It has been a long time now and the time for experimentation without any positive results has passed us by. Bacteria and Fruit Flies have quick life cycles and we can study hundreds and thousands of generations...and we have. Evolution does not occur. Even when labs are trying to cause it and pushing the mutations. Fruit flies not only remain fruit flies, when you try to get them to "evolve" they just go back to being fruit flies. If you actually believe in scientific methods to test theories, throw Darwin away. He has been tried and his hypothesis failed.
Fruit Flies Not Evolving 09/30/2010
Sept 30, 2010 — A long-running experiment trying to get fruit flies to evolve has failed. A research team forced selection on the flies to explore the limits of natural selection. Only minor changes were detected after 600 generations. The research team was disappointed and surprised; there was even less evolution in these sexual organisms than in similar experiments with microbes, like bacteria and yeast (but see 07/12/2010). And all this was under ideal lab conditions. Success is even less likely in the wild.
The Editor’s summary of a paper in Nature was titled, “Experimental evolution reveals resistance to change” and ended that the authors “conclude that unconditionally advantageous alleles rarely arise, are associated with small net fitness gains, or cannot fix because selection coefficients change over time.” Nature this week published the results of a 35-year study by UC Irvine and University of Southern California (USC). Here is the abstract:1
Experimental evolution systems allow the genomic study of adaptation, and so far this has been done primarily in asexual systems with small genomes, such as bacteria and yeast. Here we present whole-genome resequencing data from Drosophila melanogaster populations that have experienced over 600 generations of laboratory selection for accelerated development. Flies in these selected populations develop from egg to adult ~20% faster than flies of ancestral control populations, and have evolved a number of other correlated phenotypes. On the basis of 688,520 intermediate-frequency, high-quality single nucleotide polymorphisms, we identify several dozen genomic regions that show strong allele frequency differentiation between a pooled sample of five replicate populations selected for accelerated development and pooled controls. On the basis of resequencing data from a single replicate population with accelerated development, as well as single nucleotide polymorphism data from individual flies from each replicate population, we infer little allele frequency differentiation between replicate populations within a selection treatment. Signatures of selection are qualitatively different than what has been observed in asexual species; in our sexual populations, adaptation is not associated with ‘classic’ sweeps whereby newly arising, unconditionally advantageous mutations become fixed. More parsimonious explanations include ‘incomplete’ sweep models, in which mutations have not had enough time to fix, and ‘soft’ sweep models, in which selection acts on pre-existing, common genetic variants. We conclude that, at least for life history characters such as development time, unconditionally advantageous alleles rarely arise, are associated with small net fitness gains or cannot fix because selection coefficients change over time.In other words, they looked for evidence of a “selective sweep” – the signature of a beneficial mutation becoming fixed in the population – and could not find it. They did the selection artificially, forcing the fly embryos to evolve toward faster embryonic development. Despite lots of mutations, they found the flies resistant to change. Not only that, the flies underwent “reverse evolution” – they said, “forward experimental evolution can often be completely reversed with these populations, which suggests that any soft sweeps in our experiment are incomplete and/or of small effect” (a soft sweep meaning selection is acting on standing variation instead of new mutations). Possibly any beneficial mutations were hindered by linked deleterious alleles (canceling out the benefit) or antagonistic pleiotropy (in which one good mutation to a gene can cause one or more bad effects elsewhere). Either way, the evolution is like one step forward, one or more steps back.
There was even more bad news for neo-Darwinian theory: the lab situation was more optimistic than the wild, where adaptive evolution is expected to occur. You can get a lot of variation and mutation to appear in genomes, but no unconditionally beneficial mutations. Their last paragraph expressed surprise at this, with a subtext of disappointment:
Our work provides a new perspective on the genetic basis of adaptation. Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments. This suggests that selection does not readily expunge genetic variation in sexual populations, a finding which in turn should motivate efforts to discover why this is seemingly the case.This experiment was begun in 1975. After 35 years and 600 generations, accelerated by artificial selection, the net evolution (in terms of adaptation and improvement in fitness) was negligible if not nil.
1. Burke, Dunham et al, “Genome-wide analysis of a long-term evolution experiment with Drosophila,” Nature 467, 587-590 (30 September 2010); doi:10.1038/nature09352.
Natural selection is always presumed to be the wonder-worker that can produce eyes, ears, sonar, flippers, jaws, hearts, and brains with its gradual, step-by-step improvement of natural variation, without design (07/20/2010, 05/04/2010). OK, where is it? It doesn’t work theoretically (09/28/2010, 06/11/2010, 03/21/2010, 03/17/2003), it doesn’t work rhetorically (04/17/2010), it doesn’t work historically (08/05/2010), and it doesn’t work experimentally (09/22/2010). It doesn’t work in the lab, and it works less in the wild. Unless you include “reverse evolution,” (06/26/2010), it doesn’t work at all. Game over, Charlie (05/14/2010). Stop the hype (08/13/2010).
