aaah good new fashion neo-eugenics. I always op that gene therapy and cybernetics to the already born will be far more popular then the very controversial biorobotics and genetic engineering of new babies.
Evolution and instincts
- Thread starter one_raven
- Start date
Robert Jameson
Registered Senior Member
WellCookedFetus
I read the article you referred me to on the nylon bug. It is interesting but I do not think it satisfies the questions that sceptics such as myself have in regard to this issue. The first problem is this. While the odds of this type of beneficial mutation (frame shift) happening through random mutation is great it does happen and is within the range of probabilities that are possible. But for random mutation, and then the random recombination of DNA, to be the driving force of new and more complex gene functions the maths does not stack up.
From Chapter 10 of God Gametes (Finding New Genes) which can be downloaded free at www.e-publishingaustralia.com
It is evident that species do acquire new genes. This can only happen by changes to existing genes or wholesale importation of new genes and we know that either option must have happened or significant evolutionary changes would not have been possible.
As pointed out, there may be examples where slight mutations have conferred a wholly new function on a gene. Some Darwinists seem to think their argument would be strengthened if they could provide numerous examples where mutations conferred a new genetic function. In fact any confirmed increase in the number of genes created this way, and the greater changes to sequencing that these require, diminish the likelihood that they could have happened by chance. The substitution of only a half dozen nucleotides in the average size gene allows for 10(14) new possible gene-sequences.
But we know that new gene-sequences have to be found or evolution would never happen. The fact that it does is not in dispute. Higher incidents of new genes and larger changes to the genetic sequence strengthen the argument for design because they are less likely to have happened by chance.
If a new gene function were created in a ‘so called’ closed laboratory experiment this could not be explained by Cosmic Ancestry or God Gametes. Cosmic Ancestry needs to demonstrate that the new gene function was imported from space. God Gametes says it could never be a closed system experiment unless all universal forces were excluded.
Suppose for example a total of ten successive ‘so-called’ closed system experiments were to produce ten completely new genes that were functional and environmentally adaptive. If such a remarkable experiment were to happen it may be doubted, even by Darwinists, that a purely random process could produce such a result.
Someone might ask if the experiments were really closed and it may then be noted that gravity is an external force and could have had some influence on the result. It was probably not considered necessary to close off light from the sun. We must also remember that the experiments would have had billions of neutrinos passing through them every second.
If there is a life force it is not known by what means it is transmitted. It is therefore argued by God Gametes that experiments relating to the source of life and the function of living creatures should never be considered closed.
river-wind
Thanks for your response to my posts. I was going to answer in detail the points you made on eyes, wolves and social sex but thought I would be going over a lot of the same arguments I have put up earlier in this thread. I guess some people will believe it could just happen and others (like myself) think there has to be more to it. Maybe I could better explain where I am coming from by reference to your “strings and buttons” analogy. There is an important principle here that can be used to show how, once a design has reached a critical point, the numbers seem to fall into place more easily and this has no doubt been an important factor in the evolution of greater complexity.
But there are problems relating this analogy to life on earth. It takes as given the strings and buttons and also the energy required to move them. This is similar to what Darwinists have done. They do not explain matter in the universe, energy, the forces that control it and the property of life. If you take all these as given and then say “look at all these remarkable things that can just happen if you flip the dice enough times”. There had to be something to kick start it all in the same way that your strings and buttons exercise will not work unless you have some strings and buttons and the energy to move them.
>>> by peer review, he means that it has to stand up to the analysis of other scientists. Usually this is done by publishing in a scientific journal, and then allow others to try and debunk the theory. if it gets debunked, then it is gone. if it survives, then it becomes part of the common culture as is accepted as "fact" (even though it's still really only just a theory which has stood up to criticism for a while) <<<
I asked WellCooked what he meant by “peer” because I do not think the scientific establishment would think of me as a peer. I would love to have some of my work published in a science journal but I am not holding my breath?
>>> While lacking access to university supplies makes things harder, it does not make them impossible. there have been many historical cases where huge advances in scientific theory were dreamt up by people not working in a Uni lab. Like Einstein. <<<
And Charles Darwin himself. In fact most of the paradigm shifts in thinking have come from amateurs who have had to fight the establishment all the way. Some having gone to their graves vilified but later having been proven correct in their views.
>>> … you have a lot of the science you talk about down. But keep reading, there's always something new to learn. <<<
Thanks I will. Can you believe I studied history at uni and did not take any interest in science until I was in my late 40’s. I have a lot of catching up to do?
I read the article you referred me to on the nylon bug. It is interesting but I do not think it satisfies the questions that sceptics such as myself have in regard to this issue. The first problem is this. While the odds of this type of beneficial mutation (frame shift) happening through random mutation is great it does happen and is within the range of probabilities that are possible. But for random mutation, and then the random recombination of DNA, to be the driving force of new and more complex gene functions the maths does not stack up.
From Chapter 10 of God Gametes (Finding New Genes) which can be downloaded free at www.e-publishingaustralia.com
It is evident that species do acquire new genes. This can only happen by changes to existing genes or wholesale importation of new genes and we know that either option must have happened or significant evolutionary changes would not have been possible.
As pointed out, there may be examples where slight mutations have conferred a wholly new function on a gene. Some Darwinists seem to think their argument would be strengthened if they could provide numerous examples where mutations conferred a new genetic function. In fact any confirmed increase in the number of genes created this way, and the greater changes to sequencing that these require, diminish the likelihood that they could have happened by chance. The substitution of only a half dozen nucleotides in the average size gene allows for 10(14) new possible gene-sequences.
But we know that new gene-sequences have to be found or evolution would never happen. The fact that it does is not in dispute. Higher incidents of new genes and larger changes to the genetic sequence strengthen the argument for design because they are less likely to have happened by chance.
If a new gene function were created in a ‘so called’ closed laboratory experiment this could not be explained by Cosmic Ancestry or God Gametes. Cosmic Ancestry needs to demonstrate that the new gene function was imported from space. God Gametes says it could never be a closed system experiment unless all universal forces were excluded.
Suppose for example a total of ten successive ‘so-called’ closed system experiments were to produce ten completely new genes that were functional and environmentally adaptive. If such a remarkable experiment were to happen it may be doubted, even by Darwinists, that a purely random process could produce such a result.
Someone might ask if the experiments were really closed and it may then be noted that gravity is an external force and could have had some influence on the result. It was probably not considered necessary to close off light from the sun. We must also remember that the experiments would have had billions of neutrinos passing through them every second.
If there is a life force it is not known by what means it is transmitted. It is therefore argued by God Gametes that experiments relating to the source of life and the function of living creatures should never be considered closed.
river-wind
Thanks for your response to my posts. I was going to answer in detail the points you made on eyes, wolves and social sex but thought I would be going over a lot of the same arguments I have put up earlier in this thread. I guess some people will believe it could just happen and others (like myself) think there has to be more to it. Maybe I could better explain where I am coming from by reference to your “strings and buttons” analogy. There is an important principle here that can be used to show how, once a design has reached a critical point, the numbers seem to fall into place more easily and this has no doubt been an important factor in the evolution of greater complexity.
But there are problems relating this analogy to life on earth. It takes as given the strings and buttons and also the energy required to move them. This is similar to what Darwinists have done. They do not explain matter in the universe, energy, the forces that control it and the property of life. If you take all these as given and then say “look at all these remarkable things that can just happen if you flip the dice enough times”. There had to be something to kick start it all in the same way that your strings and buttons exercise will not work unless you have some strings and buttons and the energy to move them.
