Post by Randall Lord on Mar 7, 2007 17:41:08 GMT -5
www.rationalresponders.com/forum/yellow_number_five/evolution_of_life/5274
Each one of the twenty two numbers represents one fallacious ID/Creation argument. Every one is ridiculous and deserves debunking. Let us start with the most basic stupidity…
Fallacy #1: Evolution is blind luck
If a person says this, you might as well just walk out and leave. This most basic of errors shows that they have no understanding of basic science. Evolution is a carefully guided process.
Organisms adapt to their environment through natural selection, meaning that the environmental factors both cull the herd and remove organisms with unfavorable traits, and propagate those with favorable traits. The mechanism for this is the second rule of evolution: Evolution is brought about by genetic mutation. An organism cannot adapt to its environment per se. It is the genes that must adapt, and that process takes millions of years.
The next rule is that the determinate of what constitutes an advantage is the environment. The rest of it is really simple, Evolutionary models study this axiom because it is complex. An environment includes lots of factors like other animals, temperature, gas concentration, climate etc. etc. This axiom is the driver of evolution, the guide, Adam Smith’s invisible hand. Genetic mutation is random. It is up to the environment to nurture useful genes and ensure they get passed on, and to eliminate poor genes. This is the fundamental rule of natural selection.
This incredibly ridiculous error, to state that evolution is luck, is a confusion of genetic mutation which is luck, and evolution which is the process that selects the genes and makes sense of the randomness of mutation.
Fallacy #2 Advantageous mutation is impossible
This one is ridiculous. To understand why, a short overview of genetic mechanisms and biochemistry is necessary.
DNA is made up of polymerated strings of bases, which are nucleotides bound to sugar-phosphate backbones. DNA has two functions:
Holds the code to create various proteins from amino acids
Regulating the rate of producing proteins: By definition, one gene is a string of nucleotides that codes for one protein
The language of DNA is base-pairs. DNA is entirely comprised of four molecules. Cytosine, Guanine, Adenine and Thymine. These are the nucleotides. The nucleotides are complementary. Like magnets, they will only fit to a certain opposite. G fits with C and A fits with T (A also fits with U, Uracil, but that is an RNA base). So there are only four possible base-pairs: CG, GC, TA and AT. But these four pairs will dictate every single protein imaginable.
Chemistry has absolutely everything to do with nucleic pairing. A fits with T and C with G. They are dipolar covalents. One side is slightly positively charged, the other negative. They will bind to each other much more easily if they correspond. Trying to fit A with C or T with G is sort of like trying to force two north magnets together. This kind of error can only happen in an abundance of adenosine triphosphate. It's like protons. Have you ever wondered why they don’t repel? They smash into each other with such force that they bind (gluons). (DNA doesn’t smash into each other of course, but you get the idea. So if you have a CGAT on one string, you will of course have GCTA on the other. This is called complementary encoding, and is the basis of DNA.
There are four ways that DNA can innovate.
Intragenic mutation: Errors during mitosis can swap base-pairs around, creating new strings of bases, and a new gene
Segment Shuffling: Two different genes can recombine and form two new hybrids
Duplication error: Sometimes during mitosis, a parent cell will by accident only pass part of it’s genome to the daughter cell, thus it retains a redundant copy of a gene string. This copy is completely free to mutate based on random frequency probability.
Horizontal/vertical Transfer: During sexual reproduction, organisms exchange genes. If the organism is a diploid meaning that it’s offspring has the code of two parents, then it’s offspring will have a completely new genome, combing both parents. This is the most successful method of innovation. Or an organism, particularly prokaryotes, can actually exchange genes by means of one actually encoding a packaged gene for another, which incorporates it into the genome. This is horizontal transfer, a tool that Eukaryota do not have
There are two types of genes. Introns and exons, which have these separate functions. Exons code for proteins. Introns are mostly junk or redundant, but they flank all the exons. Sometimes they are just punctuation, dictating where a gene starts and stops, but their most important function by far is to regulate the speed of protein transcription, a mechanism we will look at it more detail later. Exons dictate how a protein will be assembled. They do this because a protein is essentially a string of amino acids or a polypeptide. Therefore, exons dictate the order of amino acids in a protein. They do this by representing each amino acid with a codon. A codon is three nucleotides. Three nucleotides make up an amino acid. There are 20 possible amino acids, but 64 possible codons, therefore, exons are highly sensitive. They are also sensitive because they are ordered very precisely. For instance, let’s look at a simple string of three codons in a gene: AGG CTT GCC. Now let’s assume that an extra base is accidentally inserted (Like a G for example). The new string would be totally different, it would look like this. GAG GCT TTG CC, so every base would be shifted down one, and the entire gene would change. This would be completely devastating. This is why DNA repair mechanisms quickly target such errors.
On the other hand, Introns, which are not so sensitive or precisely executed, or are sometimes just junk or redundant, mutate based solely on random frequency. As there are 44 codons that don't correspond to an amino acid, these are used in introns. Therefore, the next axiom of evolution is that evolution is driven by the Introns. Obviously it is more complicated, Introns can become exons during shuffling/shifting, and exons can become Introns, and sometimes exons can be mutated harmlessly, so long as the mutation changes only a tiny chunk of the gene, but this rule still applies.
