show how mistaken I am duplication of genes / random mutation / pure selection for the position, they seek advice from the "overwhelming evidence that this is based mostly on trikromaattinen imaginative and prescient of primates ( eight ), the absorption of mammals ( 9 ) and improvement improvements in all metasases via the diversification of the HOX genes ( 10 ). guesses, articles merely describe the presence of genes. The authors of the articles do not even attempt to argue – to not mention experimentally – that the diversification and integration of genes into slightly totally different actions might have happened via blind Darwin processes
. My instance of a guide and stated: “Everyone knows that Darwinian processes can produce complex hemoglobin from a simpler myoglobin because myoglobin genes are similar to hemoglobin genes” and is made with it. Clearly, they might fairly choose their very own examples to ask the question.
Hemoglobin has rather more superior oxygen binding properties than myoglobin. In contrast, the protein groups to which the evaluators refer – opsins (vision), odor receptors (odor), and Hox proteins – all do just about the same as others: opsins take in mild, odor receptors bind perfume molecules, Hox proteins bind DNA . I’ve no objections to assume that proteins in these distinct courses are on account of gene overlap. How they will successfully fold the organism's biology is a separate question. My guess is that the brand new odorant receptors and opines might fit by probability and selection. The new Hox proteins can be a lot, far more troublesome.
Not all kinds of proteins have the identical position, so, as or not, differences should be made. In the half of Chapter 9 entitled "Evolution with Gene Overlap", I write: 7
Everybody – including me – thought we knew rather more than we did. Nevertheless, nobody can now make the other mistake and bounce to the conclusion that the event of a protein perform can’t happen by way of the classical Darwinian mechanism. As I mentioned in chapter 6, cichlid rhodopsin has apparently changed several occasions between two wavelength delicate shapes, and the current Andean written research found some extent mutation that prompted its hemoglobin to bind oxygen more strongly. These and comparable simple examples are simple. Nevertheless, every time multiple amino acid substitutions or other mutations are required to offer a substantially totally different exercise to the overlapping protein, there can not be any doubt that the transition occurred by means of Darwin's evolutionary processes. Some may be, but not many.
The inspectors appear to be just like the brand new world monkey species Aotus trivirgatus in the paper they have stated eight, which has misplaced its practical opsin gene, leaving the species a monochrome vision. Monkeys can only see in black and white, and the reviewers see only a random mutation and a pure selection. Nevertheless, there isn’t any a priori purpose that the likelihood could not be discovered alongside the design and vice versa. Those who claim that every thing was ultimately born randomly carry a heavy burden of exhibition that’s even attainable. Inspectors and no paper they confer with don’t even attempt to do so.
Even worse, the reviewers do not even interrupt to think about how the decaying processes raised by Darwin Devolves have an effect on any of their illustrated situations. Genetic degradation is faster than constructive modifications. Would any selective strain that the gene overlap might theoretically improve first decrease with quicker, extra degradable modifications? In that case, there might be no strain left to decide on a slower mutation when it lastly arrived. And when the gene occurred in a replica, might a quicker degradable mutation remove the selective strain to further change it? At every stage, quicker and numerous decaying mutations would compete passionately towards any critics' dream. Still, they don't even seem to take pleasure in such ideas.
3. Controlled Laboratory Improvement
Lenski and co-authors point out a doc on experimental improvement: “And in 2012 Andersson et al. showed that new functions can develop rapidly in a suitable environment ( 11 ). Behe does not accept any of these studies… ”It turned out that I checked this paper9 shortly after it got here and commented on the Discovery Institute's website. Feedback are easily discovered with a number of mouse clicks.
In my writing on paper is known as "Limit the maze, it helps to be in mind." 10 It emphasizes that researchers actively guided the system over the holes and corners to the desired outcomes:
Exceptionally intelligent manipulation of researchers is transferred to on-line complementary supplies. Studying the brief part of the Complementary Supplies and Strategies part, entitled "Selection of Bifunctional HisA Mutants", is enough to see the absurdity that the outcomes have been taken as a model for unmanaged Darwinian evolution…
- histidine, because the previous work showed that mutations that give the power to make tryptophan destroyed the power to make histidine.