>>> by peer review, he means that it has to stand up to the analysis of other scientists. Usually this is done by publishing in a scientific journal, and then allow others to try and debunk the theory. if it gets debunked, then it is gone. if it survives, then it becomes part of the common culture as is accepted as "fact" (even though it's still really only just a theory which has stood up to criticism for a while) <<<
I asked WellCooked what he meant by “peer” because I do not think the scientific establishment would think of me as a peer. I would love to have some of my work published in a science journal but I am not holding my breath?
>>> While lacking access to university supplies makes things harder, it does not make them impossible. there have been many historical cases where huge advances in scientific theory were dreamt up by people not working in a Uni lab. Like Einstein. <<<
And Charles Darwin himself. In fact most of the paradigm shifts in thinking have come from amateurs who have had to fight the establishment all the way. Some having gone to their graves vilified but later having been proven correct in their views.
>>> … you have a lot of the science you talk about down. But keep reading, there's always something new to learn. <<<
Thanks I will. Can you believe I studied history at uni and did not take any interest in science until I was in my late 40’s. I have a lot of catching up to do?
it is not important if other people think you are a 'peer'. Peer is about following the rules established by the scientific community. You don't have to add your resume when you submit a paper. You are not judged on your educational background. You are judged on your manuscript.
I pointed out a major no-no/not done/reputation killer/flaw in your approach. Take it as friendly advice, or just ignore it (but be ignored in the scientific world as consequence).
I pointed out a major no-no/not done/reputation killer/flaw in your approach. Take it as friendly advice, or just ignore it (but be ignored in the scientific world as consequence).
Robert Jameson
Registered Senior Member
As mentioned previously I do not intend to waste my time with the scientific establishment. I am an outsider with a radical idea. There is 100% chance that my concept will be thrown out regardless of its merits. Try this web site address that will lead you to the “The Helicobacter Story”.
http://www.abc.net.au/rn/science/ss/stories/s782213.htm
In particular note the section on John Likoudis. (About one third into the article.) The only mistake he made was being right. Or you might like to do some reading on Australian nurse Elizabeth Kenny.
http://www.abc.net.au/rn/science/ss/stories/s782213.htm
In particular note the section on John Likoudis. (About one third into the article.) The only mistake he made was being right. Or you might like to do some reading on Australian nurse Elizabeth Kenny.
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why don't you post in the pseudoscienceforum if you don't care about the opinion of scientists?
Robert Jameson
Registered Senior Member
I have a thread there but I do not think my work is pseudoscience. I am certainly not a believer in all that stuff about alien abductions etc.
There might be some people here that will judge my ideas on their merits. There are no doubt many scientists who do not always conform to the “establishment” or ‘mainstream” points of view.
There might be some people here that will judge my ideas on their merits. There are no doubt many scientists who do not always conform to the “establishment” or ‘mainstream” points of view.
what are the merits of your work?
Robert Jameson
Registered Senior Member
That is for you and others to judge?
Well...I noticed that you reject my judgement by reasoning that I am part of the establishment. Hence I am not allowed to judge the merits of your work. In your opinion I am incompetent to do so.
therefore I have to ask you to tell me the merits.
therefore I have to ask you to tell me the merits.
Robert Jameson
Registered Senior Member
The Lamarckians
Spuriousmonkey; I am happy to have you review my work. I do not know if you are part of the establishment and I do not care so long as you judge my work on its merits and not some pre-conceived notion of what people want to believe is correct.
A lot of the argument has focused on the fact that evolution of new species can happen very quickly and new and adaptable genes can be found by the random process of natural selection. The following focuses on the immune system where it is known that the mutation rate is high and new antibodies for fighting invading antigens are found very quickly. The God Gametes theory argues that some guiding hand is needed for the coding of new genes; whether these genes are in the immune system or for adaptable new species.
The Lamarckians
Many observers are not convinced that random mutations can be responsible for building complex body parts or for driving the evolutionary process. And the various theories espousing ‘divine creation’ have little appeal to an analytical mind. We therefore find that some form of Lamarckian driven evolution is a tempting alternative.
So believers in ‘the inheritance of acquired traits’ have never gone away. The following looks at Lamarck himself and a number of notable supporters, an interesting lot who remind us that life has both a good side and bad.
(In an effort to keep these posts brief the sections on Jean Baptiste de Lamarck and other Lamarckians Charles Darwin, his grandfather Erasmus Darwin, Paul Kammerer, T.D.Lysenko and Ted Steele have been removed but the articles on Kammerer and Lysenko are referred to in this post. For readers who are interested these extracts are taken from Chapter 12 of God Gametes which can be downloaded free from www.e-publishingaustralia.com )
Normal Mutation Rate:
Cell division and recombination is normally an extremely accurate process. It is needed for replacing old cells in our bodies with new and for carrying the genetic code from one generation to the next. A good example to demonstrate this is the histone H4 gene. It is found in almost all plants and animals and is normally coded for by the same 306 base pairs of DNA. Remarkably, almost exactly the same sequence for this gene (304 of the 306 base pairs) is found in peas and cows, lineages that most likely diverged over a billion years ago.13
This is equivalent to a single copying error in one million, million. It is obviously an extremely high fidelity rate but it overstates the normal accuracy rate for gene division and recombination. To explain this we look again at the histone H4 gene. 304 of the 306 base pairs in this gene have been copied accurately since the divergence of cows and peas. There were no doubt many more mistakes made but histone 4 is necessary for the structural engineering of chromosomes and is essential for life. Individuals that received defective copies of this gene most likely would not have survived, or if they lived would not have reproduced. Natural selection has forced conformity to a gene-sequence that worked.
Even without selection pressure however, the mutation rate is low. The probability of any one nucleotide being miscopied on any one occasion is about one in a billion. It is estimated that in the absence of natural selection it would still take 5 million generations to degrade 1% of our DNA.14
Variable Mutation Rate:
Mutations are mistakes and most are deleterious. All cancers are caused by somatic gene mutation that results in an abnormal function of an otherwise normal cell. For example skin cancers may become unresponsive to ‘growth-limiting’ or death-inducing’ signals and take on a life of their own. Cancer cells may then mutate further or create autonomous (satellite) organisms within a host body.16
But it is important to recognise the difference between somatic mutations that are harmful and the beneficial mutations that occur in the antibody variable region genes. We would expect any mistakes made in replication of DNA to be detrimental but the mutation of B lymphocytes demonstrates an extraordinarily high level of control that delivers a benefit to the living organism in which it occurs.
The somatic mutation rate in rearranged antibody variable region genes, V(D)Js, will increase during an immune response. When the antibody V-region is exposed to an antigen the selected B cells mutate its V(D)J genes at a rate of 1/1,000 to 1/10,000 bases per replication event. This is about a million times higher than the normal mutation rate of germline transmitted genes.17
Targeted Mutation:
Mutations in antibody variable region genes are precisely targeted. They are localised to the rearranged (VDJ) genes and the non-coding flanking DNA sequence and are not found upstream near the Promoter site (P) or downstream beyond the Enhancer/Matrix Attachment Region.18 These mutations are found in certain places along the chromosomes called VDJ coding regions (or in lay jargon, ‘hot spots’). Even within these VDJ coding regions the mutations are distributed in a non-random way. They tend to accumulate in ‘hypervariable regions’ forming antigen-binding sites. Their non-random patterns of distribution are referred to as Wu-Kabat structures.19
The targeting of somatic mutations needs to be precise. The DNA sequences that encode for variable (V) genes are separated from the constant (C) regions and the (P) regions that control the expression of the genes. This makes it possible to mutate the V-regions while conserving the normal function of the gene.20
Stopping Mutations:
We have already discussed how the presence of foreign antigens will produce an immune response. It is important to realise that the immune system cannot tolerate working at maximum capacity all the time especially if this means a high mutation rate of DNA. There needs to be a way to switch on the immune system when germs invade a body and to stop it when a suitable antibody is found.