Next headline on: Terrestrial Zoology • Genetics • Darwin and Evolutionary Theory
"Self-replicating molecules?In his monumental work, The Ancestor’s Tale,7 Richard Dawkins traced the supposed ancestry of humanity back through all the evolutionary ages to the very first supposed common ancestor of all life. He supposed this original ancestor to have been an RNA-type of life form, although he admitted ignorance of the precise details.8 His choice of an original RNA life form is well-founded because RNA is the only known molecule that can do all of the three basic functions of life: (a) store coded information, (b) combine with itself and other RNAs to create molecular machines, and (c) self-replicate (but only in a very limited manner under very special circumstances).
However, recent studies showing how living cells actually replicate have made this ‘RNA world’ concept ludicrously unrealistic.
A central problem in cell division (that is, what living cells actually do, as opposed to Dawkins’ imagined self-replication) is that a large proportion of the whole genome is required for the normal operation of the cell—probably at least 50% in unspecialized body cells and up to 70–80% in complex liver and brain cells. When it comes time for a cell to divide, not only does the DNA have to continue to sustain normal cell operations, it also has to sustain the extra activity associated with cell division.
This creates a huge logistic problem—how to avoid clashes between the transcription machinery (which needs to continually copy information for ongoing use in the cell) and the replication machinery (which needs to unzip the whole of the DNA double-helix and replicate a ‘zipped’ copy back onto each of the separated strands).
The cell’s solution to this logistics nightmare is truly astonishing.9 Replication does not begin at any one point, but at thousands of different points. But of these thousands of potential start points, only a subset are used in any one cell cycle—different subsets are used at different times and places. Can you see how this might solve the logistics problem?
A full understanding is yet to emerge because the system is so complex; however, some progress has been made:
- The large set of potential replication start sites is not essential, but optional. In early embryogenesis, for example, before any transcription begins, the whole genome replicates numerous times without any reference to the special set of potential start sites.
- The pattern of replication in the late embryo and adult is tissue-specific. This suggests that cells in a particular tissue cooperate by coordinating replication so that while part of the DNA in one cell is being replicated, the corresponding part in a neighbouring cell is being transcribed. Transcripts can thus be shared so that normal functions can be maintained throughout the tissue while different parts of the DNA are being replicated.
- DNA that is transcribed early in the cell division cycle is also replicated in the early stage (but the transcription and replication machines are carefully kept apart). The early transcribed DNA is that which is needed most often in cell function. The correlation between transcription and replication in this early phase allows the cell to minimize the ‘downtime’ in transcription of the most urgent supplies while replication takes place.
- There is a ‘pecking order’ of control. Preparation for replication may take place at thousands of different locations, but once replication does begin at a particular site, it suppresses replication at nearby sites so that only one copy of the DNA is made. If transcription happens to occur nearby, replication is suppressed until transcription is completed. This clearly demonstrates that keeping the cell alive and functioning properly takes precedence over cell division.
- There is a built-in error correction system called the ‘cell-cycle checkpoints’. If replication proceeds without any problems, correction is not needed. However, if too many replication events occur at once the potential for conflict between transcription and regulation increases, and/or it may indicate that some replicators have stalled because of errors. Once the threshold number is exceeded, the checkpoint system is activated, the whole process is slowed down, and errors are corrected. If too much damage occurs, the daughter cells will be mutant, or the cell’s self-destruct mechanism (the apoptosome) will be activated to dismantle the cell and recycle its components.
- An obvious benefit of the pattern of replication initiation being never the same from one cell division to the next is that it minimizes the effect of any errors that are not corrected.
The impossible conundrumNow comes the impossible conundrum. Keeping in mind the cake analogy, lets recall that the vast majority of information in humans is not ingredient-level information (code for proteins) but meta-information—instructions for using the ingredients to make, maintain and reproduce functional human beings.
Evolutionists say that all this information arose by random mutations, but this is not possible. Random events are, by definition, independent of one another. But meta-information is, by definition, totally dependent upon the information to which it relates. It would be quite non-sensical to take the cooking instructions for making a cake and apply them to the assembly of, say, a child’s plastic toy (if nothing else, the baking stage would reduce the toy to a mangled mess). Cake-cooking instructions only have meaning when applied to cake-making ingredients. So too, the logistics solution to the cell division problem is only relevant to the problem of cell division. If we applied the logistics solution to the problem of mate attraction via pheromones (scent) in moths it would not work. All the vast amount of meta-information in human beings only has meaning when applied to the gene content of the human genome.
Even if we granted that the first biological information came into existence by a random process, the meta-information needed to use that information could not come into existence by the same random (independent) process because meta-information is inextricably dependent upon the information that it relates to.