- The added histidine would have stopped the production of the protein,
- Later, once they discovered mutations to supply tryptophan, they eliminated the histidine from the medium to promote mutation-restoring mutations
. How Nature's Missing – Until Nature directs events in the direction of the aim.
Sure, ”Andersson et al. confirmed that new features can develop quickly in an appropriate setting ”, however beneath the steerage of an clever agent. As I write in Darwin Devolves, Lenski found himself devastated by the devastating, random mutation and choice of his devastating 60,000 era improvement undertaking.
I need to emphasize: Lenski et al. it doesn’t seem to differentiate between experiments where scientists maintain their palms off and those where researchers actively manipulate the system. Perhaps they don't see the distinction.
Stale Arguments, Numerous Answers
Inspectors recycle previous, beforehand revealed books that have been either heavily inadequate or irrelevant (or both), previous hand-waving evaluations. not to point out in the present day.
1. First trial:
Behe also ignores the fact that some of his earlier arguments have been disbanded ( 2 ). He incorporates an extended annex claiming that the blood coagulation cascade is, for instance, an irreversible complicated, but does not point out the straightforward, elegant system of Kenneth Miller for its gradual improvement ( 3 )
Lensk's reference # three is a philosophy of biology anthology since 2009 from 11, which brought out the Miller chapter, originally written for an earlier (2004) essay titled Debating Design.12 revealed by Cambridge College Press. it contained only a transient reference to blood clotting. I have additionally contributed to the work earlier chapter 13, which was also repeated at a later antologiassa.14 Lukuani referred to as "irreducible Complexity:. Back to Darwin's evolution" It protected each blood coagulation cascade and flagellum towards Darwin's protests, including Miller's protests. Inspectors didn’t both see or determine to disregard my determine. I want to emphasize that the evaluators blame me for not discussing Miller, which was revealed in the e-book that I replied to in his article
Discovering the Darwin god in his e-book in 199915 Miller made a pen that could possibly be referred to as charity referred to as "System" for the development of blood coagulation. nevertheless it was so drawn (mixed with the description of the fashionable clotting cascades of vertebrates and invertebrates, the actual "system" consisted of one piece), which makes Ernst Mayr's "masking principle". as a paradigm of scientific discipline. Later, Miller revealed on his website16 some material that had been minimize from his e-book and added extra hand-wobblers. An identical, more clearly introduced common state of affairs for constructing a cascade was sent earlier by Harvard Grad scholar on the Web.17 I pointed out this state of affairs of critical problems twenty years ago.18 The evaluators don’t mention this. 2nd instance:
… or the truth that the ancestral fibrinogen gene has been found in spiked glands ( 4 ).
The researcher of stated reference # 4 is a man named Russell Doolittle, an impressive researcher, now a retired biochemistry professor at the College of San Diego and a member of the Academy of National Sciences who spent most of his 50-year career in a blood coagulation cascade. I talked about his work in the Darwin black field in 1996,19, and I argued there was, in truth, a cascade of the irreducibly complicated. In an addendum to Darwin Devolves20, I will inform you an occasion in 1997 where he wrote an essay on the Boston Evaluate journal revealed by MIT to contest me. Within the essay, he gained by describing some of the current experimental work completed by other researchers:
Lately, the plaminogen gene [sic — plasminogen is a protein that helps remove blood clots after a wound has healed] was removed from mice, and predictably these mice had thrombotic problems as a result of fibrin clots could not be eliminated. Not long after, the same staff dropped the fibrinogen gene [fibrinogen supplies the protein building material for the meshwork clot structure] in the second mouse row. Once more, predictably, these mice have been troublesome, though on this case the issue was bleeding. And what did you assume happened when these two strains have been crossed? For all sensible functions, mice missing each genes have been normal! Contrary to the claims relating to the complexity to be lowered, the whole body of proteins just isn’t needed. Music and concord can come from a smaller orchestra.
Nevertheless it seems that Doolittle misinterpreted the paper he was speaking about.22 In truth, mice with two cascade proteins are very sick: their blood did not clot; those bleeding; Ladies die during being pregnant. Promising evolutionary intermediates aren’t. Study more about Darwin Devolves. Here I solely make two brief factors. 1) Russell Doolittle is a prime researcher in blood coagulation and improvement. Still, we will shortly see his mistakes – stating the paper about dying mice – that he doesn't understand how blood clotting might have advanced by means of the Darwin process. (If he is aware of he might easily have mentioned the paper describing it.) If Russell Doolittle doesn't know, no one knows, no one at all – definitely Kenneth Miller and the reviewers. The second thing is equally essential. 2) Russell Doolittle knows concerning the overlap of the gene, but the info was not helpful in making an attempt to elucidate the event of the blood coagulation cascade.