When a gene has mutated to a point where it has binding affinity to the antigen, the mutation must stop. Further mutation would degrade the new antibody to the stage of losing affinity with the antigen and likely cause a loss of normal cell function. A ‘stop’ signal is therefore sent to the somatic mutation process that turns off the production of reverse transcription (RT) mutatorsome.21
Finding the Correct Code:
We discussed how the formulae for fighting foreign invaders are not written into our DNA. Our immune system functions differently from other parts of our body for normally the genetic code to build body parts is written into our species genome. But our immune system will not find the gene-sequences for a million antibody specificities encoded in our DNA. They have to sequence for new antibodies as each group of antigens invade. This means they must abandon the genetic formulae they believe no longer useful, and acquire new ones.
The above mutational process has only described how mutation rates change, how they are focused on certain areas and happen at a given time but not how new genetic codes are found. It might be assumed that if genes mutate quickly, there is a greater likelihood they will hit on the correct formulae for fighting an antigen by accident. The following however, looks at why it is impossible for the immune system to find correct genetic codes for fighting invading germs by chance and makes the point that this must also be a non-random process. We know that the function of cells is controlled and that new antibodies are being found for fighting foreign invaders. The argument so far appears to be that a high mutation rate is responsible for finding the correct gene-sequences but God Gametes does not believe this can happen. In the exercise that follows we will not question the many non-random aspects of the immune system but look instead at the probability of finding correct gene-sequences after the old have been mutated.
We ask you to imagine a genetic code for an antibody that is firstly mutated, then rearranged to fight an invading antigen. Let us turn back several pages to look at the sub-sections on Paul Kammerer and T.D.Lysenko. Kammerer’s is 335 words long and 1,724 characters while Lysenko’s is 199 words and 1,101 characters. Please try to imagine that the Kammerer sub-section is a gene with 1,724 base pairs coding for an antibody, while in an appropriate character role we have Lysenko an invading antigen with a total of 1,101 base pairs.
Let us now imagine that the 1,724 base pairs for Kammerer are not arranged in a way that can bind to Lysenko. Part of Kammerer’s DNA will need to be mutated and rearranged before he can fight off the invading Lysenko so let us say that 25 base pairs in Kammerer need to be mutated and the words Trofim Denisovich Lysenko (23 characters and 2 spaces) inserted in their place.
We will attempt to calculate the chance of hitting on the correct characters by reference to the standard typewriter keyboard. In this exercise we limit our keys to the 26 characters in the alphabet and one space. To calculate the probability therefore it is (1/27) to the power of 25, or (1/27) X (1/27) X (1/27) … 25 times. This gives a figure of about 600,000 million, million, million, million, million. So Kammerer has a probability of 60(-34) of hitting on the correct formula if the selective process is purely random.
It is sometimes argued that the selective process can hold in place parts of the formula while others are being found by chance. For example it is suggested that every time a correct character falls into the right place, it is saved. This of course would make it far easier than waiting for the whole formula to be found in a single try but for this to happen, Kammerer would need to know what he is looking for. He cannot hold in place correct characters without knowing the formula. For example there are a million possible invading antigens. In our example, we know the one invading is T.D.Lysenko but Kammerer does not. All he knows is that a foreign antigen has invaded and he must find an antibody to kill it. If he can find the sequence Trofim Denisovich Lysenko he can kill it and only then will he know his formula works. The process is purely random until the correct gene-sequence is found. This ‘cumulative’ approach favoured by Richard Dawkins is discussed further in the next chapter (Chapter 13) on Probability.
It could be argued that randomly finding the correct characters on a standard keyboard is far more difficult than selecting the right nucleotide by chance. There is some truth in this because there are only four nucleotides but we have allowed for 26 characters and one space on the keyboard. But the above calculation has probably understated the probability. Firstly we have allowed for the exact number of characters to be changed. If less than 25 were mutated, or more than 25, the new gene-sequence would not be a perfect fit. More importantly, we have not been concerned with where the original gene-sequence was mutated. If the mutations were random it is likely they are scattered which would almost certainly mean some areas needing to be conserved would be mutated and the area designated for the new gene-sequence left unchanged. It would be a statistical impossibility to randomly mutate the exact area where the new gene-sequence needed to be inserted.
The coding for new antibodies is not random and is not driven by natural selection. There is a non-random process driving the rate of mutations, where they are located, when they start and stop and also the sequencing of new genetic formulae.
Spuriousmonkey; I am happy to have you review my work. I do not know if you are part of the establishment and I do not care so long as you judge my work on its merits and not some pre-conceived notion of what people want to believe is correct.
A lot of the argument has focused on the fact that evolution of new species can happen very quickly and new and adaptable genes can be found by the random process of natural selection. The following focuses on the immune system where it is known that the mutation rate is high and new antibodies for fighting invading antigens are found very quickly. The God Gametes theory argues that some guiding hand is needed for the coding of new genes; whether these genes are in the immune system or for adaptable new species.
The Lamarckians
Many observers are not convinced that random mutations can be responsible for building complex body parts or for driving the evolutionary process. And the various theories espousing ‘divine creation’ have little appeal to an analytical mind. We therefore find that some form of Lamarckian driven evolution is a tempting alternative.
So believers in ‘the inheritance of acquired traits’ have never gone away. The following looks at Lamarck himself and a number of notable supporters, an interesting lot who remind us that life has both a good side and bad.
(In an effort to keep these posts brief the sections on Jean Baptiste de Lamarck and other Lamarckians Charles Darwin, his grandfather Erasmus Darwin, Paul Kammerer, T.D.Lysenko and Ted Steele have been removed but the articles on Kammerer and Lysenko are referred to in this post. For readers who are interested these extracts are taken from Chapter 12 of God Gametes which can be downloaded free from www.e-publishingaustralia.com )
Normal Mutation Rate:
Cell division and recombination is normally an extremely accurate process. It is needed for replacing old cells in our bodies with new and for carrying the genetic code from one generation to the next. A good example to demonstrate this is the histone H4 gene. It is found in almost all plants and animals and is normally coded for by the same 306 base pairs of DNA. Remarkably, almost exactly the same sequence for this gene (304 of the 306 base pairs) is found in peas and cows, lineages that most likely diverged over a billion years ago.13
This is equivalent to a single copying error in one million, million. It is obviously an extremely high fidelity rate but it overstates the normal accuracy rate for gene division and recombination. To explain this we look again at the histone H4 gene. 304 of the 306 base pairs in this gene have been copied accurately since the divergence of cows and peas. There were no doubt many more mistakes made but histone 4 is necessary for the structural engineering of chromosomes and is essential for life. Individuals that received defective copies of this gene most likely would not have survived, or if they lived would not have reproduced. Natural selection has forced conformity to a gene-sequence that worked.
