miss_bun wrote:
Lokiare wrote:
No, its a good example of naturally selecting for an advantageous gene that already exists which does nothing to hold up the idea that new genetic data was introduced somewhere. Huge difference. In other words it neither supports the evolutionary theory nor disproves it.
You're pulling the assumption that the gene already exists out of nowhere. You are asserting that the gene already existed based on the assumption that new traits can't evolve, and using the that assertion (that the genes already existed recessively rather than evolving) as evidence that new traits can't evolve.
No sorry. If we are talking about the moths, its widely known that the different colors are recessive and dominant traits.
If we are talking about the lizards, I've already talked about how the gene pool wouldn't have been big enough to support them let alone for them to magically grow an organ in just a few generations (hint: not even serious evolutionists will claim creating a new organ in just 30 generations).
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I've already seen his work debunked, but if you haven't you may want to check out
http://religiopoliticaltalk.com/fraud-in-my-sons-textbook-my-part-of-a-conversation-with-a-professor-at-a-local-college/ You'll have to forgive that it is on a religious website, the actual article is fact filled and very scientific.
This "article" by PapaGiorgio is not peer reviewed, and unscientific. I read the entire thing, and it is nothing but a bunch of questions asked by someone who is clearly biased, asks questions that serve only as evidence of his lack of understanding and relevant education, and in addition to not being peer reviewed or even published by a legitimate publication at all, he doesn't actually even make any assertions as far as I can tell, never mind any that actually debunk the study. This article contains no facts that I can see, beyond those quoted in the original study. It has about as much weight and scientific merit as a comment on someone's youtube video.
That article simply pokes holes in the validity of the research process used. It doesn't need to be a scientist pointing out the flaws like the assumption of birds eating the moths or the fact that he only observed a few hundred and that is not enough to do a reliable statistical analysis. However later on down the article he quotes scientist authored books on the subject. Here are some samples:
" I recommend the chapter that explains the actual parameters to Kettlewells experiment (chpt 6), it is fascinating, and would mute any further discussion. Just two “unnatural” examples can also be found in the popular press:
“The moths filmed being eaten by the birds were laboratory-bred ones placed onto tree trunks by Kettlewell; they were so languid that he once had to warm them up on his car bonnet (hood).” Calgary Herald, p. D3, 21 March 1999.
“University of Massachusetts biologist Theodore Sargent helped glue moths onto trees for the famous NOVA documentary. He says textbooks and films have featured ‘a lot of fraudulent photographs’.” J.A. Coyne, Nature 396(6706):35–36. & The Washington Times, p. D8, 17 January 1999."
"The Nitty Gritty – Sargent’s Work (from Of Moths and Men)
In a series of experiments between 1965 and 1969, Sargent tried to replicate Kettlewell’s background-preference work. He got contradictory results, and concluded that the moths’ resting places were genetically predetermined, not selected, as Kettlewell believed, by individual moths noting whether their “circumocular tufts” matched the background. Sargent has also found that the plants eaten by the larvae may induce or repress the expression of such “melanism” in adult moths (see Sargent T.R. et al. in M.K. Hecht et al, Evolutionary Biology 30:299–322, Plenum Press, New York, 1998)."
So it is a valid article because it talks about and quotes peer reviewed studies in books.
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First it shows that his experiments were flawed and not statistically sound, then it shows he like many others made many assumptions and ignored important data like the fact that the coloration can be altered by the larvae being eaten before they are colored, the natural resting place is in fact under branches and leaves and not on the trunk of the tree, and other facts. At best the author is misinformed, at worst he's intentionally perpetrating these false hoods.
Again, I read this article. Please cite examples from the text. I couldn't find any.
