It probably should not be surprising that this new mechanism is as circuitous as a Rube Goldberg device. After all, the mechanism just happened to happen, and so is not exactly elegant. In fact, it consists of a rather unlikely series of steps, as follows:
1. Gene are sometimes duplicated, for reasons we don't fully understand (somehow evolution did that even though there was no reason, but it worked really well in the end).
2. Duplicate genes lead to excessive quantities of the protein. (bad)
3. Too many copies of the protein leads to dosage imbalance. (bad)
4. Small population size means inefficient selection. (usually bad, but good in this case)
5. Inefficient selection means the duplicate genes are not deleted quickly. (bad, but later good)
6. The duplicate genes become mutated. (good)
7. Some of these mutations affect expression levels via microRNA interactions, alleviating dosage imbalance. (good)
8. Some other mutations affect the protein structure, causing less compact, and less stable proteins. (bad, but later good)
9. These proteins are fortunately stabilized by binding with other proteins. (good)
10. These protein-protein interactions cause higher complexity. (good)
As you can see the process got off to a bad start. It did not look promising, but evolution has a way of finding a way to produce, one way or another. That's how evolution works--it creates complexity (see Step 10).
In this case, the complexity of the process almost matches the complexity of the designs it created. And interestingly, it dispenses with the outdated idea of natural selection driving the design. As one evolutionist explained:
the origins of some key aspects of the evolution of complexity may have their origins in completely nonadaptive processes.
Fortunately, evolutionists are rapidly determining how everything came about.
Intelligent design is accused of not being science because it is not testable.
ReplyDeleteBy the same criterion, I don't see that the above "Rube Goldberg scenario" is testable either, and therefore it is not science.
Intellegent design is testable as a historical theory as Stephen Meyer takes pains to illuststrate in his book, "Signature in the Cell." By the criterion that he uses, which he describes as the same criterion that Darwin used for historical science, I don't see that the above scenario is testable. In other words it is not testable by any criterion.
Fernández & Chen: This selection pressure is apparent in unicellular organisms, but is mitigated in higher eukaryotes. In human, this effect reveals a capacitance toward dosage imbalance. This capacitance is not expected in organisms with larger population size, where evolutionary forces are more efficient at promoting adaptive functional innovation and purifying selection, thus curbing the concentration imbalance arising from gene duplication.
ReplyDeleteThe relationship between selection and population size has been established for generations. Gene duplication can occur during recombination. The paper reads as straightforward evolutionary science.
I Think you might enjoy this site Dr. Hunter:
ReplyDeleteIs evolution pseudoscience?
Excerpt:,,, Thus, of the ten characteristics of pseudoscience listed in the Skeptic’s Dictionary, evolution meets nine. Few other pseudosciences—astrology, astral projection, alien abduction, crystal power, or whatever—would meet so many.
http://creation.com/is-evolution-pseudoscience
I wonder what Mr. skeptic himself, Michael Shermer, would think of that analysis. LOL
"The paper reads as straightforward evolutionary science."
ReplyDeleteMost definitely.
I'll post the abstract here. Others can judge whether the conclusions are really as you present them:
ReplyDelete"Proteins rely on associations to improve packing quality and thus maintain structural integrity. This makes packing deficiency a likely determinant of dosage sensitivity, that is, of the fitness impact of concentration imbalances relative to the stoichiometry of the protein complexes. This hypothesis was validated by examining evolution-related dosage imbalances: Duplicates of genes encoding for deficiently packed proteins are less likely to be retained than genes coding for well-packed proteins. This selection pressure is apparent in unicellular organisms, but is mitigated in higher eukaryotes. In human, this effect reveals a capacitance toward dosage imbalance. This capacitance is not expected in organisms with larger population size, where evolutionary forces are more efficient at promoting adaptive functional innovation and purifying selection, thus curbing the concentration imbalance arising from gene duplication. By examining miRNA target dissimilarities within human gene families, we show that the capacitance is operative at a post-transcriptional regulatory level: The higher the packing deficiency of a protein, the more likely that its paralogs will be dissimilarly targeted by miRNA to mitigate dosage imbalance. For families with low capacitance, paralog sequence divergence and family size correlate tightly with packing deficiency, just like in unicellular eukaryotes. Thus, a major component of human tolerance toward dosage imbalances is rooted in the paralog-discriminating capacity of miRNA regulation. The results may clarify the evolutionary etiology of aggregation-related diseases, since aggregation is often promoted by overexpression (a dosage imbalance) and aggregation propensity is associated with extreme packing deficiency."
Evolutionists adapt to new scientific findings by concocting a never ending litany of highly speculative mechanisms for evolution. This is a key proof of evolution in action. Therefore evolution is a fact. Or, is this proof of intelligent design? To have intelligent design intelligence is required. No, I guess this must be proof of evolution.
ReplyDeleteMichael Lynch has published a number of interesting papers and a book on the topic of the contribution of non-adaptive processes to complexity. Although the idea sounds non-intuitive, the mechanisms are both highly plausible and strongly supported by population-genetic inferences (regarding effective population size). In this regard Lynch's thesis is not simply highly speculative or post-hoc.