Now that you understand genetic mutation mechanisms, this can be applied to how advantage mutation works.
Intron mutation can change more than just transcription rate. It can change the protein fold. So, in all likelihood an organism won’t end up with one enzyme or protein morphing into another, but an identical polypeptide folding into a new enzyme. Only exon mutation will "change" an enzyme because it will change some codons, thereby changing the protein string order. From a probability standpoint, the odds of gaining a useful mutation because you can fold a protein in a new way vastly outweigh the possibility that you can get from producing a new protein. Mutations can have chain reactions on the cycle. Same string but different protein will produce a different catalytic function therefore will change another intron somewhere else down the line, or perhaps change an exon and make a new protein which, because it is bound to the cycle, not random, will be useful. If mutations operated independently, and outside the cycle, evolution would never get off the ground.
It can be understand like this:
A useless mutation occurs: Nothing happens
A bad mutation occurs: The cell dies, or the error is targeted because it is disrupting the cycle
A good mutation occurs: A new protein, rate of transcription or fold function is made. This is useful. It alters the cycle, producing a knock on effect.
For a mutation to occur which can be preserved, junk must be turned into non-junk. It is really easy to play with the introns. The prokaryotes that are the basis of life have almost no junk DNA. It is evident that such small organisms evolved to have conservative genomes. They have useful introns. It may seem extremely unreasonable in terms of probability but DNA mutates all the time. If the shift is Duplicate error, a popular method, then the gene advantage can be conserved, because it is a redundant piece. Evolution is just mathematics. As long as a gene exists, it will fight to survive...at the chemical level there exists a ruthless primal battle in which the best of the best are constantly being selected, and the weak crushed. The only phenotype affecting genes that are conserved are the ones that affect reproductive capacity. That will cause it to be conserved and cumulatively mutated upon. This is the mathematics of evolution.
Genetic drift drives evolution. Some mutations are good, some are bad, most do nothing, but through the endless cycles, organisms evolve. The analogy I like to use is the telemarketer. About 90% of people hang up on them, but the 10% who say yes make the enterprise quite profitable.
The statement advantage mutation is impossible is a confusion of possibility and probability. Advantage mutation almost never happens…the operative word being ALMOST. But if you have mutations working at quantum speed and three billion years on your hand, your odds improve dramatically.
The knock-on effect is a good demonstrator. All proteins do only one thing, they act as a catalyst for the body's catabolic chemical reactions. Without proteins, you would have to set yourself on fire to release enough energy to perform respiration. This is obviously not practical. All proteins lower the activation energy for a chemical reaction by providing an active site which works like a lock and key model. The chemical fits into the protein receptor and is broken into smaller molecules. Therefore, one can imagine that a different fold will mean that protein will have a different catabolic function which could offer a significant advantage if it allows an organism to synthesize a new chemical. The most effective way to do this would probably be base-pair swap exon mutation, which will only change a small chunk of an exon. Normally, the amino confirmation will predispose a protein to fold in a certain way, although this process is not understood (that would be the Levinthal Paradox). Natural selection, it seems, has selected a chemical interaction set which encourages the protein to fold, because in it's primary and secondary state, it is useless.
Protein folding is also a useful demonstrator of life's autoregulatory weirdness. They fold into elegant shapes after being translated from mRNA only for a tiny piece of it to serve as an active site. The hemoglobin molecule is the bizarre case and point. It is a colossal macromolecular protein snugly wrapping a single haemite (iron). This is somewhat akin to building a nuclear powered transformer to plug in a lamp.
There are 100 nucleic acids and 300 amino acids that exist in nature, we use only 4 and 22. The sugars and phosphates snap together to form the base backbone in the exact same way that nucleic acids bond together. From a chemical standpoint, the phosphorylate-saccharide (ribose)-nucleic acid structure is sensible. There are 100 nucleic acids and 300 amino acids that exist in nature, we use only 4 and 22. There is no reason why life could not be based on other amino acids and nucleic acids. The sugars and phosphates snap together to form the base backbone in the exact same way that nucleic acids bond together. From a chemical standpoint, the phosphorylate-saccharide (ribose)-nucleic acid structure is sensible.
We can look at the knock-on effect with respect to folding like this:
1) A small mutation changes a few codons
2) A different protein is made with a new fold
3) This catalyzes a chemical in a different fashion, most likely a new product
4) This new product has a different effect on the cell membrane receptors, which keep up the autocatalytic cycle. It causes a different command to be followed, as transcription is driven when a stimuli causes a protein to bind to the introns that flank the necessary exon.
Transgenic technology has revealed that changing a gene can start making a gene down the line do bizarre things. Why? Simple. Genes can control each other. The knock-on is established by introns controlling exons which in turn produce proteins which control introns which control exons which… you understand. If evolution operated like individual genes doing individual things, it would not get on the ground.
