Cofty, whatever you see or say, the above are the reasons for what I believe, similar to your initial post. That's what you believe, isn't it? You are allowed to say your say, but I am not? Like it or lump it.
Posts by Vidqun
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71Evolution is a Fact #38 - The Origin of Complex Cells
by cofty inin 1966 microbiologist kwang jeon was studying a population of amoebae in the lab when they began to die off unexpectedly.
he noticed thousands of tiny dots in the cytoplasm of each individual which turned out to be a bacterial infection.
most of them weakened and died but surprisingly a small percentage recovered and seemed to be back to normal.
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71
Evolution is a Fact #38 - The Origin of Complex Cells
by cofty inin 1966 microbiologist kwang jeon was studying a population of amoebae in the lab when they began to die off unexpectedly.
he noticed thousands of tiny dots in the cytoplasm of each individual which turned out to be a bacterial infection.
most of them weakened and died but surprisingly a small percentage recovered and seemed to be back to normal.
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Vidqun
And I quote: "The Wiki article reveals a few flaws with the theory symbiogenesis." Go and look it up. I could not access your article, so I used Wiki instead.
I used the Wiki-article to point out the flaws, and I wrote it out and commented on the article. No copy and paste. Makes me think: Farting against thunder, flogging a dead horse, yeah, both of you. Cantleave, is that the best you can do?
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71
Evolution is a Fact #38 - The Origin of Complex Cells
by cofty inin 1966 microbiologist kwang jeon was studying a population of amoebae in the lab when they began to die off unexpectedly.
he noticed thousands of tiny dots in the cytoplasm of each individual which turned out to be a bacterial infection.
most of them weakened and died but surprisingly a small percentage recovered and seemed to be back to normal.
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Vidqun
You've said it and I repeat: "OBJECTIONS TO THIS THEORY AND ARTICLE ARE ALL MINE." I used the article and OBJECTED to some of the contents. I used the article as backbone and commented and/or objected to it. What is so difficult about that?
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71
Evolution is a Fact #38 - The Origin of Complex Cells
by cofty inin 1966 microbiologist kwang jeon was studying a population of amoebae in the lab when they began to die off unexpectedly.
he noticed thousands of tiny dots in the cytoplasm of each individual which turned out to be a bacterial infection.
most of them weakened and died but surprisingly a small percentage recovered and seemed to be back to normal.
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Vidqun
Cofty, what is wrong with you? Please follow the numbers.
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71
Evolution is a Fact #38 - The Origin of Complex Cells
by cofty inin 1966 microbiologist kwang jeon was studying a population of amoebae in the lab when they began to die off unexpectedly.
he noticed thousands of tiny dots in the cytoplasm of each individual which turned out to be a bacterial infection.
most of them weakened and died but surprisingly a small percentage recovered and seemed to be back to normal.
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Vidqun
Here’s a few calculations by scientists and researchers. I am not good with Maths so I cannot verify them. I have to take their word for it:
“The likelihood of developing two binding sites in a protein complex would be the square of the probability of developing one: a double CCC (chloroquine complexity cluster), 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the entire world in the past 4 billion years, so the odds are against a single event of this variety (just 2 binding sites being generated by accident) in the history of life. It is biologically unreasonable.”
Michael J. Behe PhD. (from page 146 of his book “Edge of Evolution”)
Evolution vs. Functional Proteins (“Mount Improbable”) – Doug Axe and Stephen Meyer – Video
https://www.youtube.com/watch?v=7rgainpMXa8
Regardless of how the trials are performed, the answer ends up being at least half of the total number of password possibilities, which is the staggering figure of 10^77 (written out as 100, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000). Armed with this calculation, you should be very confident in your skepticism, because a 1 in 10^77 chance of success is, for all practical purposes, no chance of success. My experimentally based estimate of the rarity of functional proteins produced that same figure, making these likewise apparently beyond the reach of chance.
http://www.evolutionnews.org/2.....35561.html
On the Origin of Mitochondria: Reasons for Skepticism on the Endosymbiotic StoryJonathan M. – January 10, 2012
Excerpt: While we find examples of similarity between eukaryotic mitochondria and bacterial cells, other cases also reveal stark differences. In addition, the sheer lack of a mechanistic basis for mitochondrial endosymbiotic assimilation ought to — at the very least — give us reason for caution and the expectation of some fairly spectacular evidence for the claim being made. At present, however, such evidence does not exist — and justifiably gives one cause for skepticism.