ReplyDeleteIf one suspends one's disbelief for a moment, it makes some sense to consider that while small scale Darwinian selection may optimise a given trait within the bounds of nucleotide substitutions, larger changes require a qualitatively different evolutionary event. That this might require a release from the tight bounds of highly efficient selection. However, given sufficient mutation input, it become statistically probable that rarely a duplication will be retained in a population despite modestly negative fitness effects. This becomes increasingly likely in populations of reduced size. Again, this is fundamental population genetics. Such changes, incidentally are rare, in line with the prediction that the should be because they are generally eliminated by purifying selection.
This might seem unsatisfying to ultradarwinists or like a cop-out to those who reject outright naturalistic evolution (particularly if lacking a sound knowledge of the literature), however it is in line with current evolutionary theory.
abimer,
ReplyDeleteFrom what I can tell, Cornelius doesn't even accept that antibiotic resistance occurs through evolution by natural selection. so good luck convincing him that Lynch's insightful work has any merit.
Hi nano -
ReplyDeleteI guess I am just trying to point out that such work sits within a solid theoretical framework with substantial empirical support - and so is not simply posturing and handwaving from sinister Darwinists.
I realise how optimistic it is to expect a word of it to have an impact on anyone here. Cornelius, of course, strictly sticks to expressing negatives here, i.e. he never openly endorses any theory regarding origins, despite his affiliations. Before committing to too much he seems to abandon his own threads and 'respond' instead with new posts.
Some acase of anitbiotic reistamce are actually epigenetic. No evolution is involved. And some cases seem to be the result of a mutation that damages some structure or function in the cell. The antibiotic resistance is a lucky side effect that provides a benefit only when the bacteria is exposed to the antibiotic. But this process cannot turn a bacteria in to a blue whale.
ReplyDeletesorry, typos:
ReplyDelete"acase" should be cases, "reistamce" should be resistance
my bad
nat,
ReplyDeletebut you do agree that in some cases antibiotic resistance occurs through evolution by natural selection? I am not claiming that this is proof that all species descended through evolutionary processes. i am simply pointing out that the fact that evolution by natural selection is a real process. Apparently Cornelius does not accept this fact.
This comment has been removed by the author.
ReplyDeleteMr Hunter, perhaps you ought to consider modifying your tag-line to "Superstition drives 'science,' and it matters."
ReplyDeleteIlion:
ReplyDelete===
perhaps you ought to consider modifying your tag-line to "Superstition drives 'science,' and it matters."
===
Yes, it does seem like superstition at times. But I use "religion" because, at bottom, it quite literally is religious belief motivating and justifying evolution.
Of course atheists are evolutionists, but their arguments are borrowed from the theists (following in the tradition of David Hume, 250 years ago).
Their denial is most telling. They feign innocence, claiming they are merely testing out the creationist's religious claims.
But the creationists never made those claims. And even if they did, falsifying them wouldn't make evolution a fact.
An old saying is that theology is queen of sciences. Another one is that science is religion's handmaiden. The more things change, the more they stay the same.
Ilion:
ReplyDeleteThat natural selection sometimes works is self evident. Some animasl are bigger faster etc. But it has not been demonstrated that this can is sufficient to change one species into another.
I'm always amazed at the ubiquitous use of the terms, used by abime above, "solid theoretical framework" and "substantial empirical support"
ReplyDeleteIf there is anything that Darwinism supremely lacks it is precisely empirical support.
There is none whatsoever!
Everything, beyond mere adaptation and variation, is entirely speculative with ZERO empirical support! Zip, zilch, nada!
What is wrong with these people anyway?
Conclusion: Darwinian "reasoning" - if I may abuse the term - causes metal illness.
It's called "acute cognitive dissonance".
They all have it bad. But the curious thing is that, something like leprosy, the victim usually doesn't know he has it until its too late.
"So it came about from 1860 onward that new believers [Darwinists] became in a sense mentally ill, or, more precisely, either you became mentally ill or you quitted the subject of biology, as I had done in my early teens. The trouble for young biologists was that, with everyone around them ill, it became impossible for them to think they were well unless they were ill, which again is a situation you can read all about in the columns of Nature [magazine]." (Hoyle, F., Mathematics of Evolution)
Cognitive dissonance drives Darwinism and it matters. ;-)
Hitch -
ReplyDelete"If there is anything that Darwinism supremely lacks it is precisely empirical support.
There is none whatsoever!"
When you say such things all you are really declaring is that you do not know of any!!
Allow me to educate you.
When we compare the gene sequences of all life on Earth - bacteria, Archaea, animals, plants nd fungi - we find about 500 genes which exist in all living things. These are called 'immortal genes'.
How have they endured in tact in all things? Are they immune to random mutation?
What geneticists have found is that the bases that make up the immortal genes are sometimes less similar than the resulting protein sequence.
