Putting the Darwinian debate in its place.

David Berlinski: Does Darwin Matter?

David Berlinski

you write about affect the way we live? Why should the Darwin question matter to people who don't normally concern themselves with scientific theories?

DB: I think of the Darwinian debate in the way that Dickens thought of Jardynce v Jarndyce in Bleak House. It is awfully easy to be sucked into it, and once suckered, awfully difficult to get out. I have seen it so often. A man wakes and because has read a book or scanned an essay, he is persuaded that he can make a contribution. He is eager to make it. He offers his opinion on the Internet and is gratified by the prospect of the congratulations that he is shortly to receive. No one pays the slightest attention. He then discovers that to be heard, it is necessary that he amplifies his level of abuse. He does that, referring to the Discovery Institute as the Dishonesty Institute. Repeating the phrase as he moves his bowels affords him an unexpected pleasure. As his influence remains insignificant, his indignation mounts. In the morning, he scuttles to his computer to check his own postings; satisfied when he finds them, and beside himself when he fails. His appetite for conflict sharpens. He becomes determined to exaggerate every issue; and to magnify trivialities. Sooner or later, his Internet presence seems real, and his real life unreal. He ends in the state achieved by almost every Internet blogger: He commences to gibber repetitively. Glen Davidson, who posts to David Klinghoffer's blog, has recently entered the gibbering state.

It is all very sad. I have warned about the phenomenon many times.

Does Darwin matter? Yes, of course it matters. It matters a great deal. It matters whether the theory is true because for better or worse we value the truth and struggle to find it; but it would matter far more were we able to say once and for all that the theory is false. Darwinism involves a way of thought in biology, and were it to go, it would take a great many assumptions along with it. Just think of vitalism, for example. To say a word in its favor is at once to be accused of the cheapest kind of intellectual sentimentality. We know better and if we do not know better, theydo. But hold on, please do. If by vitalism one means something like the 19th century idea of a vital fluid that informs living systems, then I am with them. That is so much sentimentality. But if by vitalism one means the thesis that living systems cannot be completely explained in terms of their physics or their chemistry -- what then? Something must explain the difference, no? And if it is not a fluid, as naïve 19th-century biologists sometimes thought, it does not follow that it is nothing.

Nothing in biology makes sense except in the light of evolution.

This remark is half right: Nothing in biology does make sense. It is for the biology of the future to start making sense of it. If that in the end involves religious ideas or even religious I, that's fine with me. Let's ask the questions first, and reject the wrong answers when we know that they are wrong.

Pakistan:a country with an army or an army with a country?:Pros and Cons.

Leviathan vs.Darwin

Crocodile eyes are fine-tuned for lurking
By Jonathan Webb

A new study reveals how crocodiles' eyes are fine-tuned for lurking at the water surface to watch for prey.
The "fovea", a patch of tightly packed receptors that delivers sharp vision, forms a horizontal streak instead of the usual circular spot.
This allows the animal to scan the shoreline without moving its head, according to Australian researchers.
They also found differences in the cone cells, which sense colours, between saltwater and freshwater crocs.
Published in the Journal of Experimental Biology, the findings suggest that although the beasts have very blurry vision underwater, they do use their eyes beneath the surface.

This is because light conditions are different in salt and freshwater habitats, but only underwater - and the crocodiles' eyes show corresponding tweaks.
"There's generally more blue light in saltwater environments, and more red light in freshwater environments. Animals tend to adapt to this," explained Nicolas Nagloo, a PhD student at the University of Western Australia.
He and his colleagues studied eyeballs from juvenile "salties" and "freshies", shipped to the university from a crocodile farm in Broome.
When they measured the light absorbed by single photoreceptors in the retina, they found that those of the freshwater crocs were shifted towards longer, redder wavelengths compared with their saltwater cousins.

Finding this skewed sensitivity in crocodiles was unexpected, Mr Nagloo said, because the famous predators were only semi-aquatic and did their hunting, feeding and mating on land."It's surprising because these guys can't actually focus underwater. [But] light sensitivity seems to be important to them," he told BBC News.
"That tells us there's potentially some aspect of their behaviour underwater that we're not aware of yet."
The team also studied the density of receptors across the crocodile retina. In this regard, the two species were more similar.
Overall, crocodile vision appears to be less precise than ours, achieving a clarity some six or seven times lower than the human eye. But their "foveal streak" is a striking adaptation that suits their lifestyle perfectly.
The fovea is a dent in the retina, containing a huge concentration of receptor cells. The indentation arises because other cells, which transmit visual information to the brain, are shifted to the sides."Typically, the fovea is circular and located in the centre of the retina. It provides animals with an area of very high visual clarity, in a small area of their visual environment," Mr Nagloo said.
It is this small patch of high-resolution information that allows us, for example, to read; but we humans have to move our eyes around to drink in details across a scene.
"In the case of crocodiles... it's spread across the middle of the retina, and it gives them maximum clarity all along the visual horizon."
This arrangement reflects the predator's iconic ability to lurk with just its eyes above the water, waiting motionless for prey to wander too close to the river's edge.Other animals, particularly mammals like deer and rabbits that live in open spaces and themselves face predation, are known to possess a similar "visual streak". But that is a more subtle feature than the furrow-shaped fovea of the crocodile, Mr Nagloo said.
"A visual streak is just an elevated cell density, in an elongated shape. A fovea takes that to the extreme - the number of photoreceptors is so high that they have to move the transmitters away, to make room for them. So the wiring is different.
"I haven't seen any other animals with this kind of specialisation."