See above. I quoted a few. There is a very long one toward the middle that proves the original experiments were very poor and contradict later findings. In fact to avoid confusing I'll just quote it here:
"The following point is important to the understanding of how these moths change color and how this may have also impacted the population change in coloration:
[Sargent] noticed that the caterpillars eating the new-growth pine were growing more slowly that the ones in the other container, and they pupated and eclosed later. In both groups all the male moths were melanics, and among females overall there was a fifty-fifty ratio of typicals and melanics. This meant that, assuming the melanism was controlled by a sex-linked dominant allele, the melanic female had mated with a heterozygous melanic male. However, there was a statistically significant difference between the two groups. More than two-thirds of new-growth-fed female moths were melanic, while two-thirds of the group fed on old-growth needles were typical. A second experiment on 8 July yielded similar results. Sargent believed he had hit paydirt. “Something in the new-growth needles was favouring the expression of adult melanism,” Sargent explains….
…. Although Sargent would undoubtedly be described by nine out of ten eyewitnesses as “quiet and unassuming” – a mild, grandfatherly figure frequently overlooked by waiters in restaurants – he is a dangerous iconoclast in the eyes of the industrial melanism establishment. He finally published, with two co-authors, a devastating analysis of the classic industrial melanism story in 1998 (see below), concluding that “there is little persuasive evidence, in the form of rigorous and replicated observations and experiments, to support [the classical] explanation at the present time.” Although it enraged the community of his peers – Bruce Grant called it a “dreadful review” and a “hatchet job” – Sargent’s article was not the decisive confrontation of the peppered moth wars. That erupted in the 5 November 1998 issue of Nature, in a review written by Jerry A. Coyne, professor of ecology and evolution at the University of Chicago, of a new book by Michael E.N. Majerus. The book, called Melanism: Evolution in Action, was a watershed event. Methodologically and incisively analyzing every flaw in Kettlewell’s experiments and in the industrial melanism paradigm, Majerus’s book left no doubt that the classic story was wrong in almost every detail. [I separated it here for ease]:
a. Peppered moths, if left to their own devices, do not rest on tree trunks;
b. bird vision is nothing like human vision [referring to Kettlewell's vision scale that were part of his original thesis];
c. Kettlewell was wrong about how peppered moths choose their resting sites;
d. the high densities of moths he used may have skewed the results;
e. the method of release was faulty, and on and on.
The various predation have not replicated his results particularly well, and other “factors” kept having to be invoked to squeeze the data into the standard industrial melanism model. “The findings of [scientists since Kettlewell],” Majerus concluded, “show that the précised description of the basic peppered moth story is wrong, inaccurate, or incomplete, with respect to most of the component parts.”
The reader who makes his way through Majerus’s mountains of evidence is rather stunned to arrive at his verdict: that the basic story, while “undoubtedly more complex and fascinating than most biology textbooks have space to relate”, is perfectly fine. “My view of the rise and fall of the melanic peppered moth is that differential bird predation in more or less polluted regions, together with migration, are primarily responsible, almost to the exclusion of other factors.”
Jerry Coyne (who reviewed Majerus’s book), however, was “horrified.” The sheer magnitude of the problems itemized in the book filled him with dismay and something like shame. After all, he too had been teaching the “standard Biston story” for years. When he dug out Kettlewell’s original papers he found that things were even worse than he thought. How was it that the experiment that Coyne called the “prize horse in our stable of examples” had been accepted unquestionably all this time? …(continued below)"
That was a quote from a peer reviewed scientist's book.
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Ok, first off, this is easily proven nonviable. In order for there to be enough genetic data to prevent
inbreeding mutations, there would have to more than 10 lizards.
First of all, please cite proof of this specific number, and second realize that inbreeding mutations are
new traits evolving that did not exist before. Something like 70% of inbreeding mutations are harmful, and most of the rest are either weakly expressed or completely neutral, but that does not change the fact that these are changes in the gene structure and not preexisting but recessive traits being expressed, and that some are even beneficial. You just cited evidence that debunks your entire stance.
No, sorry I did not cite evidence that debunks my stance. Inbreeding mutations are not new traits.
They are recessive traits that are not desirable for survival. Not new genetic data.
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I highly doubt an entire organ suddenly popped into existence over 30 generations.
"I highly doubt" is not evidence, and isn't worth mentioning if you are trying to convince anyone of anything.