http://www.evolutionnews.org/2.....54891.html
Bacteria Too Complex To Be Primitive Eukaryote Ancestors – July 2010
Excerpt: “Bacteria have long been considered simple relatives of eukaryotes,” wrote Alan Wolfe for his colleagues at Loyola. “Obviously, this misperception must be modified…. There is a whole process going on that we have been blind to.”,,, For one thing, Forterre and Gribaldo revealed serious shortcomings with the popular “endosymbiosis” model – the idea that a prokaryote engulfed an archaea and gave rise to a symbiotic relationship that produced a eukaryote.http://www.creationsafaris.com.....#20100712b
Bacterial Protein Acetylation: The Dawning of a New Age – July 2012
Excerpt: Bacteria have long been considered simple relatives of eukaryotes. Obviously, this misperception must be modified. From the presence of a cytoskeleton to the packaging of DNA to the existence of multiple post-translational modifications, bacteria clearly implement highly sophisticated mechanisms to regulate diverse cellular processes precisely.http://darwins-god.blogspot.co.....wning.html
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71
Evolution is a Fact #38 - The Origin of Complex Cells
by cofty inin 1966 microbiologist kwang jeon was studying a population of amoebae in the lab when they began to die off unexpectedly.
he noticed thousands of tiny dots in the cytoplasm of each individual which turned out to be a bacterial infection.
most of them weakened and died but surprisingly a small percentage recovered and seemed to be back to normal.
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Vidqun
Perhaps now is a good time to clarify some of the terminology: Symbiogenesis cannot be replicated in a lab (and not endosymbiosis as previously stated). There is a difference. I cannot dispute the process of endosymbiosis which can be demonstrated. However the complete process of symbiogenesis (the evolutionary theory that explains the origin of eukaryotic cells from prokaryotic cells by symbiosis) cannot as yet be demonstrated.
What should also be kept in mind, is the process of adaptation at work, which is confirmed by Dr. K. W. Jeon.
It is suggested that the presence of a potent P2 in the X-bacterial gene is an adaptation for the endosymbiotic bacteria to survive within a potentially hostile intracellular environment. 1
The following discusses the organisms or possible organisms involved in Dr. Jeon’s experiment. Important to note that these organisms remain individual and identifiable as specific species.
The X-bacteria which initiated organismic association with the D strain of Amoeba proteus in 1966 as parasites have changed to obligate endosymbionts on which the host depends for survival. Owing to the difficulty in cultivating the bacteria in vitro, the identity of X-bacteria has not been determined. The life cycle of X-bacteria is similar to that of Legionella spp. in soil amoebae. 2
Not sure why this oversight has occurred, but what is described here is the typical (or atypical) immune response of the Amoeba organism, which is not unusual at all. Our immune system has similar response mechanisms to counter invading bacteria and viruses.
This indicates that phylogenetically and ecologically diverse bacteria which thrive inside amoebae exploit common mechanisms for interaction with their hosts, and it provides further evidence for the role of amoebae as training grounds for bacterial pathogens of humans. 3
Again, one should not accept as fact that these organisms are a new species. The warning is sounded by two renowned biologists:
On the basis of the structural and physiological changes brought about by the endosymbionts of xD amoebae as described above, one could consider the the symbiont-bearing xD strain a new species of Amoeba. However, until evidence for genetic differences between D and xD amoebae is obtained, it would be more prudent to treat xD amoebae as belonging to a variant strain. 4
There are huge barriers to overcome in the proposed process of symbiogenesis. I believe the barriers are insurmountable:
Barriers to endosymbiogenesis
The transformation of an independent endosmbiont into an organelle faces tremendous barriers. The hurdles include the transfer of much of the endosymbiont’s genetic material to the host’s nucleus, the acquisition of the proper regulatory and targeting sequences to ensure that the transferred gene not only is expressed but possesses the correct targeting information to redirect it into the plastid. This, of course, leads us to the significant challenge of acquiring the appropriate protein import apparatus to ensure that the targeted proteins are properly imported and sorted within the organelle. There is also the issue of integrating and regulating metabolic pathways. 5
We will see that the archaeal translation machinery is neither bacterial, nor eukaryotic, but customized to the archaea. Indeed some parts of the archaeal translation machinery and those of bacteria or eukarya have similar sequence and/or structures since all life forms share the same task of decoding information carried by mRNA and translating the message into the amino acid sequences of proteins. However, the archaeal translation machinery can’t be exchanged with those of bacteria or eukarya, including ribosomes, tRNAs, and translation factors. Thus, there exists an evolutionarily unbridgeable gap between archaea and eukarya and bacteria in translation, just as in DNA replication and transcription.
