Topic: Ain't No Good Mutations Here (Read 1250 times)
I listened to a segment on NPR the other day on this. Surprising not more of us are sick, for according to our DNA we're fucked.
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Beneficial Mutations?
Beneficial mutations in any sense are extremely rare in our world today. Those that can be considered "beneficial" in specific situations always involve the loss of some function and generally result in the deterioration of the creature's overall health. For instance, sickle-cell anemia is considered a beneficial mutation because it protects many Africans against malaria, yet sickle-cell anemia itself is a very serious disease.
It's all tradeoffs, some mutations are bad under circumstances that organism has right now has but would be beneficial under others. People more susceptible for diabetes are more resilient to starvation once very beneficial today for half of the world not so important now etc.Beneficial mutations in any sense are extremely rare in our world today. Those that can be considered "beneficial" in specific situations always involve the loss of some function and generally result in the deterioration of the creature's overall health. For instance, sickle-cell anemia is considered a beneficial mutation because it protects many Africans against malaria, yet sickle-cell anemia itself is a very serious disease.
Quote
If the evolutionary model of origins were reality, we should expect to see a number of beneficial mutations that were the result of added information. Instead, it appears that we each receive a damaged, deteriorating version of a once excellently engineered, fully functioning genetic code.
Or those without beneficial (under their circumstances) mutations would find themselves dead after few generations and those with them will be known as normal with mostly fresh and somewhat harmless mutations.Quote
‘This disparity would have worked against producing the code by natural selection in the first place. An example of this method of degradation is illustrated by the words "amino acid" which would be changed to "amano acad," then to "amaao aaad," and finally to "aaaaa aaaa" if the letter "a" dominated. Another mutation can change the "a'" back to an "m" or another letter but, in this illustration, the overall trend would be to the letter "a'" and would eventually stabilize largely at a set of "a" letters with a few converting back to the other letters from time to time.'
Or "aaaaa aaaa" will be non existent because their "amaao aaad," parents will have many instant death mutations.We live in quite exciting times btw. price for full genome sequencing is falling faster than price of single transistor on IC
http://blogs.discovermagazine.com/sciencenotfiction/2010/06/25/genomics-has-bad-news-for-the-singularity/#.UNPBktFx1Mg
By the way can you propose some alternative to the theory of evolution that would be useful for predicting future and would fit to data?
Article Source
AIN'T NO GOOD MUTATIONS HERE
Most of the mutations in our DNA are only 5,000-10,000 years old, according to a study by the Exome Sequencing Project at the National Institutes of Health. That's a good thing, then, because a recent article in the American Journal of Human Genetics says we're all rife with genetic mistakes, and it's hard to find any that have benefited us at all. We might not have been able to handle many more years of DNA deterioration.
Researchers on the 1000 Genome Project used genetic data from 179 individuals and found that all had between 40 and 110 potentially disease-causing mutations in their DNA. The individuals had 281-515 actual substitutions each, but the trouble only really started when both parents had passed on a mutation in the same gene. The researchers, estimated, "(about)400 damaging variants and (about)2 bona fide disease mutations per individual."
Not every damaging mutation shows up immediately. Some might increase one's chances for heart disease. Another might simply weaken the kidneys or slow the production of insulin. The body is also good at covering for an improperly functioning gene, using backup systems or compensating in some way when a gene isn't doing its job right. When all else fails, though, mutations tend to cause disease.
The researchers have been working to develop and fill out the Human Gene Mutation Database with the more dangerous genetic defects, giving doctors a tool in diagnosing inherited diseases. It is distinctly noticeable that while some mutations are not as destructive as others, the researchers are not developing a database of all the improvements made by random changes in the genetic code.