Knock-on effects work all across the genome. After all, what do genes do, they produce proteins, or they regulate the production of proteins. What do those proteins do? Well...everything: The big functions are of course:
-Catabolism of biochemical families (nucleotides, coenzyme factors, carbohydrates)
-Anabolism (glycogen synthesis, lipid synthesis)
-RNA synthesis control
-Ion channels and membranes (cell membranes, nerve membranes, particularly oligolipoproteins for myelin) , transport mechanisms including inorganic transport, ion flux and carrying
-Exocrine systems and secretory pathways/chemical production
-endocrine systems and hormone control Autocatalysis
-Maintenance of cell signal transduction and energy release metabolic pathways
The thing to notice about all of these is they are all dependant on biochemical triggers. You change one thing, you change a cascade. Making a new ion channel will change the electrochemical gradient or allow a different material influx, which will affect how protein receptors bind to introns. A new ion channel could trigger a hitherto unused intron. There are so many complex factors to genetic evolution, it is not a clear cut process.
The discovery of genes was probably one of the most important in the history of science. Before genomic sequencing, the human body or indeed any organism or indeed a single celled organism seemed unbearably complex. Of course, with the advent of new molecular biology techniques that was swept away. Everything can be explained in terms of metabolic pathways building macromolecules with remarkable properties. There are only thirteen families of Biochemicals (Terpenoids, Flavanoids, Carotenoids, Polyketides, Alkaloids Peptides, Polypeptides, Amino Acids, Nucleic Acids, Steroids, Enzyme Cofactors, Carbohydrates, Lipids and Tetrapyrroles). Everything can be explained in terms of these, and the manufacture, regulation, secretion and synthesis of these…can be explained by DNA. This explains everything from simple sugar metabolism all the way to the Progenitor…the stem cell with the potential to make a human body.
Fallacy #3 The probability of advantage mutation taking place is too low.
This error is almost exactly the same as the second.
With regard to probability, think about this. Things work at quantum speed at the size of molecules. Cells are always undergoing mitosis, copying, shifting, transcription, translation, receiving and processing chemical signals. Imagine the genome as a supercomputer and the environment, the determinate of what constitutes a genetic advantage that causes more reproduction like the password. The supercomputer has to guess the password. It does so by brute force. Go through the permutations. Mutations are happening so fast, so often, some are being chucked out in a blur, some are useless and ignored, the ones that are chucked out are automatically repaired because they are getting in the way, and then finally, the computer finds a permutation. Since this is not a disruptor, it is retained in much the same way that a useless mutation would be, passed on to children, who reproduce more...etc etc.
The environment is always playing around with genes, it just takes millions of years to nurture the ones it likes.
From a probability and mathematical standpoint, evolution makes perfect sense. There is a good example of this for contemporary society. The survival advantage of trait is inversely proportional to the amount of time it takes. It is relatively easy to observe genotype transition today. For instance, in parts of Africa where malaria is most prevalent, the allele containing the single copy of sickle-cell anemia can be found in almost 100% of the population. Another good instance of this is common lawn grass. Consider dandelions, a totally nuisance type of weed. As people of suburbia ruthlessly take their lawnmowers to the grass, the dandelions that happens to have genetic combinations that inhibit it’s Auxin growth factors find it useful because they are far more likely to survive, too short to be cut by the blades. These pass their genotype to their children who in turn will be unusually short and survive the lawnmower blades while their tall counterparts perish and in time, a new species, the lawnlion, may arise.
Fallacy #4 Life is too diverse to be explained by gene mutation
No it isn’t. Phenotype depends on genotype and the genotype does not change very much. When I hear creationists talk of the incredible diversity of life, I laugh. What makes life remarkable is how similar it is. The greatest diversity in life is seen among the prokaryotes, the humble single celled bacteria. We have more in common with a mouse than an Escheria coli has in common with Mycoplasmodium genetalium.
The phenotype refers to the trait. This is determined by external features and internal anatomy. Of course, today we understand that phenotype depends on genotype. The speciation variable is not that huge. A human shares 99% of his DNA with a chimpanzee. That means that 1% (5,000 genes) produces 5,000 proteins that the chimps do not have, or transcribes them at a different rate, or folds them differently (new theory suggests that human protein folding is far more complex). We only differ in 2 amino acids (out of 22 known to life) but these two can create vast combinations of proteins. These proteins control advanced neurogenesis, hair follicle growth, skin collagen makeup, eye colour variables, hormone-stimulated growth, all the ways in which we differ from chimps. Evolution works with scaffolding. The vast majority of genes in all mammals are the same, the genes that control enzymatic response, angio and vasculogenesis, the genes that control immunological responses and stem cell arrangements, they control basic development of brain functions that all mammals have, they control metabolism, mitosis, apoptosis, sensory development, the development of spermatogenesis in male mammals and mammary glands in females. By far and large, the genome across the mammalian class is identical. Massive changes in phenotype are caused by a few changes in genes. Even with the simple banana, 50% of our genotype is identical. This groundbreaking work was done by Richard Dawkins, who wrote about the crucial part of the genotype in his book The Selfish Gene.