The above comparisons of a few molecules involved in the information processing in the three domains of life reveals several interesting phenomena: 1) Molecular machines are employed as modules, that is, a process is either bacterial-like or eukaryote-like. 2) Each machine is a molecular mosaic of modules that is fine-tuned to meet the unique need of an organism. 3) The machines for DNA replication, transcription, and translation in bacteria, archaea, and eukarya are unique and specific for each domain of life, and thus, can’t be exchanged. 4) Functional annotations of genes based on sequence homology comparisons can be misleading because they only take into account isolated parts of proteins, not the entire gene. 5) Organism-specific protein extensions, such as the CTD of eukaryotic Rpb1, can be the determinant factor of life vs. death for the specific organism.
We will see that the archaeal translation machinery is neither bacterial, nor eukaryotic, but customized to the archaea. Indeed some parts of the archaeal translation machinery and those of bacteria or eukarya have similar sequence and/or structures since all life forms share the same task of decoding information carried by mRNA and translating the message into the amino acid sequences of proteins. However, the archaeal translation machinery can’t be exchanged with those of bacteria or eukarya, including ribosomes, tRNAs, and translation factors. Thus, there exists an evolutionarily unbridgeable gap between archaea and eukarya and bacteria in translation, just as in DNA replication and transcription.
The above comparisons of a few molecules involved in the information processing in the three domains of life reveals several interesting phenomena: 1) Molecular machines are employed as modules, that is, a process is either bacterial-like or eukaryote-like. 2) Each machine is a molecular mosaic of modules that is fine-tuned to meet the unique need of an organism. 3) The machines for DNA replication, transcription, and translation in bacteria, archaea, and eukarya are unique and specific for each domain of life, and thus, can’t be exchanged. 4) Functional annotations of genes based on sequence homology comparisons can be misleading because they only take into account isolated parts of proteins, not the entire gene. 5) Organism-specific protein extensions, such as the CTD of eukaryotic Rpb1, can be the determinant factor of life vs. death for the specific organism. 6
At variance with the earlier belief that mitochondrial genomes are represented by circular DNA molecules, a large number of organisms have been found to carry linear mitochondrial DNA. Studies of linear mitochondrial genomes might provide a novel view on the evolutionary history of organelle genomes and contribute to delineating mechanisms of maintenance and functioning of telomeres. Because linear mitochondrial DNA is present in a number of human pathogens, its replication mechanisms might become a target for drugs that would not interfere with replication of human circular mitochondrial DNA. 7
1. Abstract: “A novel strong promoter of the groEx operon of symbiotic bacteria in Amoeba proteus.” Abstract: Dr K.W. Jeon, Department of Zoology, University of Tennessee, Knoxville, TN 37996-0810, USA.
2. Abstract: “Phylogenetic characterization of Legionella-like endosymbiotic X-bacteria in Amoeba proteus: a proposal for ‘Candidatus Legionella jeonii’ sp. nov.”
3. Abstract: “The Genome of the Amoeba Symbiont “Candidatus Amoebophilus asiaticus” Reveals Common Mechanisms for Host Cell Interaction among Amoeba-Associated Bacteria.”
4. Symbiosis as a Source of Evolutionary Innovation: Speciation and Morphogenesis, by Lynn Margulis and René Fester, p. 125.
5. Molecular Phylogeny of Microorganisms, by Aharon Oren and R. Thane Papke, p. 198.
6. “Information Processing Differences Between Archaea and Eukarya—Implications for Homologs and the Myth of Eukaryogenesis,” by C. L. Tan and J. P. Tomkins.