Even without selection pressure however, the mutation rate is low. The probability of any one nucleotide being miscopied on any one occasion is about one in a billion. It is estimated that in the absence of natural selection it would still take 5 million generations to degrade 1% of our DNA.14
Variable Mutation Rate:
Mutations are mistakes and most are deleterious. All cancers are caused by somatic gene mutation that results in an abnormal function of an otherwise normal cell. For example skin cancers may become unresponsive to ‘growth-limiting’ or death-inducing’ signals and take on a life of their own. Cancer cells may then mutate further or create autonomous (satellite) organisms within a host body.16
But it is important to recognise the difference between somatic mutations that are harmful and the beneficial mutations that occur in the antibody variable region genes. We would expect any mistakes made in replication of DNA to be detrimental but the mutation of B lymphocytes demonstrates an extraordinarily high level of control that delivers a benefit to the living organism in which it occurs.
The somatic mutation rate in rearranged antibody variable region genes, V(D)Js, will increase during an immune response. When the antibody V-region is exposed to an antigen the selected B cells mutate its V(D)J genes at a rate of 1/1,000 to 1/10,000 bases per replication event. This is about a million times higher than the normal mutation rate of germline transmitted genes.17
Targeted Mutation:
Mutations in antibody variable region genes are precisely targeted. They are localised to the rearranged (VDJ) genes and the non-coding flanking DNA sequence and are not found upstream near the Promoter site (P) or downstream beyond the Enhancer/Matrix Attachment Region.18 These mutations are found in certain places along the chromosomes called VDJ coding regions (or in lay jargon, ‘hot spots’). Even within these VDJ coding regions the mutations are distributed in a non-random way. They tend to accumulate in ‘hypervariable regions’ forming antigen-binding sites. Their non-random patterns of distribution are referred to as Wu-Kabat structures.19
The targeting of somatic mutations needs to be precise. The DNA sequences that encode for variable (V) genes are separated from the constant (C) regions and the (P) regions that control the expression of the genes. This makes it possible to mutate the V-regions while conserving the normal function of the gene.20
Stopping Mutations:
We have already discussed how the presence of foreign antigens will produce an immune response. It is important to realise that the immune system cannot tolerate working at maximum capacity all the time especially if this means a high mutation rate of DNA. There needs to be a way to switch on the immune system when germs invade a body and to stop it when a suitable antibody is found.
When a gene has mutated to a point where it has binding affinity to the antigen, the mutation must stop. Further mutation would degrade the new antibody to the stage of losing affinity with the antigen and likely cause a loss of normal cell function. A ‘stop’ signal is therefore sent to the somatic mutation process that turns off the production of reverse transcription (RT) mutatorsome.21
Finding the Correct Code:
We discussed how the formulae for fighting foreign invaders are not written into our DNA. Our immune system functions differently from other parts of our body for normally the genetic code to build body parts is written into our species genome. But our immune system will not find the gene-sequences for a million antibody specificities encoded in our DNA. They have to sequence for new antibodies as each group of antigens invade. This means they must abandon the genetic formulae they believe no longer useful, and acquire new ones.
The above mutational process has only described how mutation rates change, how they are focused on certain areas and happen at a given time but not how new genetic codes are found. It might be assumed that if genes mutate quickly, there is a greater likelihood they will hit on the correct formulae for fighting an antigen by accident. The following however, looks at why it is impossible for the immune system to find correct genetic codes for fighting invading germs by chance and makes the point that this must also be a non-random process. We know that the function of cells is controlled and that new antibodies are being found for fighting foreign invaders. The argument so far appears to be that a high mutation rate is responsible for finding the correct gene-sequences but God Gametes does not believe this can happen. In the exercise that follows we will not question the many non-random aspects of the immune system but look instead at the probability of finding correct gene-sequences after the old have been mutated.
We ask you to imagine a genetic code for an antibody that is firstly mutated, then rearranged to fight an invading antigen. Let us turn back several pages to look at the sub-sections on Paul Kammerer and T.D.Lysenko. Kammerer’s is 335 words long and 1,724 characters while Lysenko’s is 199 words and 1,101 characters. Please try to imagine that the Kammerer sub-section is a gene with 1,724 base pairs coding for an antibody, while in an appropriate character role we have Lysenko an invading antigen with a total of 1,101 base pairs.
Let us now imagine that the 1,724 base pairs for Kammerer are not arranged in a way that can bind to Lysenko. Part of Kammerer’s DNA will need to be mutated and rearranged before he can fight off the invading Lysenko so let us say that 25 base pairs in Kammerer need to be mutated and the words Trofim Denisovich Lysenko (23 characters and 2 spaces) inserted in their place.
We will attempt to calculate the chance of hitting on the correct characters by reference to the standard typewriter keyboard. In this exercise we limit our keys to the 26 characters in the alphabet and one space. To calculate the probability therefore it is (1/27) to the power of 25, or (1/27) X (1/27) X (1/27) … 25 times. This gives a figure of about 600,000 million, million, million, million, million. So Kammerer has a probability of 60(-34) of hitting on the correct formula if the selective process is purely random.
It is sometimes argued that the selective process can hold in place parts of the formula while others are being found by chance. For example it is suggested that every time a correct character falls into the right place, it is saved. This of course would make it far easier than waiting for the whole formula to be found in a single try but for this to happen, Kammerer would need to know what he is looking for. He cannot hold in place correct characters without knowing the formula. For example there are a million possible invading antigens. In our example, we know the one invading is T.D.Lysenko but Kammerer does not. All he knows is that a foreign antigen has invaded and he must find an antibody to kill it. If he can find the sequence Trofim Denisovich Lysenko he can kill it and only then will he know his formula works. The process is purely random until the correct gene-sequence is found. This ‘cumulative’ approach favoured by Richard Dawkins is discussed further in the next chapter (Chapter 13) on Probability.
It could be argued that randomly finding the correct characters on a standard keyboard is far more difficult than selecting the right nucleotide by chance. There is some truth in this because there are only four nucleotides but we have allowed for 26 characters and one space on the keyboard. But the above calculation has probably understated the probability. Firstly we have allowed for the exact number of characters to be changed. If less than 25 were mutated, or more than 25, the new gene-sequence would not be a perfect fit. More importantly, we have not been concerned with where the original gene-sequence was mutated. If the mutations were random it is likely they are scattered which would almost certainly mean some areas needing to be conserved would be mutated and the area designated for the new gene-sequence left unchanged. It would be a statistical impossibility to randomly mutate the exact area where the new gene-sequence needed to be inserted.
The coding for new antibodies is not random and is not driven by natural selection. There is a non-random process driving the rate of mutations, where they are located, when they start and stop and also the sequencing of new genetic formulae.
river-wind
Valued Senior Member
bacteria often meet up w/ each other and exchange DNA. when this occurs, the new DNA produces proteins in the bacteria, and new abilities are bestowed apon the bacteria. this is exactly how recombinant DNA is dealt with- feed a vat of bateria strips of DNA w/ marker attached, then search for the individuals who have sucked up the DNA you gave them, and discard the rest. how do you think Insulin is made today? The Insulen gene sequence was added to bacteria, who then begane producing large quantities of insulin, even though it did nothing good for the bacteria themselves.
New genes, *if turned on*, will confer new abilities to the cell in question. successful continuation of that new ability depends on too many factors to go over right now, but the biggest ones are :1)if the new ability causes the death of the cell, the ability will obviously not continue. 2)if the new ability causes the cell to outcompete it's nextdoor neighbors, it will most likely thrive.
why does the DNA of the anti body need to bind tot he antigen?????