This rule has a logical follow up: Small genetic changes can make massive phenotype changes. This is why the constant claims that “sometimes fossils are found in the wrong striations” is an idiot idea. In phenotype it may appear to be very different and cannot fit in the taxonomy, but now with recent advances in genetics, we can track tiny mutations with huge consequences, comparing genotypes with a keystroke. If the mutated gene in question sits atop a master chain, then a single mutation can make a huge change. For instance, in a petal flower, if a single protein is changed on the master chain, then a stem will grow in place of a flower. We used to class organisms by phenotype. Not anymore, the completely obvious axiom to be drawn is that DNA is the universal software language of evolution. There are 300 amino acids and 100 nucleotides that exist in nature, but all life is based on only 22 amino acids and a mere four nucleotides.
Fallacy #5 A symbiosis disproves evolution as it could not have come about through mutation.
Actually, symbiotic relationships are fundamental to evolution. There are countless examples, organotrophic bacteria in our guts, the mitochondria in every cell in our body, the chloroplasts in every plant cell.
The symbioses error is part of a larger error known as linear evolution fallacy. Creationists assert that large numbers of fossils found in spurts like the Cambrian are contradictory to the slow, gradual mutation which is evolution’s foundation. They misunderstand something known as punctuated equilibrium. Let us take the Cambrian as an example.
Genetics is only one of the mechanisms of evolution. Another crucial crux is that organisms can form symbiosis relations to survive. To understand it, we must travel back in time to the Mesoproterozoic, when the Earth was very different.
In fact, the Earth was mostly Carbon Dioxide. Simple Prokaryotic life forms survived by metabolizing Carbon Dioxide. They were happy and there was no need for them to evolve. They slotted perfectly into the simple taxonomy, into the mud and shale and very warm climate that made up the ancient Earth. But trouble was brewing. The by-product of their metabolism was oxygen, a gas that was toxic to these little prokaryotes. As oxygen in the atmosphere increased, it started to resemble more and more what we see today: A 21% oxygen atmosphere. As soon as the oxygen reached this number, it caused a bacterial apocalypse. Oxygen is highly reactive and toxic, it interfered with their metabolic systems and protein synthesis. Only a few hardy bacteria survived. They were the ones buried deep in the mud and shale, who could escape to the anoxic world, but it could not last. Eventually, a new class of protozoa arose by the very same process of genetic evolution I covered in detail before. These new cells could metabolize oxygen and thus gave rise to the next stage in evolution: The dawn of the Eukaryotes. The arisal of Eukaryota from prokaryotes is one of two known examples of rapid punctuated equilibrium. The other one is the arisal of proto-cells from self-replicating bimolecular structures. These two events are the quantum leaps in evolution, the understanding gaps where intelligent design still lurks. But both can be explained by catastrophic environmental changes that brought about rapid evolution. Obviously evolution cannot hinge on quantum leaps, it has long stretches of slow evolution, where all organisms drive to operate in better symbiosis with the environment.
Every cell in every advanced organism is more or less the same. A fluid filled membrane with a nucleus containing a series of base pairs that encode for all the proteins that make up the organism, surrounded a cytoplasm swimming with Lyosomes and Peroxisomes and other organelles that play a function in life. The endosymbiosis theory states that the oxygen-hating bacteria of the old world found their home in symbioses with the Eukaryotes. They became our mitochondria, safe from the oxygen of the outside world, metabolizing gases and powering their new homes. Indeed, there is vast evidence to support this (notice this is called endosymbiosis theory, not hypothesis).
The extraordinary structural similarities between Prokaryotes and mitochondria is obvious, they can be traced directly from very ancient proto bacteria that had highly simplified metabolic systems, perhaps making hydrogen sulfide, scratching out a living in the ancient shale and warm mud (Hydrogen sulfide metabolism is what gives Lithotrophes their distinctive yellow glow) Because of the symbioses, looking at our mitochondria is like looking back in time. They haven’t had to evolve, just like their oxyphobic brethren of the Mesoproterozoic world did not. And of course, the fact that this is the only organelle besides the nucleus that has its own genetic code is a clear indicator of endosymbiosis. We used to think the nucleolus contained all the genes. No more. Deep inside the twisting folds of the metabolic catalysis that operates inside our mitochondria is a tiny genome. 60,000 base pairs that contain the structural encoding to perform the metabolic pathways that keep us alive.
Charles Darwin knew there must be a Mesoproterozoic origin for the explosion. He thought the molecular stage was being set for a massive jump in life. He was right. The rise of the Eukaryotes was crucial. Oxygen is much more reactive than Carbon Dioxide, therefore metabolism involving it is much faster. Eukaryotic evolution could work so much faster because it was based upon a much faster fuel. Mitosis and breeding speed increased, and clumps of quasi-independent cells would clump to form tissues that would later make up plant-like organisms, as the process of photosynthesis developed from the simple carbon dioxide metabolism.
The punctuated equilibrium is obvious and brings up a standard mathematic rule. The harsher the environment, the faster the evolution and the steeper the advantage gradient. An environment has got to have some limiting factors, because if an organism is in happy symbiosis with the environment, nothing will happen. The prokaryotes that first inhabited the Earth did not evolve for a billion years, they just happily existed until their oxygen metabolism changed the atmospheric gas concentration to the point that most of them died, and that forced an end to their Camelot-esque existence in the warm mud and shale of the Mesoproterozoic.
Fortunately the environment is a cold hearted bastard who is always harsh as hell. The planet has gone through seven ice ages in the last 700,000 years, three mass extinctions since life began and numerous other cataclysms.