Let me make it clearer then. That is impossible by any means, even if we assume new neutral or positive genetic mutations are added during each of the 30 generations.
After looking around for a bit,
it turns out that these lizards do have the organ that was supposedly evolved. They just have it at a younger stage of life.
They also note that the changes occurred with a change in population density. As everyone knows when cricket and grasshopper population density swells they undergo physiological changes and become
locusts.
So what we have here is zero evidence for evolution until someone sequences the DNA to tell if it was a genetic loss or a new gene that caused the cecal valves to remain to adulthood. In short "Not enough information".
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As I said, there wasn't enough genetic data in 10 lizards to produce a viable population of lizards for more than a few generations without extreme birth defects and infertility which would have wiped them out.
Cite evidence please.
Citation:
"The "50/500" rule of thumb initially advanced by Franklin (1980) and Soule (1980) comes the closest of any to attaining "magic number" status (Wilcox 1986). This rule prescribes a short-term effective population size (Ne) of 50 to prevent an unacceptable rate of inbreeding, and a long-term Ne of 500 to maintain overall genetic variability. The Ne=50 prescription (termed "the basic rule" by Soule 1980) corresponds to an inbreeding rate of 1% per generation, approximately half the maximum rate tolerated by domestic animal breeders (Franklin 1980). The Ne=500 prescription is an attempt to balance the rate of gain in genetic variation due to mutation with the rate of loss due to drift, and is based on a genetic study of bristles in Drosophila (Franklin 1980)."
You need way more than 10 lizards. 10 lizards 5 being male and 5 being female would equal an inbreeding rate of way over 1%.
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That link is forbidden to me for some reason. Most of the examples given though I bet are easily disproved as recessive genes or a loss of data allowing some already existing mechanism to work. I've gone over dozens of these kinds of articles and they always claim to have proven evolution as fact, but upon closer inspection they always fail to show anything other than recessive genes or loss of genetic traits.
You bet?
Yes, I can't be 100% sure because I can't read the article. However every single article I've been able to access with a little bit of research turns out to be a recessive gene or a loss of genetic traits.
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Except you can't make a mathematical model based on a lack of knowledge or information. Its those unknown unknowns that get you. The probabilities you talk about ignore an entire section of variables in favor of a 'lets just assume this for now' which totally goes against science.
What section of variables is ignored? Science is about using the best explanation for what we see. A bunch of stuff isn't getting made up to support these explanations, we've seen these mutations. At a macro level, and at a bacterial level, which we DO have DNA sequencing for:
http://www.newscientist.com/article/dn1 ... ktv9VOcF8EYep, that one has been debunked for awhile. The article erroneously claims that this bacteria can't metabolize citrate, when in fact they have the ability to metabolize citrate in an non-oxidized environment.
Here is a better article that explains it more fully, though with the same 'evolution' slant.
Here is the Wikipedia article on the subject, and here is a quote that shows that it wasn't new genetic data but simply a gene duplication:
"In 2012, a team of researchers working under Lenski reported the results of a genomic analysis of the Cit+ trait that shed light on the genetic basis and evolutionary history of the trait.[5] The researchers had sequenced the entire genomes of twenty-nine clones isolated from various time points in the Ara-3 population's history. They used these sequences to reconstruct the phylogenetic history of the population, which showed that the population had diversified into three clades by 20,000 generations. The Cit+ variants had evolved in one of these, which they called Clade 3. Clones that had been found to be potentiated in earlier research were distributed among all three clades, but were over-represented in Clade 3. This led the researchers to conclude that there had been at least two potentiating mutations involved in Cit+ evolution. The researchers also found that all Cit+ clones sequenced had in their genomes a duplication mutation of 2933 base pairs that involved the gene for the citrate transporter protein used in anaerobic growth on citrate, citT. The duplication is tandem, resulting in two copies that are head-to-tail with respect to each other. This duplication immediately conferred the Cit+ trait by creating a new regulatory module in which the normally silent citT gene is placed under the control of a promoter for an adjacent gene called rnk. The new promoter activates expression of the citrate transporter when oxygen is present, and thereby enabling aerobic growth on citrate. Movement of this new regulatory module (called the rnk-citT module) into the genome of a potentiated Cit- clone was shown to be sufficient to produce a Cit+ phenotype. However, the initial Cit+ phenotype conferred by the duplication was very weak, and only granted a ~1% fitness benefit. The researchers found that the number of copies of the rnk-citT module had to be increased to strengthen the Cit+ trait sufficiently to permit the bacteria to grow well on the citrate, and that further mutations after the Cit+ bacteria became dominant in the population continued to accumulate that refined and improved growth on citrate. The researchers conclude that the evolution of the Cit+ trait suggests that new traits evolve through three stages: potentiation, in which mutations accumulate over a lineage's history that make a trait accessible; actualization, in which one or more mutations render a new trait manifest; and refinement, in which the trait is improved by further mutations."