Mutations and Evolution:
In order for evolution to work on a grand scale, changing one family of creatures into another family of creatures, beneficial mutations must appear to add new information to the genetic code. Without mutations, there are no major evolutionary steps. Yes, the genetic information already existing within a species can vary due to natural selection, but this always strains out information; it never adds new, previously non-existent coding to the genome. Yet, while Darwinists claim that rare, beneficial mutations do exist, the math shows that random mutations result in the net removal of functional programming from the genetic code rather than adding to it.
Beneficial Mutations?
Beneficial mutations in any sense are extremely rare in our world today. Those that can be considered "beneficial" in specific situations always involve the loss of some function and generally result in the deterioration of the creature's overall health. For instance, sickle-cell anemia is considered a beneficial mutation because it protects many Africans against malaria, yet sickle-cell anemia itself is a very serious disease.
Sickle cell anemia is a genetic disorder in which the red blood cells take a long, thin, sickle-like shape instead of the round donut shape of a healthy red blood cell. While this deformity prevents the body from carrying malaria, protecting people in high-malaria areas from dying from the disease, the sickle cell anemia is itself dangerous. Sickle cell blood cells carry less oxygen than normal cells. The misshapen cells also tend to clump up and get stuck in blood vessels, leading to infection and organ damage. Sickle-shaped cells often die after only 10-20 days, while healthy red blood cells live an average of 120 days before they die.
People with the mutation from only one parent can live normally because they have the genes from the other parent still producing correctly-shaped blood cells. The sickle-shaped cells are also produced, but the body doesn't have to depend on them. Those with the sickle cell mutation from both parents, however, have a problem. Their body functions in a state of constant oxygen deprivation, and it struggles to produce enough red blood cells to replace the dying ones, greatly reducing general health. The life expectancy for men with sickle-cell anemia is only 42 years.
If sickle cell anemia is the best beneficial mutation out there, our hopes for evolving through mutations are empty and doomed to disappointment. It is true that bacteria that develop a specific dysfunction may survive in the presence of antibiotics, but those same bacteria are still weaker and quicker to die when exposed to the outside world. A person with no arms may be less likely to contract a virus, because he can't rub his nose with infected fingers, but few people will argue that it's better to go around in life without arms. The fact is, examples of truly beneficial mutations are massively lacking.
Loss Of Information:
The real trouble with mutations takes us down to the DNA level. We learn in high school biology that our genetic code is made up of DNA, long strands of the nucleotide bases adenine, guanine, thymine, and cytocine – A G T and C for short. These four bases provide the digital code for our system, similar to the way 0s and 1s make up binary code for computers. In the cell, during the process of translation, these nucleotides get read in groups of three, called codons. Each codon is like a little train car of three letters that code for an amino acid, which go on to make up proteins. For instance, the codon AAA codes for the amino acid lysine and TGG codes for the amino acid tryptophan. (During transcription, thymine is replaced with uracil - U - to make the codon UGG.)
There isn't just one code for many amino acids, though. Lysine can also be coded by AAG. Cysteine can be coded by both TGT and TGC, and the amino acids serine, arginine, and leucine all have six possible codes. Other proteins on the other hand, like tryptophan, only have that single code available to make them.
This causes a problem for the statistics of mutations. If there are errors in the transcription process and letters are not copied correctly (a source for mutations), certain amino acids are going to be favored over others. For instance, if AAG is accidentally transcribed as AAA, it won't necessarily harm the body because AAA still codes for lysine (provided the cell has high enough levels of tRNA for the alternate codon). If TGG for tryptophan gets changed to TTG, though, it will cause leucine to be made. If TAA gets changed to TTA, it will also make leucine and if CAA for Glutamine gets turned to CTA, again leucine benefits. Statistically, an error is highly likely to accidentally make leucine and highly unlikely to make tryptophan.
