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Topic: can some aspect of Darwinism be falsified?
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Bruce Fast
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Member # 924
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posted 12. June 2006 14:38
Zachriel, my question is genuine, not rhetorical. As a member of the peanut gallery I am lost as to what Penny proposes, or what it means. I am quite comfortable with the concept of the hypothesis. A little "this proposal hasn't been established in science" is not a problem.
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Zachriel
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posted 12. June 2006 16:36
Bruce Fast: "Zachriel, my question is genuine, not rhetorical."
That's how I took it. (Perhaps you missed my reply one post above the one you apparently responded to. The latter post was meant to modify the previous comment which may have inadvertently left the impression that Penny considers it a settled issue.)
Zachriel: Kimura's original neutral theory assumed that over longer timescales, detrimental mutations would disappear from a population. This does not apply to slightly detrimental mutations over shorter timescales. Direct studies were not available at that time.
You might also follow the link provided to the actual article. If it still isn't clear, let me know what questions you might have and I'll try to respond with whatever insight I might garner.
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Bruce Fast
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posted 12. June 2006 17:18
I see, so Penny suggests that a mildly detremental mutation may take a while to filter out of the genome. One might add that a detremental mutation in a recessive gene may be more difficult to filter out. Alas, I find this to be a reasonable concept.
[ 12. June 2006, 17:19: Message edited by: Bruce Fast ]
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peter borger
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posted 13. June 2006 02:35
This is the link to Penny's article:
http://www.nature.com/nature/journal/v436/n7048/full/436183a.html
have alook at figure 1. It shows the J-curve for mutations rates. Slow in ancient times, fast in modern times.
Moreover, Penny writes:
quote:
There is the challenge of formulating a single theory that operates smoothly over disparate timescales, from current heterozygosity to the long-term rate of evolution. In addition, a single mutation rate () does not really exist. Even for nucleotides there are many 'mutation rates', at least one between each pair of nucleotides, and these can be estimated separately using three-dimensional matrices12. The J-shaped curve cannot rest until a single theory holds for it: we live in interesting times.
We live in interesting times indeed: the fall of all aspects of Darwinian Theory.
A single mutation rate does not exist because mutations are not purely random. I have also argued this from the observations doen by Wyckof et al, who found that selection does not appear to act on genes with high mutation rates.
Welcome GUToB.
peebee
[ 13. June 2006, 02:40: Message edited by: peter borger ]
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peter borger
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posted 13. June 2006 02:51
quote:
peter borger: "Penny's paper tries to reconcile the very high intraspecies mutations rates with the low frequencies found in interspecies comparisons."
Zachriel: Kimura's original neutral theory assumed that over longer timescales, detrimental mutations would disappear from a population. This does not apply to slightly detrimental mutations over shorter timescales. Direct studies were not available at that time.
The Darwinians do their calculations assuming that all organism have a common ancestor and that is why the are actually able to perform interspecies comparisons and find low mutations rates. Then, molecular biologists started to compare DNA sequences within species (intraspecies comparisons) and found high mutation rates (see my Cyt C example). This apparent paradox has to be reconciled with standard theory, et voila: Penny's paper.
The only data that are really helpful are DNA sequence comparison of ancient and modern organisms. And these data are available. What do these data show? Almost identical sequences in organisms alleged to be hundreds of millions years apart. You don't have to be Einstein to observe the paradoxes.
So, Penny argues, genetic changes used to be slow and now they are high.
peebee
[ 13. June 2006, 08:40: Message edited by: peter borger ]
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peter borger
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posted 13. June 2006 03:24
quote:
One might add that a detremental mutation in a recessive gene may be more difficult to filter out.
You probably mean a recessive allele?
RECESSIVE alleles are usually inactivated genes, but there is also a functional gene (Mendel called it DOMINANT) to back up the inactivated gene.
Genuine recessive genes would qualify as genetic redundancy. We know now, the genome is loaded with such recessive genes. Their discovery means the end of Darwinism, as their existence cannot be explained through selection hypothesis.
peebee
[ 13. June 2006, 03:25: Message edited by: peter borger ]
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peter borger
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posted 13. June 2006 05:58
quote:
Have a look at figure 1. It shows the J-curve for mutations rates. Slow in ancient times, fast in modern times.