DNA doesn't do the binding, the proteins coded for by the DNA does. And proteins can be re-folded in multiple ways independant of the DNA that coded for them. catalists, lowest energy states, mis-transcription, etc. can all result in slightly different versions of a protein molecule. the individual that folds most of it's proteins in the right way will survive. this could come down to what food the guy is eating, and may have nothing to do with DNA mutation. It may also be that out of 6 billion people 2 have a mutation that allow for them to incorrectly fold protein x, which in turn causes them to fight off a given pathogen better then others. You don't need an entire strand of DNA to change for this system to work.
You just need alot of death to select those few who, by chance, have the item you are looking for. I will not mutate to accomidate the SARS virus is I come into contact with it. But it may be that I have a mutation which may allow me to fight SARS better then the next guy. so he dies, I live, all my kids have my mutation against SRAS, 3 generations down the road, the entire population of the world is SARS immune, and there was no hand of God *nessesary* for things to work out. I could choose to believe that God put that helpful mutation in me, but it's not required for things to work.
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Robert Jameson
Registered Senior Member
Originally posted by river-wind
why does the DNA of the anti body need to bind to the antigen?
I did not mean to imply that they did and I do not think that many people would have interpreted my words to that effect. Do you expect me to break into the “Kammerer – Lysenko” analogy with a chemistry lesson on how DNA codes for protein?
It may also be that out of 6 billion people 2 have a mutation that allow for them to incorrectly fold protein x, which in turn causes them to fight off a given pathogen better then others.
But the immune system can find new antibodies within hours.
I will not mutate to accommodate the SARS virus if I come into contact with it.
You may not find the right antibody to accommodate it but you (or your immune system) will certainly do a lot of mutating -:
From Chapter 12 of God Gametes
The somatic mutation rate in rearranged antibody variable region genes, V(D)Js, will increase during an immune response. When the antibody V-region is exposed to an antigen the selected B cells mutate its V(D)J genes at a rate of 1/1,000 to 1/10,000 bases per replication event. This is about a million times higher than the normal mutation rate of germline transmitted genes.17
Equally important however is the fact that this extraordinarily high mutation rate has been coupled to a selection process that removes deleterious mutations and saves those that are helpful. A beneficial immune response has been made possible by a non-random mutation rate and the selection of the mutant gene-sequences best able to fight the invading antigen.
Targeted Mutation:
Mutations in antibody variable region genes are precisely targeted. They are localised to the rearranged (VDJ) genes and the non-coding flanking DNA sequence and are not found upstream near the Promoter site (P) or downstream beyond the Enhancer/Matrix Attachment Region.18 These mutations are found in certain places along the chromosomes called VDJ coding regions (or in lay jargon, ‘hot spots’). Even within these VDJ coding regions the mutations are distributed in a non-random way. They tend to accumulate in ‘hypervariable regions’ forming antigen-binding sites. Their non-random patterns of distribution are referred to as Wu-Kabat structures.19
The targeting of somatic mutations needs to be precise. The DNA sequences that encode for variable (V) genes are separated from the constant (C) regions and the (P) regions that control the expression of the genes. This makes it possible to mutate the V-regions while conserving the normal function of the gene.20
Stopping Mutations:
We have already discussed how the presence of foreign antigens will produce an immune response. It is important to realise that the immune system cannot tolerate working at maximum capacity all the time especially if this means a high mutation rate of DNA. There needs to be a way to switch on the immune system when germs invade a body and to stop it when a suitable antibody is found.
When a gene has mutated to a point where it has binding affinity to the antigen, the mutation must stop. Further mutation would degrade the new antibody to the stage of losing affinity with the antigen and likely cause a loss of normal cell function. A ‘stop’ signal is therefore sent to the somatic mutation process that turns off the production of reverse transcription (RT) mutatorsome.21
Darwinism argues that all evolutionary changes are caused by mutation and that mistakes in zipping up DNA during cell division will sometimes confer an adaptive advantage and that this has been the driving force of evolution. The Darwinian paradigm needs this to be a random process. If it could be shown that mutations were not random, we need an explanation of their cause.
The above provides overwhelming evidence that mutations are not random. The rates at which they occur are not constant. The places where DNA mutates are precisely targeted and their timing is tightly controlled by the immune system. Neither Darwinism nor conventional science can provide an answer for non-random mutations.
References above point to the text below-:
Steele, Edward J.; Lindley, Robyn A. and Blanden, Robert V. Lamark's Signature, How retro genes are changing Darwin's natural selection paradigm. Allen & Unwin, Australia. 1998.
why does the DNA of the anti body need to bind to the antigen?
I did not mean to imply that they did and I do not think that many people would have interpreted my words to that effect. Do you expect me to break into the “Kammerer – Lysenko” analogy with a chemistry lesson on how DNA codes for protein?
It may also be that out of 6 billion people 2 have a mutation that allow for them to incorrectly fold protein x, which in turn causes them to fight off a given pathogen better then others.
But the immune system can find new antibodies within hours.
I will not mutate to accommodate the SARS virus if I come into contact with it.
You may not find the right antibody to accommodate it but you (or your immune system) will certainly do a lot of mutating -:
From Chapter 12 of God Gametes
The somatic mutation rate in rearranged antibody variable region genes, V(D)Js, will increase during an immune response. When the antibody V-region is exposed to an antigen the selected B cells mutate its V(D)J genes at a rate of 1/1,000 to 1/10,000 bases per replication event. This is about a million times higher than the normal mutation rate of germline transmitted genes.17
Equally important however is the fact that this extraordinarily high mutation rate has been coupled to a selection process that removes deleterious mutations and saves those that are helpful. A beneficial immune response has been made possible by a non-random mutation rate and the selection of the mutant gene-sequences best able to fight the invading antigen.
Targeted Mutation:
Mutations in antibody variable region genes are precisely targeted. They are localised to the rearranged (VDJ) genes and the non-coding flanking DNA sequence and are not found upstream near the Promoter site (P) or downstream beyond the Enhancer/Matrix Attachment Region.18 These mutations are found in certain places along the chromosomes called VDJ coding regions (or in lay jargon, ‘hot spots’). Even within these VDJ coding regions the mutations are distributed in a non-random way. They tend to accumulate in ‘hypervariable regions’ forming antigen-binding sites. Their non-random patterns of distribution are referred to as Wu-Kabat structures.19
The targeting of somatic mutations needs to be precise. The DNA sequences that encode for variable (V) genes are separated from the constant (C) regions and the (P) regions that control the expression of the genes. This makes it possible to mutate the V-regions while conserving the normal function of the gene.20
Stopping Mutations:
We have already discussed how the presence of foreign antigens will produce an immune response. It is important to realise that the immune system cannot tolerate working at maximum capacity all the time especially if this means a high mutation rate of DNA. There needs to be a way to switch on the immune system when germs invade a body and to stop it when a suitable antibody is found.
When a gene has mutated to a point where it has binding affinity to the antigen, the mutation must stop. Further mutation would degrade the new antibody to the stage of losing affinity with the antigen and likely cause a loss of normal cell function. A ‘stop’ signal is therefore sent to the somatic mutation process that turns off the production of reverse transcription (RT) mutatorsome.21
Darwinism argues that all evolutionary changes are caused by mutation and that mistakes in zipping up DNA during cell division will sometimes confer an adaptive advantage and that this has been the driving force of evolution. The Darwinian paradigm needs this to be a random process. If it could be shown that mutations were not random, we need an explanation of their cause.