Each one of the twenty two numbers represents one fallacious ID/Creation argument. Every one is ridiculous and deserves debunking. Let us start with the most basic stupidity…
Fallacy #1: Evolution is blind luck
If a person says this, you might as well just walk out and leave. This most basic of errors shows that they have no understanding of basic science. Evolution is a carefully guided process.
Organisms adapt to their environment through natural selection, meaning that the environmental factors both cull the herd and remove organisms with unfavorable traits, and propagate those with favorable traits. The mechanism for this is the second rule of evolution: Evolution is brought about by genetic mutation. An organism cannot adapt to its environment per se. It is the genes that must adapt, and that process takes millions of years.
The next rule is that the determinate of what constitutes an advantage is the environment. The rest of it is really simple, Evolutionary models study this axiom because it is complex. An environment includes lots of factors like other animals, temperature, gas concentration, climate etc. etc. This axiom is the driver of evolution, the guide, Adam Smith’s invisible hand. Genetic mutation is random. It is up to the environment to nurture useful genes and ensure they get passed on, and to eliminate poor genes. This is the fundamental rule of natural selection.
This incredibly ridiculous error, to state that evolution is luck, is a confusion of genetic mutation which is luck, and evolution which is the process that selects the genes and makes sense of the randomness of mutation.
Fallacy #2 Advantageous mutation is impossible
This one is ridiculous. To understand why, a short overview of genetic mechanisms and biochemistry is necessary.
DNA is made up of polymerated strings of bases, which are nucleotides bound to sugar-phosphate backbones. DNA has two functions:
Holds the code to create various proteins from amino acids
Regulating the rate of producing proteins: By definition, one gene is a string of nucleotides that codes for one protein
The language of DNA is base-pairs. DNA is entirely comprised of four molecules. Cytosine, Guanine, Adenine and Thymine. These are the nucleotides. The nucleotides are complementary. Like magnets, they will only fit to a certain opposite. G fits with C and A fits with T (A also fits with U, Uracil, but that is an RNA base). So there are only four possible base-pairs: CG, GC, TA and AT. But these four pairs will dictate every single protein imaginable.
Chemistry has absolutely everything to do with nucleic pairing. A fits with T and C with G. They are dipolar covalents. One side is slightly positively charged, the other negative. They will bind to each other much more easily if they correspond. Trying to fit A with C or T with G is sort of like trying to force two north magnets together. This kind of error can only happen in an abundance of adenosine triphosphate. It's like protons. Have you ever wondered why they don’t repel? They smash into each other with such force that they bind (gluons). (DNA doesn’t smash into each other of course, but you get the idea. So if you have a CGAT on one string, you will of course have GCTA on the other. This is called complementary encoding, and is the basis of DNA.
There are four ways that DNA can innovate.
Intragenic mutation: Errors during mitosis can swap base-pairs around, creating new strings of bases, and a new gene
Segment Shuffling: Two different genes can recombine and form two new hybrids
Duplication error: Sometimes during mitosis, a parent cell will by accident only pass part of it’s genome to the daughter cell, thus it retains a redundant copy of a gene string. This copy is completely free to mutate based on random frequency probability.
Horizontal/vertical Transfer: During sexual reproduction, organisms exchange genes. If the organism is a diploid meaning that it’s offspring has the code of two parents, then it’s offspring will have a completely new genome, combing both parents. This is the most successful method of innovation. Or an organism, particularly prokaryotes, can actually exchange genes by means of one actually encoding a packaged gene for another, which incorporates it into the genome. This is horizontal transfer, a tool that Eukaryota do not have
There are two types of genes. Introns and exons, which have these separate functions. Exons code for proteins. Introns are mostly junk or redundant, but they flank all the exons. Sometimes they are just punctuation, dictating where a gene starts and stops, but their most important function by far is to regulate the speed of protein transcription, a mechanism we will look at it more detail later. Exons dictate how a protein will be assembled. They do this because a protein is essentially a string of amino acids or a polypeptide. Therefore, exons dictate the order of amino acids in a protein. They do this by representing each amino acid with a codon. A codon is three nucleotides. Three nucleotides make up an amino acid. There are 20 possible amino acids, but 64 possible codons, therefore, exons are highly sensitive. They are also sensitive because they are ordered very precisely. For instance, let’s look at a simple string of three codons in a gene: AGG CTT GCC. Now let’s assume that an extra base is accidentally inserted (Like a G for example). The new string would be totally different, it would look like this. GAG GCT TTG CC, so every base would be shifted down one, and the entire gene would change. This would be completely devastating. This is why DNA repair mechanisms quickly target such errors.
On the other hand, Introns, which are not so sensitive or precisely executed, or are sometimes just junk or redundant, mutate based solely on random frequency. As there are 44 codons that don't correspond to an amino acid, these are used in introns. Therefore, the next axiom of evolution is that evolution is driven by the Introns. Obviously it is more complicated, Introns can become exons during shuffling/shifting, and exons can become Introns, and sometimes exons can be mutated harmlessly, so long as the mutation changes only a tiny chunk of the gene, but this rule still applies.