Darwinism and S.D.L algorithm II

How Did Birds Get Their Wings? Bacteria May Provide a Clue to the Genomic Basis of Evolutionary Innovation, Say Evolutionists

That evolution occurred is known to be a fact but how evolution occurred is not known. In particular we are ignorant of how evolutionary innovations arose. Of course biological novelties and innovations arose from a series of random chance events, but it is less than reassuring that we cannot provide more detail. How exactly did the most complex designs spontaneously arise? What mechanisms overcame, over and over, the astronomical entropy barriers, by sheer luck of the draw? As Craig MacLean’s and Andreas Wagner’s, and coworker’s, new PLOS Genetics paper begins, “Novel traits play a key role in evolution, but their origins remain poorly understood.” Could it be that evolution is not actually a fact? No, not according to evolutionists. And this new paper claims to provide the basis for how the seemingly impossible became the mundane.

The paper begins by summarizing the many proposed genetic mechanisms for the evolution of biological innovations:

An evolutionary innovation is a new trait that allows organisms to exploit new ecological opportunities. Some popular examples of innovations include flight, flowers or tetrapod limbs [1,2]. Innovation has been proposed to arise through a wide variety of genetic mechanisms, including: domain shuffling [3], changes in regulation of gene expression [4], gene duplication and subsequent neofunctionalization [5,6], horizontal gene transfer [7,8] or gene fusion [9]. Although innovation is usually phenotypically conspicuous, the underlying genetic basis of innovation is often difficult to discern, because the genetic signature of evolutionary innovation erodes as populations and species diverge through time.

1. Mayr E. Animal Species and Evolution. Cambridge: MA: Harvard University Press; 1963.

2. Pigliucci M. What, if anything, is an evolutionary novelty? Philos Sci. 2008;75: 887–898. Available:http://philpapers.org/rec/PIGWIA

3. Patthy L. Genome evolution and the evolution of exon-shuffling—a review. Gene. 1999;238: 103–14. Available: http://www.ncbi.nlm.nih.gov/pubmed/10570989 pmid:10570989

4. True JR, Carroll SB. Gene co-option in physiological and morphological evolution. Annu Rev Cell Dev Biol. 2002;18: 53–80. doi: 10.1146/annurev.cellbio.18.020402.140619. pmid:12142278

5. Zhang J. Evolution by gene duplication: An update. Trends Ecol Evol. 2003;18: 292–298. doi: 10.1016/S0169-5347(03)00033-8.

6. Bergthorsson U, Andersson DI, Roth JR. Ohno’s dilemma: evolution of new genes under continuous selection. Proc Natl Acad Sci U S A. 2007;104: 17004–9. doi: 10.1073/pnas.0707158104. pmid:17942681

7. Boucher Y, Douady CJ, Papke RT, Walsh DA, Boudreau MER, Nesbø CL, et al. Lateral gene transfer and the origins of prokaryotic groups. Annu Rev Genet. 2003;37: 283–328. doi: 10.1146/annurev.genet.37.050503.084247. pmid:14616063

8. Wiedenbeck J, Cohan FM. Origins of bacterial diversity through horizontal genetic transfer and adaptation to new ecological niches. FEMS Microbiol Rev. 2011;35: 957–976. doi: 10.1111/j.1574-6976.2011.00292.x. pmid:21711367

9. Thomson TM, Lozano JJ, Loukili N, Carrió R, Serras F, Cormand B, et al. Fusion of the human gene for the polyubiquitination coeffector UEV1 with Kua, a newly identified gene. Genome Res. 2000;10: 1743–56. pmid:11076860 doi: 10.1101/gr.gr-1405r

The unspoken problem here is, as usual, serendipity. The various proposed genetic mechanisms for the evolution of biological innovations all suggest an amazing bit of fortuitous luck. For random chance events just happened to create these various complicated structures and mechanisms (such as horizontal gene transfer and protein domains their shuffling) which then produced new evolutionary breakthroughs.

Evolution didn’t know what was coming. Evolution did not plan this out, it did not realize that horizontal gene transfer would lead the way to new biological worlds. The evolution of horizontal gene transfer would require a long sequence of random mutations, many of which would not provide any fitness advantage. And when the construction project was completed, and the first horizontal gene transfer capability was possible, there would be no immediate advantage.

This is because there would have been no genes to transfer. The mechanism works only when it is present in more than one, neighboring, cells. One cell gives, and another cells receives. By definition the mechanism involves multiple cells.

But it doesn’t stop there. Even if the first horizontal gene transfer capability was able to spread across a population, and even if it did provide a fitness advantage to the fortunate citizens, there would not be even a hint of the enormous world of biological innovations that had just been opened.