The above provides overwhelming evidence that mutations are not random. The rates at which they occur are not constant. The places where DNA mutates are precisely targeted and their timing is tightly controlled by the immune system. Neither Darwinism nor conventional science can provide an answer for non-random mutations.
References above point to the text below-:
Steele, Edward J.; Lindley, Robyn A. and Blanden, Robert V. Lamark's Signature, How retro genes are changing Darwin's natural selection paradigm. Allen & Unwin, Australia. 1998.
The immune system is only making new antibodies, if a person has a gene that grants them some resistance to say bubonic plague toxin then that is a evolutionary advantage I think that’s what river-wind was getting at. How the immune systems mutates is NOT connected to evolution it has no relevance in mitotic or meiotic reproduction or in the mutation of any non-antigen gene.
Robert Jameson
Registered Senior Member
Quote from WellCookedFetus
How the immune systems mutates is NOT connected to evolution it has no relevance in mitotic or meiotic reproduction or in the mutation of any non-antigen gene.
This has been the traditional view but more recent findings suggest that new antibody genes find their way into the germline. The following quote is from page 187 of “Lamarck’s Signature”.
“Changed circumstances in the environment (e.g. food availability, new predators) could lead to changed habits and somatic changes in body structure and physiology. New immunological challenges could lead to new antibody genes in B lymphocytes. Over time, such changes could be integrated in the germline DNA. This would contribute to a new, enriched repertoire of hereditary variations upon which natural selection then acts to sort out the 'fittest for survival' and propagation of the line.” 7
Steele, Edward J.; Lindley, Robyn A. and Blanden, Robert V. Lamark's Signature, How retro genes are changing Darwin's natural selection paradigm. Allen & Unwin, Australia. 1998. page 187
How the immune systems mutates is NOT connected to evolution it has no relevance in mitotic or meiotic reproduction or in the mutation of any non-antigen gene.
This has been the traditional view but more recent findings suggest that new antibody genes find their way into the germline. The following quote is from page 187 of “Lamarck’s Signature”.
“Changed circumstances in the environment (e.g. food availability, new predators) could lead to changed habits and somatic changes in body structure and physiology. New immunological challenges could lead to new antibody genes in B lymphocytes. Over time, such changes could be integrated in the germline DNA. This would contribute to a new, enriched repertoire of hereditary variations upon which natural selection then acts to sort out the 'fittest for survival' and propagation of the line.” 7
Steele, Edward J.; Lindley, Robyn A. and Blanden, Robert V. Lamark's Signature, How retro genes are changing Darwin's natural selection paradigm. Allen & Unwin, Australia. 1998. page 187
How? There is neither proof nor even evidence that the antigen mutations enter the germ line! All you are stating is a hypothetical event. Please show me some evidence that such an event has been observed and perhaps a theory on the mechanism for such a transfer.
Robert Jameson
Registered Senior Member
Lamarck's Signature
WellCookedFetus
How? There is neither proof nor even evidence that the antigen mutations enter the germ line! All you are stating is a hypothetical event. Please show me some evidence that such an event has been observed and perhaps a theory on the mechanism for such a transfer.
The evidence for soma-to-germline transmission in the immune system is well presented in the book I referenced in my earlier post. If you do not have access to this publication then the following gives a brief outline of the mechanism by which the unmistakable signatures of somatic mutations end up in the species germline. Points 1 to 5 are direct quotes from page 10 of Lamarck’s Signature and Figure 13 can be viewed by downloading God Gametes at www.e-publishingaustralia.com (Note: A brief outline of the proposed soma-to-germline feed back loop is presented in God Gametes but those interested in this subject should refer to Lamarck’s Signature or other publications by Steele, Lindley and Blanden.)
Figure 13. (God Gametes)
1. “A diverse array of B lymphocytes exists prior to a foreign antigen entering the system. Each cell expresses on its surface membrane antibodies of one specificity. The variable (V)-region genes encode those parts of the antibody which form the antigen-combining site (as shown in Fig 13 of God Gametes or page 10 of Lamarck’s Signature). A foreign antigen binds to those B cells which have complementary antibodies-these cells are therefore 'selected' in a Darwinian manner ('clonal selection').
2. After antigen binding the B cell is activated and divides producing progeny which in turn also divide producing more identical progeny cells. A clone of identical cells expressing that antibody is produced ('clonal expansion'). Individual cells of the clone can mutate their variable region genes (somatic mutations), which can themselves be selected by antigen to produce a new clone.
3. Within cells of the clone, RNA copies of antibody V genes are made in the nucleus. Mature (processed) versions of these messenger RNA molecules are exported to the cytoplasm where they are translated into sequences of amino acids making up the protein chains of the antibody (see Appendix for details of translation of RNA sequences into an amino acid sequence).
4. RNA molecules encoding V genes (nucleus or cytoplasm) may be 'captured' by harmless endogenous RNA retroviruses (produced by the cell) and complementary DNA copies of the RNA made by the viral enzyme reverse transcriptase (these are called retrotranscripts or cDNAs).
5. Copies of the antibody V genes are then transferred to sperm or egg cells by the virus and integrated into the germline DNA for transmission to progeny organisms.”
WellCookedFetus
How? There is neither proof nor even evidence that the antigen mutations enter the germ line! All you are stating is a hypothetical event. Please show me some evidence that such an event has been observed and perhaps a theory on the mechanism for such a transfer.
The evidence for soma-to-germline transmission in the immune system is well presented in the book I referenced in my earlier post. If you do not have access to this publication then the following gives a brief outline of the mechanism by which the unmistakable signatures of somatic mutations end up in the species germline. Points 1 to 5 are direct quotes from page 10 of Lamarck’s Signature and Figure 13 can be viewed by downloading God Gametes at www.e-publishingaustralia.com (Note: A brief outline of the proposed soma-to-germline feed back loop is presented in God Gametes but those interested in this subject should refer to Lamarck’s Signature or other publications by Steele, Lindley and Blanden.)
Figure 13. (God Gametes)
1. “A diverse array of B lymphocytes exists prior to a foreign antigen entering the system. Each cell expresses on its surface membrane antibodies of one specificity. The variable (V)-region genes encode those parts of the antibody which form the antigen-combining site (as shown in Fig 13 of God Gametes or page 10 of Lamarck’s Signature). A foreign antigen binds to those B cells which have complementary antibodies-these cells are therefore 'selected' in a Darwinian manner ('clonal selection').
2. After antigen binding the B cell is activated and divides producing progeny which in turn also divide producing more identical progeny cells. A clone of identical cells expressing that antibody is produced ('clonal expansion'). Individual cells of the clone can mutate their variable region genes (somatic mutations), which can themselves be selected by antigen to produce a new clone.
3. Within cells of the clone, RNA copies of antibody V genes are made in the nucleus. Mature (processed) versions of these messenger RNA molecules are exported to the cytoplasm where they are translated into sequences of amino acids making up the protein chains of the antibody (see Appendix for details of translation of RNA sequences into an amino acid sequence).
4. RNA molecules encoding V genes (nucleus or cytoplasm) may be 'captured' by harmless endogenous RNA retroviruses (produced by the cell) and complementary DNA copies of the RNA made by the viral enzyme reverse transcriptase (these are called retrotranscripts or cDNAs).