Evaluators notice that in 1990 (before his mistake was written above), Doolittle found a vertebrate group with a household that resembles vertebrate fibrinogen.23 In Darwin Devolves, I speak extensively about Russell Doolittle's nonetheless fantastic From work on clotting cascade.24 However this work consists primarily of looking for sequence databases for any clotting of proteins found in any species. This sort of work can produce evidence referring to points of widespread origin, however as I’ve written many occasions, proof of widespread descent shouldn’t be proof of Darwin's mechanism. Not Doolittle and no one else has even tried to point out that random processes and decisions might have led to imaginary transitions. Right here is an excerpt of the e-book's addition to discussing a number of large problems with uncontrolled blood clotting by way of gene overlapping: 25 , akin to how you can keep nice control on the fly and alter the system sometimes. I wish happiness to anyone. …
The more, as we now have seen throughout the work, the random mutation simply breaks or breaks genes. Because the blood coagulation cascade is a finely balanced system – the other of protein perform bow that both promote or inhibit clot – change within the equilibrium by decreasing one factor must be as effective within the brief term, as confirmed by another (corresponding to an quantity of weight) by turning the swing aspect of the web page, as an alternative of including a bit to the other) . And since protein degradation is far quicker and easier, it ought to virtually all the time win. …
As for Professor Doolittle, in addition to the good majority of evolutionary biologists. All these elementary issues look really invisible to them. Proof of unusual landing routinely mixes with Darwin's mechanism of proof
3. Third Example:
Behe doubles its declare that the development of chloroquine resistance to malaria by random mutations is extremely unlikely as a result of at the least two mutations are wanted, Neither is beneficial with out another. His calculation has already been reversed (5) and it has lengthy been recognized that neutral and even harmful mutations can present a step ahead for future variations.
I replied to the reference 5 in 2009 by letter26, which was revealed in Genetics magazine along with Durrett's and Schmidt's reply 27 adopted by this trade with new answers that may be found simply on the website.28 Evaluators inform readers nothing about this. Briefly, in my solutions, I pointed out that Durrett and Schmidt, two mathematicians, misunderstood some of the system biology (which they recognized), and when this error was corrected, their calculations fit quite intently from their very own. As for the "even harmful mutations in" that provide steps, I’m glad to agree. In truth, an important level in The Edge of Evolution was that the event of chloroquine resistance with an antimalarial drug in all probability required two mutations, the primary of which was dangerous. (I am mystified as to why reviewers do not see that their first sentences with the above quote is liable for the last half of the second sentence.) Nonetheless, the necessity for neutral or harmful askelelle evolutionary path to significantly scale back the rate of Darwinian evolution, corresponding to klorokiiniresistenssin the case of
4. Fourth instance:
The 2014 research, which was not talked about by Behe, reported the discovery of two genetic pathways by means of which malaria developed via chloroquine resistance in several steps ( 6 ).
extensively in that paper shortly after it was revealed.29 Self-Touted at that time by Summers et al. (How troublesome is it to put in writing "Behe" and "Summers" on the search engine?) As they wrote in summary, "At least two mutations were enough for (low) CQ transport." The necessity for 2 particular mutations clearly explains that the parasite has made it troublesome for a few billion occasions to increase resistance to chloroquine compared to other malarial medicine, akin to atovaquone, which only require one. (The fact that there may be a number of routes to a resistive state is pink herring because, as the paper confirmed, all the paths move by way of a detrimental step. it has to face even the necessity for the smallest coordination – just two simple point mutations.