In other words, some bases can change without affecting the protein as a whole. The protein will still function. Such changes are called synonymous changes. Changes in bases which do effect the protein are called non-synonymous changes.
It is simple to calculate the odds of a mutation being either synonymous or non-synonymous. If there was no natural selection, the expected ration of nonsynonymous to synonymous mutation would be 3:1. But that is not what we find. What we actually find is a ratio of 1:3.
Only a tiny fraction of the expected nonsynonymous changes are being kept in the immortal genes. There is some force which is filtering out the nonsynonymous mutations.
Natural selection, of course, fits the bill perfectly. It perfectly describes this discrepancy. Natural selection would filter out the specifically nonsynonymous mutations.
What other explanation accounts for this? None other that has yet been drawn up. Unless of course we allow magic and fairies and gods as explanations for observed phenomenon, of course.
These are facts. This is observed data. Here is your evidence. There is far more, of course, but I hope this is small enough to be digestible.
Ritchie:
ReplyDeleteThis only demonstrates natural selection, which means that some organisms survive and some don't. No one disputes this. But what has not been demonstrated is that this can turn one species into another.
natschuster -
ReplyDelete"This only demonstrates natural selection, which means that some organisms survive and some don't."
With respect, that is not natural selection. At least, that is not ALL there is to natural selection.
Some animals will survive to reproduce and some will not. But which ones will survive? Well, the ones most suited to be sucessful in their lifestyle - the fittest - will generally be the sucessful ones. They will be the ones to survive to pass on their genes. In terms of genes, the fittest survive. This is natural selection.
And it is pretty much all there is to the theory of evolution - that random mutations occur and the ones which help the host creature survive will likely be passed on, while ones which hinder the host creature will be more likely to be eliminated. That is pretty much it. Evolution, through natural selection.
"No one disputes this. But what has not been demonstrated is that this can turn one species into another."
I beg to differ. Ring species offer a beautiful example of speciation through natural selection:
http://www.youtube.com/watch?v=CEtnyx0Yo9I
The lesser black backed gull, the herring gull, and the yellow footrd gull are a ring species, but they can readily interbreed, so they may all be one species. Again, species to species change may not be happening.
ReplyDeletenatschuster -
ReplyDeleteInteresting you mention that. Have you seen this:
http://www.youtube.com/watch?v=CEtnyx0Yo9I
Maybe I misunderstood, but at around 4:30 it did say something about the eastern sunspecies do hybridize in the eastern parts of the range. So again, if they can interbreed then maybe they are all one species. Correct me if I'm wrong.
ReplyDeleteAccording to this, they can interbreed,
ReplyDeletehttp://www.santarosa.edu/lifesciences2/ensatina2.htm.
So they may very well be one species.
violet -
ReplyDeleteThe video does indeed say that. But I suspect you are missing the point. The salamanders are not divided neatly into 'the eastern ones' and 'the western ones'. The point is that there is gradual progression of change all the way round the valley - except at the southern tip.
Dawkins makes this point a little clearer in other parts of his book (The Ancestor's Tale, if you'd like to read it. I highly recommend it), but the major deciding factor in whether to term two groups of animals as seperate species is whether they can sucessfully interbreed to produce fertile young.
But as the salamanders demonstrate, this is not a clear-cut point. Imagine you take a group of animals and divide them into two groups. Under the theory of evolution, random mutations in the DNA, filtered through natural selection, will slowly alter the two groups - but as long as the groups are kept seperate, the changes from one will not filter into the changes from the other. So, slowly, the DNA of the two groups will become more and more dissimilar.
As this happens, the chances of hybridization will go down, because a sperm from one group has less and less chance of being compatible with an egg from the other. It is not a clear, obvious line between being able to hybridize and not being able to do so.
Even creatures as different as lions and tigers may sometimes sucessfully interbreed. But the odds are very low, and any young are usually sick and often infertile.
So when do you classify your two groups as different species? When the two generally WOULDN'T breed if mixed together, even though they could? When the odds of cross-breeding producing fertile young were low? Non-existant?
So (finally), returning to the salamanders, imagine the group at the northern tip of the valley was the original group. As they spread south around the valley, the salamander's at the southern tip of each arm of salamanders resemble the other genetically less and less. Until finally they meet at the south, and the DNA of each group has been kept apart for so long that they now either chose not to, or are unable to interbreed. Those further up either side will be more smiilar to each other, and more compatible. Indeed, when you reach the very northern tip, they are completely compatible.
Does that all make sense?
But evolution means species to species change. Is that really happening with the salamanders? OR is it just intraspecies variation.
ReplyDeleteLaugh out loud -
ReplyDeleteThe longer you keep two groups apart, the more dissimilar they will grow. So this begins as intraspecies variation, but, given time, will end up as species to species change.
Imagine if all the salamanders died out due to some disaster and the only survivors were the ones at the southern tip. Biologists would probably hav little hesitation in labeling them as different species. We only label them as a ring species instead of different species because the intermediate sub-species are still living.
But is it really evolution in action, or is that speculation at best?
ReplyDelete