5. Copies of the antibody V genes are then transferred to sperm or egg cells by the virus and integrated into the germline DNA for transmission to progeny organisms.”
Robert Jameson
Registered Senior Member
From God Gametes on Professor Ted (E.J.) Steele:
Recently there have been more serious challenges to Weismann’s Barrier. In 1979 Professor Ted Steele proposed his Somatic Selection hypothesis in Somatic Selection and Adaptive Evolution. He outlined the ‘soma-to-germline’ feedback loop that attempts to explain the rapid evolution of antibody genes (V-genes). This allows for the creation of new genetic variable animals as a response to the invasion of foreign microorganisms. Steele provided a credible hypothesis for the inheritance of acquired traits based on a sound scientific premise.
Initially the scientific community scorned his views but much data to emerge over the last two decades have strengthened his case. In particular the soma-to-germline feedback loop requires the rapid mutation of DNA sequences for recognising and fighting foreign invaders. Non-random mutations of DNA sequences were not thought possible but it is now widely recognised that this happens.
Soma-to-germline feedback relies on reverse transcription. Genetic information normally flows from DNA to RNA but in the late 1950s Howard Temin discovered it can also go the other way (from RNA to DNA). Steele’s hypothesis is that RNA molecules encoding for antibody V-genes may be captured by RNA ‘retroviruses’. These then make DNA copies of the antibody V-genes that are then transferred to the sperm or egg cells where they are integrated into germline DNA for transmission to the next generation.5
It is not possible to discuss the revival of Lamarckism without commenting on the controversy it generated. Following the publication of his book Steele was described by Science Digest as “The Bad boy of Biology” and in Science as a “heretic”. Many in the scientific community reviled him while others came to his defence. In New Scientist Colin Tudge wrote “and if he (Steele) is right, we are beginning a new chapter in biology”.6 Professor Robert (Bob) Blanden, Head of Immunology and Cell Biology at the Australian National University also recognised that there may be a soma-to-germline feedback mechanism operating in the immune system. He has worked with Steele on this issue and the collaboration between Blanden and Steele has been fruitful. In 1998 they, along with Robyn A. Lindley, Senior Lecturer in the School of Information Technology and Computer Science at the University of Wollongong were confident enough of their findings to publish Lamarck’s Signature that is an open challenge to Darwinian natural selection.
Recently there have been more serious challenges to Weismann’s Barrier. In 1979 Professor Ted Steele proposed his Somatic Selection hypothesis in Somatic Selection and Adaptive Evolution. He outlined the ‘soma-to-germline’ feedback loop that attempts to explain the rapid evolution of antibody genes (V-genes). This allows for the creation of new genetic variable animals as a response to the invasion of foreign microorganisms. Steele provided a credible hypothesis for the inheritance of acquired traits based on a sound scientific premise.
Initially the scientific community scorned his views but much data to emerge over the last two decades have strengthened his case. In particular the soma-to-germline feedback loop requires the rapid mutation of DNA sequences for recognising and fighting foreign invaders. Non-random mutations of DNA sequences were not thought possible but it is now widely recognised that this happens.
Soma-to-germline feedback relies on reverse transcription. Genetic information normally flows from DNA to RNA but in the late 1950s Howard Temin discovered it can also go the other way (from RNA to DNA). Steele’s hypothesis is that RNA molecules encoding for antibody V-genes may be captured by RNA ‘retroviruses’. These then make DNA copies of the antibody V-genes that are then transferred to the sperm or egg cells where they are integrated into germline DNA for transmission to the next generation.5
It is not possible to discuss the revival of Lamarckism without commenting on the controversy it generated. Following the publication of his book Steele was described by Science Digest as “The Bad boy of Biology” and in Science as a “heretic”. Many in the scientific community reviled him while others came to his defence. In New Scientist Colin Tudge wrote “and if he (Steele) is right, we are beginning a new chapter in biology”.6 Professor Robert (Bob) Blanden, Head of Immunology and Cell Biology at the Australian National University also recognised that there may be a soma-to-germline feedback mechanism operating in the immune system. He has worked with Steele on this issue and the collaboration between Blanden and Steele has been fruitful. In 1998 they, along with Robyn A. Lindley, Senior Lecturer in the School of Information Technology and Computer Science at the University of Wollongong were confident enough of their findings to publish Lamarck’s Signature that is an open challenge to Darwinian natural selection.
river-wind
Valued Senior Member
While the idea of RNA->DNA translation is well known (iut is used in the reproductive proccess of retro viruses), I have not heard of it in reference to normal animal cells. any on-line links?
viral infection/reproduction method:
http://www.biology-online.org/1/9_pathogens.htm
If anti-body code is being passed on to offspring through RNA->DNA recombination, then why was I not born immune to the Mumps? My parents got it, produced anti-bodies to become imune from re-infection, and I was born 25 odd years later. Why did I not recieve Mumps imunity from my parents?
Cells make RNA retroviruses? Why have I never heard of this? you'd think that this would be huge information, possibly requiring a re-classification of viruses! If Mammelian cells can produce viruses, then suddenly viral infection could be considered a non-sexual reproductive stratigy. it would be huge!!!
It sounds almost like there is some confusion going on here. Human Retro viruses, AFAIK, are independant organisms from the people they infect. They reproduce by landing on a human cell, and inserting their RNA. the RNA then is re-coded as DNA, and then inserted into the Cell's DNA code. the Cell, now having been successfully mind-controlled, will produce copies of the virus, until the cell gets so full that it explodes.
During the proccess of creating these new viruses, it *has* been shown that some copies oft he host cell's DNA ends up transcripted to RNA, and ends up in some copies of the virus. If that section of RNA code is by chance the right section to encode for new anti-bodies & that virus happens to infect a reproductive cell & and the viral RNA happens to not be correct so that the cell does not begin producing virus copies, and that cell ends up being the one used to produce offspring, then *maybe* the child will end up with an inherited immunity.
now this would be different than what is normally called "inherited immunity" the antibodies and such a baby recieves from the mother while in the womb and during birth. In this case, all anitbodies are form the mother *only*. What you are talking about would suggest that offspring would have similar chances to inherit anti-body DNA from both the Mother and Father.
also, this:
http://news.bbc.co.uk/1/hi/health/503025.stm
a very interesting read, I'm still going through it:
http://216.239.51.100/search?q=cach...nology4.pdf+antibody+formation&hl=en&ie=UTF-8[/url]
it appears that the above article suggest the same thing I was taught in college. Antibodys are created as generic bits, and the are made specific through encounters w/ antigens and/or other anti-bodies, in a simmilar fasison to how honey crystalizes. Honey will remain in it's semi-liquid form forever, unless it is given a crystaline template. Once a crystaline template is introduced, the honey will slowly, molecule by molecule, lacth onto it's neightbor to form a crystaline solid. Unless that template is provided, however, honey will remain in it's semi-liquid form, possibly until the point where it is destroyed.
viral infection/reproduction method:
http://www.biology-online.org/1/9_pathogens.htm
If anti-body code is being passed on to offspring through RNA->DNA recombination, then why was I not born immune to the Mumps? My parents got it, produced anti-bodies to become imune from re-infection, and I was born 25 odd years later. Why did I not recieve Mumps imunity from my parents?
Cells make RNA retroviruses? Why have I never heard of this? you'd think that this would be huge information, possibly requiring a re-classification of viruses! If Mammelian cells can produce viruses, then suddenly viral infection could be considered a non-sexual reproductive stratigy. it would be huge!!!