If we have been evolving for millions of years, we would expect to see a high ratio of serine, arginine, and leucine codes, because statistically mutations would favor making these three amino acids. As mutations accumulated over the generations, we'd expect these codes to dominate, making it rare to ever see tryptophan and leading to a loss of information in the genetic code. Dr. Jerry Bergman writes:
‘This disparity would have worked against producing the code by natural selection in the first place. An example of this method of degradation is illustrated by the words "amino acid" which would be changed to "amano acad," then to "amaao aaad," and finally to "aaaaa aaaa" if the letter "a" dominated. Another mutation can change the "a'" back to an "m" or another letter but, in this illustration, the overall trend would be to the letter "a'" and would eventually stabilize largely at a set of "a" letters with a few converting back to the other letters from time to time.'
Creature Coding:
There are built-in mechanisms to correct errors, at least, and mutations do rarely slip through. The human race has fought through the past 5,000-10,000 years of slow disintegration fairly well. The self-correcting mechanisms would have had to have been in place at the beginning, else the gene code's deterioration would have been rapid and destructive before these self-correcting mechanisms evolved.
It is also valuable to note that organisms considered closely related can favor different codes for the same amino acid. E coli uses AAA to code for lysine 75 percent of the time, but only uses AAG one fourth of the time. Another bacteria, Rhodobacter, uses AAG 75 percent of the time - just the opposite. These two organisms, which are supposed to be more closely related, don't use codes in the same proportions, while the human being and fruit fly (not closely related) both use CTG to code for leucine just over 40 percent of the time.
Studies have also shown there to be far more deletions than insertions into the DNA code. In their article on the DNA loss in Drosophila (fruit flies) in the journal Gene in 1997, Petrov and Hartl found a "virtual absence of insertions and a remarkably high incidence of large deletions." In their article on nucleotide substitution, insertion and deletion in the human genome in Nucleic Acids Research in 2003, Zhang and Gerstein found the mutational deletion rate of base pairs to be three times as high as the insertion rate. Once again, this results in a net loss of information rather than the net gain necessary for us to have evolved from lower lifeforms.
Mutation Hot Spots
Mutations also do not occur randomly throughout the DNA code, but are generally localized in certain spots. For instance, the CG dinucleotide has a much higher chance of being involved in a mutation than any other dinucleotide – 12 times as high according to Jorde, Carey and White in Medical Genetics(1997). Of 400 codon mutations mapped on the human tumor suppressor antioncogene gene just over 91 percent occurred in four specific codons. Some of these "hot spots" result from passing around the same mutation through inheritance, but most are truly hot spots in which certain parts of the genetic code are more prone to mutation than other parts.
The basic point is this: mutation is not evenly, randomly distributed throughout the genome, which we'd expect if mutations had brought about all the precise structures in living things today.
Genome Deterioration:
Mutations are well known to cause diseases like cystic fibrosis, hemophilia, inherited osteoporosis and literally more than 1000 others. Finding descriptions of deleterious mutations takes less than half a minute. Finding truly beneficial mutations is a headache, and even the so-called beneficial mutations are due to net loss of information that, while helping an organism survive in a very specific situation, also lead to the weakening of the organism's overall health.
If the evolutionary model of origins were reality, we should expect to see a number of beneficial mutations that were the result of added information. Instead, it appears that we each receive a damaged, deteriorating version of a once excellently engineered, fully functioning genetic code.
AIN'T NO GOOD MUTATIONS HERE
Most of the mutations in our DNA are only 5,000-10,000 years old, according to a study by the Exome Sequencing Project at the National Institutes of Health. That's a good thing, then, because a recent article in the American Journal of Human Genetics says we're all rife with genetic mistakes, and it's hard to find any that have benefited us at all. We might not have been able to handle many more years of DNA deterioration.
Researchers on the 1000 Genome Project used genetic data from 179 individuals and found that all had between 40 and 110 potentially disease-causing mutations in their DNA. The individuals had 281-515 actual substitutions each, but the trouble only really started when both parents had passed on a mutation in the same gene. The researchers, estimated, "(about)400 damaging variants and (about)2 bona fide disease mutations per individual."