7. Linear mitochondrial genomes: 30 years down the line. Josef Nosek, L’Ubomir Tomaska, Hiroshi Fukuhara, and Ladislav Kovac.
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147
Challenge to Creationists
by cofty inin response to the 37 threads in my evolution is a fact series - see bottom of op for links - perry posted a link to an article "44 reasons why evolution isn't true".. i offered him a challenge on the thread and by pm.
predictably he is totally ignoring it, so i am offering the challenge to any evolution-denier who thinks they have evidence to support their position.. please present one specific piece of evidence for creationism.. my task will be to refute it with evidence within 24 hours.. then i will present one piece of evidence for evolution and your challenge will be the same.. all posts must be as succinct as reasonably possible.
entirely in your own words, without copy-paste, videos or links.. please post your interest to take part and we will set it up before the first actual post in the exchange.
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Vidqun
Cofty, you certainly have the cat by the tale here. Originally the question was: How can a prokaryotic cell (species) turn into a eukaryotic cell (new species)? There is a huge difference between the two, as the scanned illustrations show. Simple organism > more complicated organism. Researchers do not have access to primordial "prehistoric" bacteria for them to demonstrate the suggested processes, so they use existing bacteria and plants instead. Bad examples, for these do not have the ability to mutate to more complex organisms (as their hypotheses suggest). I don't know how to simplify it more. It's not a complicated argument. Or are you using smoke and mirrors to confuse the issue?
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147
Challenge to Creationists
by cofty inin response to the 37 threads in my evolution is a fact series - see bottom of op for links - perry posted a link to an article "44 reasons why evolution isn't true".. i offered him a challenge on the thread and by pm.
predictably he is totally ignoring it, so i am offering the challenge to any evolution-denier who thinks they have evidence to support their position.. please present one specific piece of evidence for creationism.. my task will be to refute it with evidence within 24 hours.. then i will present one piece of evidence for evolution and your challenge will be the same.. all posts must be as succinct as reasonably possible.
entirely in your own words, without copy-paste, videos or links.. please post your interest to take part and we will set it up before the first actual post in the exchange.
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Vidqun
Cofty, I am sorry you couldn't follow my arguments. But as you insist, only the evidence matters. Hold that thought. The following would have been especially interesting to discuss:
3) The hypotheses are demonstrated by mechanisms found in “near-living relatives,” e.g., Cyanobacteria and a-proteobacteria, as well as flowering plants and the tobacco plant. Granted, these organisms have some of the ingredients of above hypotheses. However, the processes within these organisms do not assist said organisms to transcend the species barrier, which the endosymbiotic hypothesis suggests.
prokaryote(s) + prokaryote(s) > eukaryote (new bacterium)
We all know that’s impossible without the help of the genetic engineers. One cannot gloss over these things and hope they will go away. The objections to this theory and article are all mine (and in my own words), but you respond with: "So egregious as to qualify as a deliberate lie." That's some fancy English there, but I call it clouding the issue. Yes, I know, sometimes the truth hurts.
Okay let’s call it a day. Next stop the bacterial flagellum. How about that for a next challenge.
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147
Challenge to Creationists
by cofty inin response to the 37 threads in my evolution is a fact series - see bottom of op for links - perry posted a link to an article "44 reasons why evolution isn't true".. i offered him a challenge on the thread and by pm.
predictably he is totally ignoring it, so i am offering the challenge to any evolution-denier who thinks they have evidence to support their position.. please present one specific piece of evidence for creationism.. my task will be to refute it with evidence within 24 hours.. then i will present one piece of evidence for evolution and your challenge will be the same.. all posts must be as succinct as reasonably possible.
entirely in your own words, without copy-paste, videos or links.. please post your interest to take part and we will set it up before the first actual post in the exchange.
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Vidqun
Cofty, must say, you are hard to please. None of what I wrote is copy and paste. I put it in my own words as per instruction. And I did explain to you that I was not up to date with the latest developments. When I tried to access your article, I was unsuccessful, so I went with Wiki instead. You could just have ignored the text, and responded to my objections: 1) Genome size, 2) Loss of genetic autonomy, 3) Examples used.