It sounds almost like there is some confusion going on here. Human Retro viruses, AFAIK, are independant organisms from the people they infect. They reproduce by landing on a human cell, and inserting their RNA. the RNA then is re-coded as DNA, and then inserted into the Cell's DNA code. the Cell, now having been successfully mind-controlled, will produce copies of the virus, until the cell gets so full that it explodes.
During the proccess of creating these new viruses, it *has* been shown that some copies oft he host cell's DNA ends up transcripted to RNA, and ends up in some copies of the virus. If that section of RNA code is by chance the right section to encode for new anti-bodies & that virus happens to infect a reproductive cell & and the viral RNA happens to not be correct so that the cell does not begin producing virus copies, and that cell ends up being the one used to produce offspring, then *maybe* the child will end up with an inherited immunity.
now this would be different than what is normally called "inherited immunity" the antibodies and such a baby recieves from the mother while in the womb and during birth. In this case, all anitbodies are form the mother *only*. What you are talking about would suggest that offspring would have similar chances to inherit anti-body DNA from both the Mother and Father.
also, this:
http://news.bbc.co.uk/1/hi/health/503025.stm
a very interesting read, I'm still going through it:
http://216.239.51.100/search?q=cach...nology4.pdf+antibody+formation&hl=en&ie=UTF-8[/url]
it appears that the above article suggest the same thing I was taught in college. Antibodys are created as generic bits, and the are made specific through encounters w/ antigens and/or other anti-bodies, in a simmilar fasison to how honey crystalizes. Honey will remain in it's semi-liquid form forever, unless it is given a crystaline template. Once a crystaline template is introduced, the honey will slowly, molecule by molecule, lacth onto it's neightbor to form a crystaline solid. Unless that template is provided, however, honey will remain in it's semi-liquid form, possibly until the point where it is destroyed.
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river-wind
Valued Senior Member
a few things occured to me while I was eating lunch.
1)many things in a given cell are passed on to it's decendants through means other than Nulear DNA (passing of structures in cyplasm, DNA found in chloroplasts and mitochondrion, cellular microfiliment division during cell division, etc)
2)DNA not only codes for the creation of proteins, it also codes for the rate of creation. A mutation may not just change the protein in question. it may simply increase or reduce the amount of a given protein.
3)translation inhibiting proteins can bind to mRNA strands, limiting the production of a given amino acid or protein, without effecting the DNA at all.
4)translation catalist proteins can bind to both the amino acids and the mRNA molecule, acting as a helper for tRNA. It can increase the rate of protein production w/o effecting the Nuclear DNA of the cell at all.
5) similarly to items 3 and 4, inhibitor proteins can bind to receptor cites on anit-bodys, preventing them from binding to their particular antigen, or possibly allowing them to bind to a different antigen.
Proteins first fold into alpha or beta forms (or a mixture of both), then they fold into 3-d shapes, the external-facing atoms allowing and defining the available receptor sites for binding. This limits the types of other molecules than can be bound, and by binding to one receptor site, the rest of the protein is twisted by the atomic interations with the new molecule, causing many of the other receptor site to change. So even when no protiens are destoryed or created, a simply binding of a secondary molecule can change the receptor sites of the anti-bodies, and therefor alter their function.
1)many things in a given cell are passed on to it's decendants through means other than Nulear DNA (passing of structures in cyplasm, DNA found in chloroplasts and mitochondrion, cellular microfiliment division during cell division, etc)
2)DNA not only codes for the creation of proteins, it also codes for the rate of creation. A mutation may not just change the protein in question. it may simply increase or reduce the amount of a given protein.
3)translation inhibiting proteins can bind to mRNA strands, limiting the production of a given amino acid or protein, without effecting the DNA at all.
4)translation catalist proteins can bind to both the amino acids and the mRNA molecule, acting as a helper for tRNA. It can increase the rate of protein production w/o effecting the Nuclear DNA of the cell at all.
5) similarly to items 3 and 4, inhibitor proteins can bind to receptor cites on anit-bodys, preventing them from binding to their particular antigen, or possibly allowing them to bind to a different antigen.
Proteins first fold into alpha or beta forms (or a mixture of both), then they fold into 3-d shapes, the external-facing atoms allowing and defining the available receptor sites for binding. This limits the types of other molecules than can be bound, and by binding to one receptor site, the rest of the protein is twisted by the atomic interations with the new molecule, causing many of the other receptor site to change. So even when no protiens are destoryed or created, a simply binding of a secondary molecule can change the receptor sites of the anti-bodies, and therefor alter their function.
Robert Jameson
Registered Senior Member
Quote from River wind
While the idea of RNA->DNA translation is well known (it is used in the reproductive process of retro viruses), I have not heard of it in reference to normal animal cells. any on-line links?
I researched Steels book because his findings are supportive of the God Gametes concept but as an amateur scientist I am not well qualified to advise you in this area. Ted Steele was recently dismissed from the University of Wollongong for public comments he made about soft marking and his scientific work has unfortunately been put on hold. I believe however Professor Bob Blanden is still Head of Immunology and Cell Biology in the John Curtin School of Medical Research, Australian National University. I am sure you could find on-line links to their work through the ANU (Australian National University, Canberra) But their work is well presented in Lamarck’s Signature ISBN 1-86448-796-8
From God Gametes
But it seems life for Lamarckians is destined to be controversial for Steele has now become embroiled in an issue unrelated to biology. In early 2001 dozens of academics contacted the Sydney Morning Herald (Australia) with examples of ‘soft marking’ but Steele was the only one to allow his name to be published. As a result he was dismissed from the University of Wollongong without pay or warning. Support for him came from all around the world and the National Tertiary Education Union (NTEU) took the UOW to court. The Australian Federal court ruled in his favour but the university vice-chancellor appealed. The university lost its appeal and has made a conditional offer of reinstatement. At time of writing Steele has not accepted the terms of reinstatement and is considering further legal action against the University.8
http://www.i-sis.org.uk/steele4.php
While the idea of RNA->DNA translation is well known (it is used in the reproductive process of retro viruses), I have not heard of it in reference to normal animal cells. any on-line links?
I researched Steels book because his findings are supportive of the God Gametes concept but as an amateur scientist I am not well qualified to advise you in this area. Ted Steele was recently dismissed from the University of Wollongong for public comments he made about soft marking and his scientific work has unfortunately been put on hold. I believe however Professor Bob Blanden is still Head of Immunology and Cell Biology in the John Curtin School of Medical Research, Australian National University. I am sure you could find on-line links to their work through the ANU (Australian National University, Canberra) But their work is well presented in Lamarck’s Signature ISBN 1-86448-796-8
From God Gametes
But it seems life for Lamarckians is destined to be controversial for Steele has now become embroiled in an issue unrelated to biology. In early 2001 dozens of academics contacted the Sydney Morning Herald (Australia) with examples of ‘soft marking’ but Steele was the only one to allow his name to be published. As a result he was dismissed from the University of Wollongong without pay or warning. Support for him came from all around the world and the National Tertiary Education Union (NTEU) took the UOW to court. The Australian Federal court ruled in his favour but the university vice-chancellor appealed. The university lost its appeal and has made a conditional offer of reinstatement. At time of writing Steele has not accepted the terms of reinstatement and is considering further legal action against the University.8
http://www.i-sis.org.uk/steele4.php