Not every damaging mutation shows up immediately. Some might increase one's chances for heart disease. Another might simply weaken the kidneys or slow the production of insulin. The body is also good at covering for an improperly functioning gene, using backup systems or compensating in some way when a gene isn't doing its job right. When all else fails, though, mutations tend to cause disease.
The researchers have been working to develop and fill out the Human Gene Mutation Database with the more dangerous genetic defects, giving doctors a tool in diagnosing inherited diseases. It is distinctly noticeable that while some mutations are not as destructive as others, the researchers are not developing a database of all the improvements made by random changes in the genetic code.
Mutations and Evolution:
In order for evolution to work on a grand scale, changing one family of creatures into another family of creatures, beneficial mutations must appear to add new information to the genetic code. Without mutations, there are no major evolutionary steps. Yes, the genetic information already existing within a species can vary due to natural selection, but this always strains out information; it never adds new, previously non-existent coding to the genome. Yet, while Darwinists claim that rare, beneficial mutations do exist, the math shows that random mutations result in the net removal of functional programming from the genetic code rather than adding to it.
Beneficial Mutations?
Beneficial mutations in any sense are extremely rare in our world today. Those that can be considered "beneficial" in specific situations always involve the loss of some function and generally result in the deterioration of the creature's overall health. For instance, sickle-cell anemia is considered a beneficial mutation because it protects many Africans against malaria, yet sickle-cell anemia itself is a very serious disease.
Sickle cell anemia is a genetic disorder in which the red blood cells take a long, thin, sickle-like shape instead of the round donut shape of a healthy red blood cell. While this deformity prevents the body from carrying malaria, protecting people in high-malaria areas from dying from the disease, the sickle cell anemia is itself dangerous. Sickle cell blood cells carry less oxygen than normal cells. The misshapen cells also tend to clump up and get stuck in blood vessels, leading to infection and organ damage. Sickle-shaped cells often die after only 10-20 days, while healthy red blood cells live an average of 120 days before they die.
People with the mutation from only one parent can live normally because they have the genes from the other parent still producing correctly-shaped blood cells. The sickle-shaped cells are also produced, but the body doesn't have to depend on them. Those with the sickle cell mutation from both parents, however, have a problem. Their body functions in a state of constant oxygen deprivation, and it struggles to produce enough red blood cells to replace the dying ones, greatly reducing general health. The life expectancy for men with sickle-cell anemia is only 42 years.
If sickle cell anemia is the best beneficial mutation out there, our hopes for evolving through mutations are empty and doomed to disappointment. It is true that bacteria that develop a specific dysfunction may survive in the presence of antibiotics, but those same bacteria are still weaker and quicker to die when exposed to the outside world. A person with no arms may be less likely to contract a virus, because he can't rub his nose with infected fingers, but few people will argue that it's better to go around in life without arms. The fact is, examples of truly beneficial mutations are massively lacking.
Loss Of Information:
The real trouble with mutations takes us down to the DNA level. We learn in high school biology that our genetic code is made up of DNA, long strands of the nucleotide bases adenine, guanine, thymine, and cytocine – A G T and C for short. These four bases provide the digital code for our system, similar to the way 0s and 1s make up binary code for computers. In the cell, during the process of translation, these nucleotides get read in groups of three, called codons. Each codon is like a little train car of three letters that code for an amino acid, which go on to make up proteins. For instance, the codon AAA codes for the amino acid lysine and TGG codes for the amino acid tryptophan. (During transcription, thymine is replaced with uracil - U - to make the codon UGG.)
There isn't just one code for many amino acids, though. Lysine can also be coded by AAG. Cysteine can be coded by both TGT and TGC, and the amino acids serine, arginine, and leucine all have six possible codes. Other proteins on the other hand, like tryptophan, only have that single code available to make them.