Zachriel, this demonstrates uniformitarianism wrt mutations is being abandoned. Or not?
peebee
[ 13. June 2006, 07:41: Message edited by: peter borger ]
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peter borger
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posted 13. June 2006 08:21
Let's analyse a bit of Penny's writing:
quote:
...at times less than about 1−2 million years there is an increasing acceleration, with the highest rates at the shortest times.
Question: How did Ho and coworkers anylyse this? We do not have access to the DNA of organism that lived 1-2 million years ago.
Answer: by extrapolation of the darwinian assumption of common descent. That is by interspecies comparison.
Penny continues:
quote:
The rate is highest between generations (that is, in pedigree studies), and decreases continuously for local and then for widespread populations.
Now, Penny is referring to studies within several subpopulations of one species, i.e. intraspecies comparisons.
quote:
Finally it reaches the low plateau that we know for long-term evolution.
And now he is comparing distinct species again; interspecies comparison.
No wonder that the Darwinians find a J-curve. They jump from interspecies to intraspecies to interspecies comparisons. What the actual, measured biology data show is that mutation rates are much higher then calculated under the Darwinan assumption of common descent. The genuine scientific data were obtained by measuring the differences in DNA sequences and can be trusted. Unfortunately, the real data contradict darwinian's preconceived ideas about evolution and mutation rates and thus the real data have to be reconciled with their pseudoscientific non-sense. What a non-science darwinism is.
peebee
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Bruce Fast
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posted 13. June 2006 11:52
PB, thanks for the discussion. I love it when you biologists debate each other. Any of you guys can blow the doors off of my limited knowledge, but when you are all bringing up counterpoints, I can follow them rather well.
My question, as recessive genes do seem to periodically pop up in populations (we see left-handedness and blue eyes quite often) why would you say that recessive genes are "redundant", not protected by natural selection, and not accoutable for by NDE?
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Shi
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Member # 1923
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posted 13. June 2006 11:52
Peter,
I enjoyed your insightful analysis. I hold the view that the major variations in DNA sequences are set up or created in a non-random fashion at the beginning of species split. So, human and chimps never once shared nearly 100% identity and gradually divered to today's 95-98% identity. They have always been 95-98% different ever since human and chimp diverged from their last common ancestor. Is this view consistent with your ideas?
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Shi
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Member # 1923
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posted 13. June 2006 12:04
It is NDE nonsense to say that the common ancetor of human and chimp looked like neither human or chimp. In my view, the ancestor of human is a chimp like animal. Human is created using the chimp as a template. When the first human or pair of human is created, their difference in DNA from chimp was the same as it is today and will stay the same indefinitely in the future. Random mutations, no matter how high a rate, will never be able to change significantly the degree of similarity that was set at the beginning of species split. Random mutations are reversible and will cancel each other out over time.
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Shi
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Member # 1923
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posted 13. June 2006 14:19
I can use atoms as analagy. The randomness of quanta in the hydrogen atom will never be able to change a hydrogen atom into a helium atom. Each type of atom is a unique stable state of energy. Within each atom, there is randomness of quanta. But such randomness is not without limit and contribute little to the difference between different types of atoms. A stable species is like an atom. Randomness of the building elements (DNA) of the spcies is not sufficient to fundamentally change the stability of the species.
Randomness theories cannot explain the stability of nature. If the Earth is randomly created then why it has not been randomly demolished. Randomness creates change and instability. The existance of stability in nature fasifies the notion that the cause of nature is randomness. Granted that randomness is part of nature. The reason why randomeness can coexist with stability is because randomness cancel itself out. It cannot move in one direction without also moving in the opposite direction. So, the net effect is no movement in any direction. The coin flip is random but is not going to affect the stability of the fact that a coin has a 50% chance of landing on its head. The rare event of landing 5 heads in a row is canceled by the opposite event of landing 5 tails in a row.
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christopher humphrey
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Member # 1377
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posted 13. June 2006 15:48
quote:
April 8 2005
Precursor Cells Follow Different Paths to Same
Cell Fate
Complex Behavior
"With so many genes turning on and off inside the developing cell, the potential for instability is great. In the 1960s, the theoretical biologist Stuart Kaufmann proposed that if a cell were to hit upon an arrangement in which every element affected what the others were doing, much in the manner of a feedback system, that cell would better resist perturbation. In fact, evolution appears to have selected for just such a system—genes and proteins often inhibit or activate one another. The collective behavior of this network creates a system that is so stable and self-correcting that it exerts an almost gravitational pull—the developing cell is compelled toward its fate, for instance, to become a liver cell. Kaufmann called these stable networks “attractors,” a term he borrowed from physics. But evidence for the existence of attractors was lacking .