"Deriding" of the alleged Lensk long-term evolutionary experiment
Richard Lenski has accomplished an excellent job now together with his thirty-year challenge that follows the expansion and improvement of E. coli in his laboratory. He himself interprets them inside the framework of the standard Darwin. Nice, he's undoubtedly free. Nevertheless, in Darwin Devolves, I don't assume he's making it darwinism utterly. I clarify that though the results affirm the power of random mutation and natural selection to supply useful small-scale modifications (mainly because of the breakdown of present genes), additionally they present why larger structural modifications are out of reach
1st random is random
Lenski and co-authors write within the evaluation:
There are indeed many examples of activity-related mutations which are cheap, however Behe is selective in its examples. He attracts a better half of Chapter 7 to discuss the 65,000 era Escherichia coli check, which highlights many mutations that have arisen from this degraded perform – the desired option to adapt to a easy laboratory surroundings. a new "side view" ( 1 ).
I "do not remove improved functions." Relatively, as I explicitly state, I give attention to separating useful degradable mutations from helpful constructive mutations. In different phrases, probably the most helpful mutations assist in building new "functional coded elements" (abbreviated FCTs, for example genes or control parts) or decreasing previous ones? It is merely an exercise in calculating the number of helpful mutations belonging to every class. As I initially wrote within the quarterly biology evaluate, 32 is the most typical useful mutations reported within the literature that weaken FCTs. – Sorry! Do not blame me!
I’m not going to hurt Lensk's emotions by calling a extensively reported citrate mutation33, which in his laboratory was a "side show". Fairly, I just needed to place this mutation into perspective. Here is an extended quote from Darwin Devolves to context: 34
However the onerous lesson of this chapter far exceeds the importance of this or that specific mutation. If you want to see why, contemplate the other mutations that the citrate eater has suffered on his evolutionary journey. Like all cultivation strains, citrate bacteria have misplaced the power to metabolize ribose, endure from the killing of "moving element" mutations to different genes, and even more strong degradation level mutations. And like the five other replicating cell strains, the citrate consumer has became a mutant with a strongly impaired potential to restore DNA. Regardless of the bug's fate right here, it has irrevocably lost the providers of as much as ten genes.
However not all. To be able to greatest take into consideration the gene rearrangement that gave it the power to eat citrate, a number of other mutations have been found which fine-tuned its metabolism. (Quandt, EM, et al., 2015. Elife: 4.e09696.) Even earlier than a crucial mutation, a unique mutation in a gene of a protein that makes citrate in E. . A second, later mutation to the same gene decreased its activity by about 90%. Why have been these mutations helpful? As writers write, "when citrate is the only carbon source, [computer analysis] predicts optimum growth when there is no flow [the enzyme]. In fact, any [of that enzyme] activity is harmful …" And if one thing is harmful, the random mutation is released shortly. The evaluation of the computers by the authors instructed that the citrate mutant can be much more efficient if both other usually quenched metabolic pathways have been coupled to each. It is fascinating that the ambiguous citrate mutation that has begun to brag is a side-by-side present. The random, notably noticeable change in FCT mutation can’t reverse the stream of harmful and FCT losses.
The crucial distinction is that helpful decomposing mutations are a totally totally different beast of useful constructive. Useful decomposing mutations arrive very quickly and far larger than construct. This is simply because the disruption of the gene is far simpler and quicker than constructively. As well as, useful degradable mutations are ruthless. They’ll seem before, throughout, and after the construction, and will compete vigorously with it. And when a decaying mutation is shaped within the inhabitants, the degraded gene has gone perpetually from all sides and functions
Lenski could be very proud of his work and naturally needs to emphasize the constructive. Nevertheless, I’m within the question of whether Darwin's processes have been capable of build a classy life of the machine, so I like the outcomes from a special perspective
2. "Impaired function – expected to conform to a simple laboratory environment"
a. Rationalizing the Results
"Expectation" of decaying mutations dominating laboratory improvement experiments is an entire submit hoc rationalization. Contemplate, for instance, that solely in 2013, PLoS Genetics revealed a paper entitled "Bacterial adaptation through loss of function", during which researchers systematically demonstrated that gene breakdown can virtually all the time be useful in an setting or elsewhere. Kirjoitan Darwin Devolvesissa: 35
Ainoa työ, jonka olen nähnyt, keskittyy funktiomutaatioiden häviämiseen yleisenä luokkana, joka on mielenkiintoinen itsestään, vuonna 2013 Princetonin ja Columbian yliopistojen tutkijat tutkivat kirjallisuutta ja sitten suorittivat omia kokeita, jotta voitaisiin nähdä, mitkä bakteerigeenit voivat rikkoutua ja vika kasvaisi paremmin. [Hottes, A. K., et al. 2013. Bacterial adaptation through loss of function. PLoS Genetics 9:e1003617.] He osoittivat, että "ainakin yksi hyödyllinen [loss-of-FCT] mutaatio tunnistettiin kaikissa lukuun ottamatta viittä 144: stä tarkasteltavasta tilasta." Toisin sanoen bakteeri voisi parantaa sen eroa rikkomalla geenin yli 96%: ssa tutkituista ympäristöolosuhteista ….