This causes a problem for the statistics of mutations. If there are errors in the transcription process and letters are not copied correctly (a source for mutations), certain amino acids are going to be favored over others. For instance, if AAG is accidentally transcribed as AAA, it won't necessarily harm the body because AAA still codes for lysine (provided the cell has high enough levels of tRNA for the alternate codon). If TGG for tryptophan gets changed to TTG, though, it will cause leucine to be made. If TAA gets changed to TTA, it will also make leucine and if CAA for Glutamine gets turned to CTA, again leucine benefits. Statistically, an error is highly likely to accidentally make leucine and highly unlikely to make tryptophan.
If we have been evolving for millions of years, we would expect to see a high ratio of serine, arginine, and leucine codes, because statistically mutations would favor making these three amino acids. As mutations accumulated over the generations, we'd expect these codes to dominate, making it rare to ever see tryptophan and leading to a loss of information in the genetic code. Dr. Jerry Bergman writes:
‘This disparity would have worked against producing the code by natural selection in the first place. An example of this method of degradation is illustrated by the words "amino acid" which would be changed to "amano acad," then to "amaao aaad," and finally to "aaaaa aaaa" if the letter "a" dominated. Another mutation can change the "a'" back to an "m" or another letter but, in this illustration, the overall trend would be to the letter "a'" and would eventually stabilize largely at a set of "a" letters with a few converting back to the other letters from time to time.'
Creature Coding:
There are built-in mechanisms to correct errors, at least, and mutations do rarely slip through. The human race has fought through the past 5,000-10,000 years of slow disintegration fairly well. The self-correcting mechanisms would have had to have been in place at the beginning, else the gene code's deterioration would have been rapid and destructive before these self-correcting mechanisms evolved.
It is also valuable to note that organisms considered closely related can favor different codes for the same amino acid. E coli uses AAA to code for lysine 75 percent of the time, but only uses AAG one fourth of the time. Another bacteria, Rhodobacter, uses AAG 75 percent of the time - just the opposite. These two organisms, which are supposed to be more closely related, don't use codes in the same proportions, while the human being and fruit fly (not closely related) both use CTG to code for leucine just over 40 percent of the time.
Studies have also shown there to be far more deletions than insertions into the DNA code. In their article on the DNA loss in Drosophila (fruit flies) in the journal Gene in 1997, Petrov and Hartl found a "virtual absence of insertions and a remarkably high incidence of large deletions." In their article on nucleotide substitution, insertion and deletion in the human genome in Nucleic Acids Research in 2003, Zhang and Gerstein found the mutational deletion rate of base pairs to be three times as high as the insertion rate. Once again, this results in a net loss of information rather than the net gain necessary for us to have evolved from lower lifeforms.
Mutation Hot Spots
Mutations also do not occur randomly throughout the DNA code, but are generally localized in certain spots. For instance, the CG dinucleotide has a much higher chance of being involved in a mutation than any other dinucleotide – 12 times as high according to Jorde, Carey and White in Medical Genetics(1997). Of 400 codon mutations mapped on the human tumor suppressor antioncogene gene just over 91 percent occurred in four specific codons. Some of these "hot spots" result from passing around the same mutation through inheritance, but most are truly hot spots in which certain parts of the genetic code are more prone to mutation than other parts.
The basic point is this: mutation is not evenly, randomly distributed throughout the genome, which we'd expect if mutations had brought about all the precise structures in living things today.
Genome Deterioration:
Mutations are well known to cause diseases like cystic fibrosis, hemophilia, inherited osteoporosis and literally more than 1000 others. Finding descriptions of deleterious mutations takes less than half a minute. Finding truly beneficial mutations is a headache, and even the so-called beneficial mutations are due to net loss of information that, while helping an organism survive in a very specific situation, also lead to the weakening of the organism's overall health.
If the evolutionary model of origins were reality, we should expect to see a number of beneficial mutations that were the result of added information. Instead, it appears that we each receive a damaged, deteriorating version of a once excellently engineered, fully functioning genetic code.
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