In one respect, it is easy to see why. In Kaufmann’s view, a cell hits upon a stable genetic configuration and develops into a particular cell type. But demonstrating that the entire network functions as an attractor, pulling the cell down a particular developmental path, is problematic. One could argue, as molecular biologists have, that the network is simply the consequence of individual signaling pathways instructing the cell to develop in a particular direction. There is another approach. According to Kaufmann, attractors are very robust—they cast a wide net. Two developing cells might initially exhibit wildly differing constellations of gene activity and yet they could eventually be caught up by the same stable configuration, or attractor, and become the same kind of cell. That is what Huang and his colleagues have shown."
quote:
“Our view is that a cell’s differentiation state is there as a pre-existing program, an attractor, and all you need is to tip over into it,” said Sui Huang. “You do not need very specific
instructional inputs.” —Misia Landau
From The Vesica Attractor...
If the attractor retained the shell and a symmetrical flow though the apertures, the result would be a cephalopod. This shell is not a genetic adaptation but more precisely the a receipt from paying {Schrödinger entropy debt} http://www.entropylaw.com/thermoevolution9.html
{The oolitic mass would shrink [dissipate] during this pulse into a higher ordered state.}
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Another key in the self-making ability of the embryonic material that forms the vesica attractor is in it's ability to shape-shift around the tendency of a fluid to seek an ordered path though and around a medium. This medium having a fine balance of cohesion and plasticity.
The next key is in the mineral content of the spheres. Aragonite, this form of calcium carbonate has properties that promote microbial growth and acts as a mineral substrate for initiating an autopoetic biochemical cycle. This mineral has been discovered to be a fundamental element in maintaining an autopoetic system in coral reefs and closed artificial systems such as salt water aquariums.
Another important roll of the oolites is in their ability to act as a dynamic scaffolding. As the aragonite spheres dissolve though chemical and mechanical forces, a synergy unfolds throughout the emerging structure, As the oolites shrink they become point attractors among the eukaryote cells, that have now adopted the fluid energetic pattern left by the cyanobacteria filaments. As the oolites lose mass they induce the production of new filaments that emerge from the outer cellular membranes of the eukaryotes. Anchoring proteins extend through the plasma membrane to link to the emerging cytoskeleton structure. Simply put, as the temporary oolitic scaffolding deconstructs, it constructs it's permanent replacement. These Anchoring-type junctions not only hold cells together but provide tissues with structural cohesion. These junctions are produced more abundantly in tissues that are subject to higher mechanical stress such as the outer skin and heart. Connective tissues begin forming flexible geodesic scaffolding by drawing in and connecting to points in space where the oolites have now vacated. These connecting points form the extracellular matrix, meanwhile the vesica apertures acts as a cycle attractor spiraling inward keeping a central tension as the embryo loses mass and takes shape, simultaneously providing a flow of renewing sea water though the recursive system as it pulses in time with wave cycles. The central apertures begins to coil in slack in the form of a layered network of connected cells. This dense mass of wound together cells will form heart tissue. This tension that connects eukaryote cells in a medium of cohesion is called (tensegrity). Tensegrity results in a crystallization of connections in the architecture of the emerging organism, enabling the individual cell though it's own intracellular matrix to respond to a potential fitness space. This crystallization of the recursive dynamic structure might well result in an "algorithmic self-assembly" of genetic probabilities.
http://www.iscid.org/boards/ubb-get_topic-f-26-t-000007
[ 13. June 2006, 16:09: Message edited by: christopher humphrey ]
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Bruce Fast
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posted 13. June 2006 16:44
Your post is interesting, though in all honesty most of it is floating happily above my head. Alas, I checked out the reviews of "The Origin of Order" on Amazon.com. It really appears that Kauffman is suggesting that there is a natural law which is at work, driving the development of order.
I started a new thread, "Evolution by Natural Law". This post, and Kauffman's work, seems to fit very nicely into this concept of evolution by Natural Law. I actually find that Dr. Davison's work, as well as PB's work, also are much more compatible with a "natural law" model than they are with a contingency model.
Wouldn't it be interesting to discover that neither contingency (chance) nor agcency is responsible for biodiversity, but that natural law is, just as natural law is responsible for the cosmos.
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John A. Davison
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posted 13. June 2006 21:33
"Everything is determined... by forces over which we have no control."
Albert Einstein
That says it all as far as I am concerned.
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