Lyhyt kommentti uutiskirjeen alkuperäisestä teoksesta osoittaa, että yksinkertainen ero hyödyllisten ja rakentavien mutaatioiden välillä on napsauttanut ainakin yhtä henkilöä: ”Tässä tutkimuksessa muutetaan yleisesti pidettyä näkemystä [my emphasis]jonka funktiomuutokset ovat [Stower, H. 2013. Molecular evolution: Adaptation by loss of function. Nature Reviews Genetics 14:596.]
Kuten monet ihmiset, evoluutiobiologit tarkistavat odotuksiaan kokemuksen (tai kokeellisten tulosten) valossa. Arvioijat tekevät niin täällä, ehkä tahattomasti.
b. Luonnollisesti myös
Mitä enemmän, olen omistanut hyvän osan kappaleesta 7 osoittaakseni, että funktionaaliset mutaatiot hallitsevat paitsi "yksinkertaisessa laboratorioympäristössä" myös luonnossa. Luvussa 9 kirjoitan: 36
Todellisessa maailmassa kaikki mahdolliset hyödylliset, hajoavat mutaatiot saapuvat nopeasti, voimassa, lievittääkseen minkäänlaista selektiivistä painetta organismille – ennen kuin ensimmäinen monijäämäinen ominaisuus esiintyy jopa näkymä. (Determine 9-5) The result’s that every degradative change and every damaging single-step mutation can be examined a number of occasions as an answer, or as part of an answer, to whatever selective strain a species was dealing with, and, if useful, would spread to fixation nicely before a useful multi-residue function even showed up. The place Darwinian processes dominate, the biological panorama can be expected to be suffering from broken-but-helpful genes, damaged-yet-beneficial techniques, degraded-organisms-on-crutches, ages before any fancy equipment was even out there. That’s exactly what we noticed in Chapter 7 with laboratory E. coli, pure Yersinia pestis, wild polar bears, tame dog breeds and all different organisms up to now examined.
Whatever mutation helps alleviate some selective strain by any means will immediately start to spread. Degradative mutations can typically assist relieve selective strain, they usually arrive orders of magnitude quicker than constructive mutations, each in the laboratory and within the wild.
Drawing a Conclusion
Can any necessary conclusion be drawn from this practice wreck of a evaluation? Contemplate that Richard Lenski is probably probably the most qualified scientist on the planet to assessment the argument of Darwin Devolves. Lenski has spent many years overseeing probably the most in depth, most acclaimed laboratory evolution experiment carried out thus far, for which he was elected a member of the National Academy of Sciences. His personal work is a serious focus of Darwin Devolves. He might simply and casually have identified any issues with the argument all by himself, merely by wielding Darwin’s putatively highly effective concept and his personal expertise. Yet he and his co-authors spend all the evaluation deriding the writer, barely mentioning Lenski’s own work, recounting previous criticisms by different individuals, and leaning heavily on aged theoretical conjectures as an alternative of new experimental results.
The implication is obvious. Just as Russell Doolittle unwittingly showed, merely by his mistaken citation, that no rationalization for the origin of the blood clotting cascade existed, so the reviewers show that there isn’t any reply to the issues for unguided evolution described in Darwin Devolves. Although it serves a useful position in understanding modifications on the margins of biology, as an evidence for the overarching structure of life Darwin’s principle is defunct.
- Lents, N.H., Swamidass, S.J., Lenski, R.E. 2019. The top of evolution? Science 363: 590-590.
- Behe, M.J. 2019. Woo-hoo! In Science Evaluation of Darwin Devolves, Lenski Has No Response to My Important Argument.
- Behe, M.J., 2019. Darwin Devolves: The New Science About DNA that Challenges Evolution. HarperOne, New York, pp 80-81
- Behe 2019, 225
- Behe 2019, 214.