In other words an already existing process was duplicated which allowed the bacteria to better process citrate while in an oxidated environment.
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Your confusion might be that the homunculus regressed middle man changes in each iteration. That is still the right fallacy. For instance they start with new genetic data is created, we ask how that happens, they say mutation, we point out how absurd that is and they say of mutation is caused by X (where X is another regressed middle man) and the cycle continues as each new theory has holes poked into it.
Just because you aren't aware of it or don't understand it doesn't mean it doesn't exist. Random gene recombination happens all of the time. We see this happen at a genetic level in labs. here is no "caused by X" happening. We are talking about extrapolating ideas from things that are verifiable, that there is evidence for, and every time someone shows you evidence, you say that it has been debunked, and cite something that doesn't debunk it at all, or you ignore it.
Unfortunately no one has as yet shown in the lab that this has happened. You are talking about imagining unverified speculation based on what you know. Its important to note that you can extrapolate incorrectly just as well as you can correctly.
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I'm talking about a positive change. It only takes one base pair change to become destructive. It takes 25%-50% of base pairs that create a protein to make it into the next closest protein that actual is not negative (that's not even counting positive).
I've already answered this above, and others have any other times as well, but you're still citing the mechanism that makes evolution work, and saying it proves that it doesn't. Just because most of some types of mutations such as inbreeding produce negative results doesn't mean that the mechanism doesn't exist. In the same works you've cited, it is outlined that positive change does happen, and has been documented in lab settings, as well as in nature. At a macro and micro scale.
You and others don't seem to grasp what I'm saying. Not only does it require hundreds of mutations, they have to be specific mutations and if they aren't they end up making the protein harmful to the organism. Scientists have admitted that they can't find a path of one protein evolving into another because during that path the mutations would kill the organism or render it unsuitable for its environment.
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Yet it still represents a loss of genetic data and not an addition. As I said before adaptation to an environment due to the loss of genetic data is a proven phenomenon. It does not prove in any way shape or form that things grow new genetic data and that amoebas gave rise to chimps.
Okay first, how does it represent a loss of genetic data? There is no "loss of data," there is only change. All of our dna is four nucleobases combined in different ways. But secondly, there were no chimps 500 million years ago. So by your logic, everything that is a chimp already existed as a recessive gene in the first amoebas.
Loss of functionality. It turns a useful protein into a harmful or non-useful protein. Thus its a loss.
Your second sentence is pure nonsense and isn't what I was saying.
Straw Man.
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You seem to be going far, far beyond what the second law of thermodynamics implies. The system of DNA transcription is an thermodynamically open system because energy is being transferred in, in the form of chemical bonds.
That's the production of the DNA and RNA chemical bonds, that system is open. The copying of the DNA over to the RNA and the causation of mutations is a closed system no new genetic data is inserted.
What. That you can acknowledge one and not the other blows my mind. Especially since it appears to be a distinction based on pure whim, as far as I can tell.
They are two different system. Its as simple as that. A factory that produces a specific set of gears is an open system. As soon as you go to put those gears together it is a closed system because the only thing that is happening is the placing of the gears together. You aren't adding new gears or modifying old gears by adding paint or whatever.