Now that you understand genetic mutation mechanisms, this can be applied to how advantage mutation works.
Intron mutation can change more than just transcription rate. It can change the protein fold. So, in all likelihood an organism won’t end up with one enzyme or protein morphing into another, but an identical polypeptide folding into a new enzyme. Only exon mutation will "change" an enzyme because it will change some codons, thereby changing the protein string order. From a probability standpoint, the odds of gaining a useful mutation because you can fold a protein in a new way vastly outweigh the possibility that you can get from producing a new protein. Mutations can have chain reactions on the cycle. Same string but different protein will produce a different catalytic function therefore will change another intron somewhere else down the line, or perhaps change an exon and make a new protein which, because it is bound to the cycle, not random, will be useful. If mutations operated independently, and outside the cycle, evolution would never get off the ground.
It can be understand like this:
A useless mutation occurs: Nothing happens
A bad mutation occurs: The cell dies, or the error is targeted because it is disrupting the cycle
A good mutation occurs: A new protein, rate of transcription or fold function is made. This is useful. It alters the cycle, producing a knock on effect.
For a mutation to occur which can be preserved, junk must be turned into non-junk. It is really easy to play with the introns. The prokaryotes that are the basis of life have almost no junk DNA. It is evident that such small organisms evolved to have conservative genomes. They have useful introns. It may seem extremely unreasonable in terms of probability but DNA mutates all the time. If the shift is Duplicate error, a popular method, then the gene advantage can be conserved, because it is a redundant piece. Evolution is just mathematics. As long as a gene exists, it will fight to survive...at the chemical level there exists a ruthless primal battle in which the best of the best are constantly being selected, and the weak crushed. The only phenotype affecting genes that are conserved are the ones that affect reproductive capacity. That will cause it to be conserved and cumulatively mutated upon. This is the mathematics of evolution.
Genetic drift drives evolution. Some mutations are good, some are bad, most do nothing, but through the endless cycles, organisms evolve. The analogy I like to use is the telemarketer. About 90% of people hang up on them, but the 10% who say yes make the enterprise quite profitable.
The statement advantage mutation is impossible is a confusion of possibility and probability. Advantage mutation almost never happens…the operative word being ALMOST. But if you have mutations working at quantum speed and three billion years on your hand, your odds improve dramatically.
The knock-on effect is a good demonstrator. All proteins do only one thing, they act as a catalyst for the body's catabolic chemical reactions. Without proteins, you would have to set yourself on fire to release enough energy to perform respiration. This is obviously not practical. All proteins lower the activation energy for a chemical reaction by providing an active site which works like a lock and key model. The chemical fits into the protein receptor and is broken into smaller molecules. Therefore, one can imagine that a different fold will mean that protein will have a different catabolic function which could offer a significant advantage if it allows an organism to synthesize a new chemical. The most effective way to do this would probably be base-pair swap exon mutation, which will only change a small chunk of an exon. Normally, the amino confirmation will predispose a protein to fold in a certain way, although this process is not understood (that would be the Levinthal Paradox). Natural selection, it seems, has selected a chemical interaction set which encourages the protein to fold, because in it's primary and secondary state, it is useless.
Protein folding is also a useful demonstrator of life's autoregulatory weirdness. They fold into elegant shapes after being translated from mRNA only for a tiny piece of it to serve as an active site. The hemoglobin molecule is the bizarre case and point. It is a colossal macromolecular protein snugly wrapping a single haemite (iron). This is somewhat akin to building a nuclear powered transformer to plug in a lamp.
There are 100 nucleic acids and 300 amino acids that exist in nature, we use only 4 and 22. The sugars and phosphates snap together to form the base backbone in the exact same way that nucleic acids bond together. From a chemical standpoint, the phosphorylate-saccharide (ribose)-nucleic acid structure is sensible. There are 100 nucleic acids and 300 amino acids that exist in nature, we use only 4 and 22. There is no reason why life could not be based on other amino acids and nucleic acids. The sugars and phosphates snap together to form the base backbone in the exact same way that nucleic acids bond together. From a chemical standpoint, the phosphorylate-saccharide (ribose)-nucleic acid structure is sensible.
We can look at the knock-on effect with respect to folding like this:
1) A small mutation changes a few codons
2) A different protein is made with a new fold
3) This catalyzes a chemical in a different fashion, most likely a new product
4) This new product has a different effect on the cell membrane receptors, which keep up the autocatalytic cycle. It causes a different command to be followed, as transcription is driven when a stimuli causes a protein to bind to the introns that flank the necessary exon.
Transgenic technology has revealed that changing a gene can start making a gene down the line do bizarre things. Why? Simple. Genes can control each other. The knock-on is established by introns controlling exons which in turn produce proteins which control introns which control exons which… you understand. If evolution operated like individual genes doing individual things, it would not get on the ground.