- Behe, M.J., 1996. Darwin’s Black Field: the Biochemical Challenge to Evolution. The Free Press, New York, pp. 206-207.
- Behe 2019, 214-215.
- Dulai, Okay.S. et al. 1999. The evolution of trichromatic shade vision by opsin gene duplication in New World and Previous World primates. Genome Res. 9: 629.
- Näsvall, J., et al. 2012. Real-time evolution of new genes by innovation, amplification, and divergence. Science 338: 384-387.
- Behe, M.J. 2012. To traverse a maze, it helps to have a mind.
- Miller, Okay.R. 2009. The Flagellum Unspun: The Collapse of Irreducible Complexity, in: Rosenberg, A., Arp, R. (Eds.), Philosophy of Biology: an Anthology. Wiley-Blackwell, Chichester, West Sussex, U.Okay., pp. 439-455.
- Miller, Okay.R. 2004. The Flagellum Unspun: The Collapse of Irreducible Complexity, in: Dembski, W.A., Ruse, M. (Eds.), Debating Design: from Darwin to DNA. Cambridge University Press, Cambridge, pp. 81-97.
- Behe, M.J. 2004. Irreducible Complexity: Obstacle to Darwinian Evolution, in: Dembski, W.A., Ruse, M. (Eds.), Debating Design: from Darwin to DNA. Cambridge College Press, Cambridge, pp. 352-370.
- Behe, M.J. 2009. Irreducible complexity: impediment to Darwinian evolution, in: Rosenberg, A., Arp, R. (Eds.), Philosophy of Biology: an Anthology. Wiley-Blackwell, Chichester, West Sussex, U.Okay., pp. 427-438.
- Miller, Okay.R. 1999. Discovering Darwin’s God: a Scientist’s Seek for Widespread Floor Between God and Evolution. Cliff Road Books, New York, pp. 156-157.
- Miller, Okay.R. The evolution of vertebrate blood clotting.
- Robison, Okay. 1996. Darwin’s Black Box: Irreducible complexity or irreproducible irreducibility?
- Behe, M.J. 2000. In defense of the irreducibility of the blood clotting cascade: Response to Russell Doolittle, Ken Miller and Keith Robison.
- Behe 1996, Chapter four.
- Behe 2019, 294-298.
- Doolittle, R.F. 1997. A delicate stability. Boston Evaluation, pp. 28-29.
- Bugge, T.H., et al. 1996. Loss of fibrinogen rescues mice from the pleiotropic results of plasminogen deficiency. Cell 87: 709-719.
- Xu, X., Doolittle, R.F., 1990. Presence of a vertebrate fibrinogen-like sequence in an echinoderm. Proceedings of the Nationwide Academy of Sciences USA 87: 2097-2101.
- Behe 2019, 298-301.
- Behe 2019, 300.
- Behe, M.J. 2009. Waiting longer for 2 mutations. Genetics 181: 819-820.
- Durrett, R., Schmidt, D. 2009. Reply to Michael Behe. Genetics 181: 821-822.
- Behe, M.J. 2009. Ready longer for 2 mutations.
- Behe, M.J. 2014. A key inference of The Edge of Evolution has now been experimentally confirmed.
- Summers, R.L., et al. 2014. Numerous mutational pathways converge on saturable chloroquine transport by way of the malaria parasite’s chloroquine resistance transporter. Proceedings of the Nationwide Academy of Sciences USA 111: E1759-E1767.
- Good, B.H., et al. 2017. The dynamics of molecular evolution over 60,000 generations. Nature 551: 45-50.
- Behe, M.J. 2010. Experimental evolution, loss-of-function mutations, and “The First Rule of Adaptive Evolution”. Quarterly Assessment of Biology 85: 1-27.
- Blount, Z.D., Borland, C.Z., Lenski, R.E. 2008. Historic contingency and the evolution of a key innovation in an experimental population of Escherichia coli. Proceedings of the Nationwide Academy of Sciences USA 105: 7899-7906.
- Behe 2019, p 188-190
- Behe 2019, p 191
- Behe 2019, pp 248-249
Photograph: A practice wreck, 1895, Montparnasse Station, Paris, by way of Wikimedia Commons.
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