There is thus no possible random (mutation) solution to this conundrum. Can natural selection save the day? No. There are at least 100 (and probably many more) bits of meta-information in the human genome for every bit of primary (protein-coding gene) information. An organism that has to manufacture, maintain, and drag around with it a mountain of useless information while waiting for a chance correlation of relevance to occur so that something useful can happen, is an organism that natural selection is going to select against, not favour! Moreover, an organism that can survive long enough to accumulate a mountain of useless information is an organism that does not need useless information—it must already have all the information it needs to survive!
What kind of organism already has all the information it needs to survive? There is only one answer—an organism that was designed in the beginning with all that it needs to survive."
Description of the Prize
- "The Origin-of-Life Prize" ® (hereafter called "the Prize") will be awarded for proposing a highly plausible natural-process mechanism for the spontaneous rise of genetic instructions in nature sufficient to give rise to life. The explanation must be consistent with empirical biochemical, kinetic, and thermodynamic concepts as further delineated herein, and be published in a well-respected, peer-reviewed science journal(s).
- Progress in life-origin research has been greatly impeded by a few key nagging problems. Biochemical constraints render many appealing theoretical models non productive. These biochemical constraints have received the most attention in scientific literature.
- Self-replication has been another subject of considerable research, although successes in this area have usually come from very artificial rather than natural-selection models. But perhaps the most daunting of all life-origin problems is elucidating a natural mechanism for "self-organization." Self-ordering is often confused with bona fide organization. A crucial paper providing valuable background information in this area is found at the following link: Self-organization vs.Self-ordering in life-origin models .
- Complexity, "the edge of chaos," hypercycles, Markov processes, fractals, complex adaptive systems, genetic algorithms, and directed evolution have all attracted great interest. A valuable summary of progress in these areas is summarized in another key review paper: The capabilities of chaos and complexity .
- Gene emergence relates specifically to sequence complexity, material symbol systems, decision nodes, logic gates and configurable switch-settings. The following papers provide important background information for all of these issues:
- Is your model scientifically plausible? To test this, the scientific method requires that you calculate a Universal Plausibility Metric (UPM, Xi), and that you apply the Universal Plausbililty Principle to your model. The probabilities incorporated into your UPM must be calculated correctly, factoring the probabilities of:
- 1) getting only homochiral monomers,
- 2) only peptide bonds (half the bonds that normally form between amino acids),
- 3) only biologically usable amino acids (20 out of 80 or more),
- 4) getting activated monomers that can polymerize,
- 5) getting a family member of each protein catalyst out of sequence space,
- 6) getting all needed components produced and assembled at the same place and in the correct reaction order through time, etc.
- If the UPM for your model is less than 1, your model is definitively falsified by the Universal Plausibility Principle applicable to all hypotheses, models, theories and scenarios in all fields of science.
- Winning The Origin of Life Prize would entail falsifying two null hypotheses:
- Brief summaries of these two null hypotheses can be found as Scirus SciTopic Pages:
- Also of interest are two other short summaries:
- The one-time Prize will be paid to the winner(s) as a twenty-year annuity in hopes of discouraging theorists' immediate retirement from productive careers. The annuity consists of $50,000.00 (U.S.) per year for twenty consecutive years, totalling one million dollars in payments. Formal application by submitters is required to win. Submitters must expressly consent to abide by all terms and conditions of the Prize before judging of their paper(s) can begin.
- The ability of the Foundation to underwrite these payments and to administer the Project is monitored by the well-known accounting firm of Young, Brophy & Duncan, PC, Certified Public Accountants.
Those of you who have been considering evolution as a possibility, I hope you will go to the links provided on the foundation's pages and look carefully at the daunting challenges facing a natural evolution of life. It is not within the realm of possibility.
Louis Pasteur and the scientists of his day were quite sure they had determined that even the most microscopic of life forms could not spontaneously generated from non-life. They were so sure they called it a "law."
But true Darwinist Humanist religious zealots will not let the laws of thermodynamics nor the findings of statistics to deter them from their ridiculous belief in the ability of nothing to make itself into something and then eventually into everything.
Do you really want to agree with them that this is "science?" They might as well be worshipping a tree or offering sacrifices to stone idols, these Darwinists, for all the scientific content of their fairy tales.
Life cannot and will not spontaneously generate.
Information cannot and will not be produced by natural forces.
The Universe could not create itself.
I hope some of you will join me in un-dumbing the public and begin to try to undo a few generations of endless propaganda and censorship and outright lies, all for the sake of a religion known as various things - Humanism or Naturalistic Materialism or Darwinism. Call it what you like. It has resulted in hundreds of thousands of scientists stuck on stupid and hundreds of thousands more afraid to say anything lest they be ostracized and/or lose their place in the scientific or academic community. Here is the emperor's new clothes being lived out before your eyes.