In other words, what this evolutionary narrative entails is monumental serendipity. Biological structures and mechanisms (horizontal gene transfer in this case, but it is the same story with the other hypotheses listed above) are supposed to have evolved as a consequence of a local, proximate, fitness advantage: a bacteria could now have a gene it didn’t have before.

But it just so happened that the new structures and mechanisms would also, as a free bonus, be just what was needed to produce all manner of biological innovations, far beyond assisting a lowly bacteria increase its fecundity.

This is monumental serendipity.

The science contradicts the theory

Undaunted, the new paper finds that one of the other mechanisms, gene duplication and subsequent neofunctionalization, is a key enabler and pathway to biological innovations.

That conclusion resulted from what otherwise was a fine piece of research work. The experimenters exposed different populations of Pseudomonas aeruginosa, a dangerous infectious bacteria, to 95 new sources of its favorite food: carbon.

The bacteria had to adjust to the new flavors of carbon and they did so with various genetic modifications, including various genetic mutations. In the most challenging cases (where the new carbon sources were most difficult for the bacteria to adjust to), the bacteria often produced mutations in genes involved in transcription and metabolism. And these mutations often occurred in genes where there were multiple copies, so the mutations occurred in one copy while the other copy could continue in its normal duties.

The problem is, these genetic duplicates were preexisting in the P. aeruginosa genome. This is yet another instance of serendipity.

Why? Because preexisting duplicates are not common. Only about 10% of the genes have duplicates lying around, and fortunately, the genes needed for adaptation (involving transcription and metabolism) just happened to have such duplicates.

Now there were a few instances of de novo gene duplication. That is, once the experiment began, and after the P. aeruginosa populations were exposed to the challenging diets, a total of six genes underwent duplication events. But in each and every case, the duplication events occurred repeatedly and independently, in different populations (for each of the 95 different carbon sources, the experimenters ran four parallel trials with independent populations).

This result indicates directed gene duplication. This is because it is highly unlikely that random, chance, gene duplication events just happened hit on the same gene in different populations. Here is an example calculation.

Let’s assume that in the course of the experiment, which ran for 30 days and about 140 generations of P. aeruginosa, some genes may undergo duplication events by chance. Next assume there is a particular gene that needs to be duplicated and modified in order to for P. aeruginosa to adapt to the new food source. (Note that there may be several such genes, but as we shall see that will not affect the conclusion). Given that there are four separate, independent trials, what is the probability that the gene will be duplicated in two or more of those trials?

Let P_dup be the probability that any gene is duplicated in the course of the experiment. For our gene of interest, it may be duplicated in 0, 1, 2, 3, or all 4 of the trials. The binomial distribution describes the probability, P, of each of these outcomes. To answer our question (i.e., What is the probability that the gene will be duplicated in two or more of those trials?) we sum the binomial distribution’s value for N = 2, 3 and 4. In other words, we calculate P(2) + P(3) + P(4).

This will give us the probability of observing what was observed in the experiment (i.e., the duplication events occurred repeatedly and independently, in different populations, in all 6 cases where duplication events were observed).

Well for a reasonable value of P_dup, the probability that any gene is duplicated in the course of the experiment, such as 0.0001, the probability of observing multiple duplications events for any given food source (i.e., P(2) + P(3) + P(4)) is about 60 in one billion, or 6  times 10^-8. Even worse, the probability of observing this in all 6 cases where duplication events were observed is about 5 times 10^-44.

It isn’t going to happen.

Exceptionally high rates of gene duplication, in particular genomic regions of Salmonella typhimurium, in a high growth rate medium, were observed to be about 0.001 and even slightly above 0.01 in rare cases.

If we go all out and set P_dup to an unrealistically high 0.1, our results are still unlikely. The P(2) + P(3) + P(4)) is .05, and the probability of observing this in all 6 cases where duplication events were observed is about 2 times 10^-8.

In order to raise these probabilities to reasonable levels, such that what was observed in the experiment is actually likely to have occurred, we need to raise P_dup to much higher values. For example, for a P_dup of .67 (two-thirds probability), P(2) + P(3) + P(4)) is .89, and the probability of observing this in all 6 cases where duplication events were observed is about .5.

But even this doesn’t work. For if we were to imagine unrealistically high P_dup values of 0.1 or higher, then massive numbers of duplication events would have been observed in the experiments.

But they weren’t.

Once again, the science contradicts the theory. Our a priori assumption that evolution is a fact, and that the P. aeruginosa adaptations to the new food sources were driven by random mutations, did not work. The theory led to astronomically low probabilities of the observed results.

What the observed gene duplications are consistent with is directed gene duplications. Just as mutations have been found to be directed in cases of environmental challenges, it appears that gene duplications may also be directed.

The paper’s premise, that biological innovations such as flowers and wings are analogous to bacteria adapting to new nutrient sources, is fallacious. But setting that aside, the experimental results do not make sense on evolution’s mechanism of random mutations and natural selection. Instead, the results indicate directed adaptation.

Posted by Cornelius Hunter