Knock-on effects work all across the genome. After all, what do genes do, they produce proteins, or they regulate the production of proteins. What do those proteins do? Well...everything: The big functions are of course:
-Catabolism of biochemical families (nucleotides, coenzyme factors, carbohydrates)
-Anabolism (glycogen synthesis, lipid synthesis)
-RNA synthesis control
-Ion channels and membranes (cell membranes, nerve membranes, particularly oligolipoproteins for myelin) , transport mechanisms including inorganic transport, ion flux and carrying
-Exocrine systems and secretory pathways/chemical production
-endocrine systems and hormone control Autocatalysis
-Maintenance of cell signal transduction and energy release metabolic pathways
The thing to notice about all of these is they are all dependant on biochemical triggers. You change one thing, you change a cascade. Making a new ion channel will change the electrochemical gradient or allow a different material influx, which will affect how protein receptors bind to introns. A new ion channel could trigger a hitherto unused intron. There are so many complex factors to genetic evolution, it is not a clear cut process.
The discovery of genes was probably one of the most important in the history of science. Before genomic sequencing, the human body or indeed any organism or indeed a single celled organism seemed unbearably complex. Of course, with the advent of new molecular biology techniques that was swept away. Everything can be explained in terms of metabolic pathways building macromolecules with remarkable properties. There are only thirteen families of Biochemicals (Terpenoids, Flavanoids, Carotenoids, Polyketides, Alkaloids Peptides, Polypeptides, Amino Acids, Nucleic Acids, Steroids, Enzyme Cofactors, Carbohydrates, Lipids and Tetrapyrroles). Everything can be explained in terms of these, and the manufacture, regulation, secretion and synthesis of these…can be explained by DNA. This explains everything from simple sugar metabolism all the way to the Progenitor…the stem cell with the potential to make a human body.
Fallacy #3 The probability of advantage mutation taking place is too low.
This error is almost exactly the same as the second.
With regard to probability, think about this. Things work at quantum speed at the size of molecules. Cells are always undergoing mitosis, copying, shifting, transcription, translation, receiving and processing chemical signals. Imagine the genome as a supercomputer and the environment, the determinate of what constitutes a genetic advantage that causes more reproduction like the password. The supercomputer has to guess the password. It does so by brute force. Go through the permutations. Mutations are happening so fast, so often, some are being chucked out in a blur, some are useless and ignored, the ones that are chucked out are automatically repaired because they are getting in the way, and then finally, the computer finds a permutation. Since this is not a disruptor, it is retained in much the same way that a useless mutation would be, passed on to children, who reproduce more...etc etc.
The environment is always playing around with genes, it just takes millions of years to nurture the ones it likes.
From a probability and mathematical standpoint, evolution makes perfect sense. There is a good example of this for contemporary society. The survival advantage of trait is inversely proportional to the amount of time it takes. It is relatively easy to observe genotype transition today. For instance, in parts of Africa where malaria is most prevalent, the allele containing the single copy of sickle-cell anemia can be found in almost 100% of the population. Another good instance of this is common lawn grass. Consider dandelions, a totally nuisance type of weed. As people of suburbia ruthlessly take their lawnmowers to the grass, the dandelions that happens to have genetic combinations that inhibit it’s Auxin growth factors find it useful because they are far more likely to survive, too short to be cut by the blades. These pass their genotype to their children who in turn will be unusually short and survive the lawnmower blades while their tall counterparts perish and in time, a new species, the lawnlion, may arise.
Fallacy #4 Life is too diverse to be explained by gene mutation
No it isn’t. Phenotype depends on genotype and the genotype does not change very much. When I hear creationists talk of the incredible diversity of life, I laugh. What makes life remarkable is how similar it is. The greatest diversity in life is seen among the prokaryotes, the humble single celled bacteria. We have more in common with a mouse than an Escheria coli has in common with Mycoplasmodium genetalium.
The phenotype refers to the trait. This is determined by external features and internal anatomy. Of course, today we understand that phenotype depends on genotype. The speciation variable is not that huge. A human shares 99% of his DNA with a chimpanzee. That means that 1% (5,000 genes) produces 5,000 proteins that the chimps do not have, or transcribes them at a different rate, or folds them differently (new theory suggests that human protein folding is far more complex). We only differ in 2 amino acids (out of 22 known to life) but these two can create vast combinations of proteins. These proteins control advanced neurogenesis, hair follicle growth, skin collagen makeup, eye colour variables, hormone-stimulated growth, all the ways in which we differ from chimps. Evolution works with scaffolding. The vast majority of genes in all mammals are the same, the genes that control enzymatic response, angio and vasculogenesis, the genes that control immunological responses and stem cell arrangements, they control basic development of brain functions that all mammals have, they control metabolism, mitosis, apoptosis, sensory development, the development of spermatogenesis in male mammals and mammary glands in females. By far and large, the genome across the mammalian class is identical. Massive changes in phenotype are caused by a few changes in genes. Even with the simple banana, 50% of our genotype is identical. This groundbreaking work was done by Richard Dawkins, who wrote about the crucial part of the genotype in his book The Selfish Gene.
This rule has a logical follow up: Small genetic changes can make massive phenotype changes. This is why the constant claims that “sometimes fossils are found in the wrong striations” is an idiot idea. In phenotype it may appear to be very different and cannot fit in the taxonomy, but now with recent advances in genetics, we can track tiny mutations with huge consequences, comparing genotypes with a keystroke. If the mutated gene in question sits atop a master chain, then a single mutation can make a huge change. For instance, in a petal flower, if a single protein is changed on the master chain, then a stem will grow in place of a flower. We used to class organisms by phenotype. Not anymore, the completely obvious axiom to be drawn is that DNA is the universal software language of evolution. There are 300 amino acids and 100 nucleotides that exist in nature, but all life is based on only 22 amino acids and a mere four nucleotides.