That's why endosymbiosis has not yet advanced from theory to fact, there's still too many loose ends. Yes, Cantleave did explain endosymbiosis quite nicely, and I thank him for that. And I am trying to explain to you my objections to endosymbiosis.
Do you realize the difference here? I entertain all options (as a true scientist should), whereas you will entertain only a single option. To you it's either your beloved evolution or bust! You want to make up rules as you go along and are not really interested in anybody else's opinion, especially concerning ID, because it clashes with your personal agenda, whatever that is. Could it be that you have become a disciple of Richard Dawkins. Yes, he also hated religion with a fervent hatred.
Allow me two quotes from him: "By all means let's be open-minded, but not so open-minded that our brains drop out."
"Science is interesting, and if you don't agree you can f$%k off" (quote censored). I think here he was quoting someone else.
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147
Challenge to Creationists
by cofty inin response to the 37 threads in my evolution is a fact series - see bottom of op for links - perry posted a link to an article "44 reasons why evolution isn't true".. i offered him a challenge on the thread and by pm.
predictably he is totally ignoring it, so i am offering the challenge to any evolution-denier who thinks they have evidence to support their position.. please present one specific piece of evidence for creationism.. my task will be to refute it with evidence within 24 hours.. then i will present one piece of evidence for evolution and your challenge will be the same.. all posts must be as succinct as reasonably possible.
entirely in your own words, without copy-paste, videos or links.. please post your interest to take part and we will set it up before the first actual post in the exchange.
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Vidqun
The Wiki article reveals a few flaws with the theory symbiogenesis:
1) Genome size. Cyanobacteria and a-proteobacteria are the most closely related free-living organisms to plastids and mitochondria respectively. However, plastid and mitochondria exhibit a dramatic reduction in genome size when compared to their bacterial relatives. Chloroplast genomes in photosynthetic organisms are normally 120-200kb encoding 20-200 proteins and mitochondrial genomes in humans are approximately 16kb and encode 37 genes, 13 of which are proteins.
2) Loss of genetic autonomy: The authors, i.e., Keeling and Archibald, argue that the host cell has assumed control of the regulation of the former endosymbiont's division, thereby synchronizing it with the cell's own division. The mechanisms of gene transfer are not fully known; however, multiple hypotheses exist to explain this phenomenon.
The cDNA hypothesis is based on studies of the genomes of flowering plants. Protein coding RNAs in mitochondria are spliced and edited using organelle-specific splice and editing sites. Nuclear copies of some mitochondrial genes, however, do not contain organelle-specific splice sites, suggesting a processed mRNA intermediate. The cDNA hypothesis has since been revised as edited mitochondrial cDNAs are unlikely to recombine with the nuclear genome and are more likely to recombine with their native mitochondrial genome. If the edited mitochondrial sequence recombines with the mitochondrial genome, mitochondrial splice sites would no longer exist in the mitochondrial genome. Any subsequent nuclear gene transfer would therefore also lack mitochondrial splice sites.
Bulk-flow hypothesis views escaped DNA, rather than mRNA, as the mechanism of gene transfer. According to this hypothesis, disturbances to organelles, including autophagy (normal cell destruction), gametogenesis (the formation of gametes), and cell stress, release DNA which is imported into the nucleus and incorporated into the nuclear DNA using non-homologous end joining (repair of double stranded breaks). For example, in the initial stages of endosymbiosis, due to a lack of major gene transfer, the host cell had little to no control over the endosymbiont. The endosymbiont underwent cell division independently of the host cell, resulting in many "copies" of the endosymbiont within the host cell. Some of the endosymbionts lysed and high levels of DNA were incorporated into the nucleus. A similar mechanism is thought to occur in tobacco plants, who show a high rate of gene transfer and whose cells contain multiple chloroplasts. In addition, the bulk flow hypothesis is also supported by the presence of non-random clusters of organelle genes, suggesting the simultaneous movement of multiple genes.
3) The hypotheses are demonstrated by mechanisms found in “near-living relatives,” e.g., Cyanobacteria and a-proteobacteria, as well as flowering plants and the tobacco plant. However, these processes never transcend the species barrier, which the endosymbiotic hypothesis suggests.