Fallacy #5 A symbiosis disproves evolution as it could not have come about through mutation.
Actually, symbiotic relationships are fundamental to evolution. There are countless examples, organotrophic bacteria in our guts, the mitochondria in every cell in our body, the chloroplasts in every plant cell.
The symbioses error is part of a larger error known as linear evolution fallacy. Creationists assert that large numbers of fossils found in spurts like the Cambrian are contradictory to the slow, gradual mutation which is evolution’s foundation. They misunderstand something known as punctuated equilibrium. Let us take the Cambrian as an example.
Genetics is only one of the mechanisms of evolution. Another crucial crux is that organisms can form symbiosis relations to survive. To understand it, we must travel back in time to the Mesoproterozoic, when the Earth was very different.
In fact, the Earth was mostly Carbon Dioxide. Simple Prokaryotic life forms survived by metabolizing Carbon Dioxide. They were happy and there was no need for them to evolve. They slotted perfectly into the simple taxonomy, into the mud and shale and very warm climate that made up the ancient Earth. But trouble was brewing. The by-product of their metabolism was oxygen, a gas that was toxic to these little prokaryotes. As oxygen in the atmosphere increased, it started to resemble more and more what we see today: A 21% oxygen atmosphere. As soon as the oxygen reached this number, it caused a bacterial apocalypse. Oxygen is highly reactive and toxic, it interfered with their metabolic systems and protein synthesis. Only a few hardy bacteria survived. They were the ones buried deep in the mud and shale, who could escape to the anoxic world, but it could not last. Eventually, a new class of protozoa arose by the very same process of genetic evolution I covered in detail before. These new cells could metabolize oxygen and thus gave rise to the next stage in evolution: The dawn of the Eukaryotes. The arisal of Eukaryota from prokaryotes is one of two known examples of rapid punctuated equilibrium. The other one is the arisal of proto-cells from self-replicating bimolecular structures. These two events are the quantum leaps in evolution, the understanding gaps where intelligent design still lurks. But both can be explained by catastrophic environmental changes that brought about rapid evolution. Obviously evolution cannot hinge on quantum leaps, it has long stretches of slow evolution, where all organisms drive to operate in better symbiosis with the environment.
Every cell in every advanced organism is more or less the same. A fluid filled membrane with a nucleus containing a series of base pairs that encode for all the proteins that make up the organism, surrounded a cytoplasm swimming with Lyosomes and Peroxisomes and other organelles that play a function in life. The endosymbiosis theory states that the oxygen-hating bacteria of the old world found their home in symbioses with the Eukaryotes. They became our mitochondria, safe from the oxygen of the outside world, metabolizing gases and powering their new homes. Indeed, there is vast evidence to support this (notice this is called endosymbiosis theory, not hypothesis).
The extraordinary structural similarities between Prokaryotes and mitochondria is obvious, they can be traced directly from very ancient proto bacteria that had highly simplified metabolic systems, perhaps making hydrogen sulfide, scratching out a living in the ancient shale and warm mud (Hydrogen sulfide metabolism is what gives Lithotrophes their distinctive yellow glow) Because of the symbioses, looking at our mitochondria is like looking back in time. They haven’t had to evolve, just like their oxyphobic brethren of the Mesoproterozoic world did not. And of course, the fact that this is the only organelle besides the nucleus that has its own genetic code is a clear indicator of endosymbiosis. We used to think the nucleolus contained all the genes. No more. Deep inside the twisting folds of the metabolic catalysis that operates inside our mitochondria is a tiny genome. 60,000 base pairs that contain the structural encoding to perform the metabolic pathways that keep us alive.
Charles Darwin knew there must be a Mesoproterozoic origin for the explosion. He thought the molecular stage was being set for a massive jump in life. He was right. The rise of the Eukaryotes was crucial. Oxygen is much more reactive than Carbon Dioxide, therefore metabolism involving it is much faster. Eukaryotic evolution could work so much faster because it was based upon a much faster fuel. Mitosis and breeding speed increased, and clumps of quasi-independent cells would clump to form tissues that would later make up plant-like organisms, as the process of photosynthesis developed from the simple carbon dioxide metabolism.
The punctuated equilibrium is obvious and brings up a standard mathematic rule. The harsher the environment, the faster the evolution and the steeper the advantage gradient. An environment has got to have some limiting factors, because if an organism is in happy symbiosis with the environment, nothing will happen. The prokaryotes that first inhabited the Earth did not evolve for a billion years, they just happily existed until their oxygen metabolism changed the atmospheric gas concentration to the point that most of them died, and that forced an end to their Camelot-esque existence in the warm mud and shale of the Mesoproterozoic.
Fortunately the environment is a cold hearted bastard who is always harsh as hell. The planet has gone through seven ice ages in the last 700,000 years, three mass extinctions since life began and numerous other cataclysms.