The last refuge for arguments of most Christian fundamentalist ignoramuses (including those going for an online Bachelor of Biblical Studies degree- when they don’t even have a high school degree!) is “complexity” – as made popular by the ID crowd in the Discovery Institute.
Trouble is we know now that the “ID- too complex to have evolved” meme is essentially an intellectual ‘rope a dope’ or better, a convenient trope for those who lack an extensive science background (which means more than reading a couple of books by Dawkins – when one hasn’t even read Origin of Species) . But never mind, these blabbering, blustering Babbits will continue using it so long as they are convinced most people can’t call them on it.
Let’s consider assorted claims made by a wannabe “specialist” in biological complexity who himself has never taken a single biology course, even in high school. He scribbles on his blog:
“Complex molecular systems in organisms pose a considerable challenge to Darwinian evolution . Many of the proteins within the cell need to interact together for a particular function . “
Here, the concept of “ligand” escapes him. This is defined as a compound structured in terms of it ability to bind with other compounds. Their role is particularly critical for the allosteric proteins. Key to this is “allosteric transition” wherein a molecule shifts from one to the other and back again, such as illustrated in Fig. 1. Since we know the shape-changing properties of a protein depend on the shape of its binding sites, then we know stereospecific properties are modified by the transition.
To fix ideas, in state P1 the protein will be able to recognize and therefore bind ligand L1 at one site (but not ligand, L2) whereas in state P2 it will recognize and bind ligand L2, but not Ligand L1. From this we see either ligand, L1 or L2, will have the effect of stabilizing the protein in one of two states, P1 or P2, and that L1 and L2 will be mutually antagonistic.
All of this is critical, because it shows exactly HOW proteins within a cell can interact with each other to enable a particular function. The emergence of the function arrives when one includes a third ligand, call it L(3)s which we denote as a substrate (E.g. L(3)s allows binding in some other site of the molecule than the one L1 binds). Thus the role of L(3)s is cooperative in stabilizing the protein in its active state (which recognizes the substrate)
In this guise, we see that ligands L1 and L(3)s act as activators, while L2 acts as an inhibitor. It is important to note here that the activity of a population of molecules will be proportional to the fraction of them that are in state P1, say, a fraction which will be larger or smaller depending on the relative concentrations of the ligands as well as intrinsic equilibrium between P1 and P2.
The point to be emphasized in the foregoing is that there are no direct interactions between the 3 ligands identified, all interactions occur exclusively between the protein and each ligand separately. These sort of indirect interactions are the very thing that enables biochemists to account for the subtle adaptations shown in the protein’s nonlinear response to variations in the concentration of effector agents. To wit, all known allosteric proteins are oligometric or made up of a noncovalent assembly of a few chemically identical sub-units called protonomers. Each protonomer bears a receptor for each of the ligands the protein recognizes.
The upshot of all this points to a microscopic, cybernetic system which also has arisen purely from Darwinian adaptations. For example, the synthesis of three key proteins (P1, P2, P3) is seen most clearly in the simple lactose system of Escherichia coli bacteria. This is illustrated in Fig. 2. In the diagram R is a repressor protein acting in association with a galactoside -inducer BG. T is also a repressor protein but acting in association with an operator (o) segment of DNA. Three other gene segments, G, G2 and G3 govern the the synthesis of the three proteins: P1, P2, and P3 (bottom). It is these "structure" genes that have appeared via natural selection - and makes them no longer "random", as evidenced by their gene frequencies relative to more primitive ancestors of E. coli. (See below). Meanwhile, the 'p' designated segment initiates the synthesis of messenger RNA (mRNA) while the 'i' segment embodies the "regulator" gene governing the synthesis of the repressor R. The key idea to take away here is that the repressor gene specifically recognizes the operator segment (o) to which it binds forming a very stable complex with a binding energy of ~ 15kCal. Because the processes and interactions are “teleonomic” (long distance-interactive) the synthesis can proceed without external additions.
The fundie critic goes on to write:
“Proteins are comprised of a specific sequence of building blocks , the order of which is encoded in DNA . According to evolution , such sequences can only be the result of random mutation , yet random processes cannot produce information “
Again, he misuses the term “random” here which we already explained in an earlier blog:
http://brane-space.blogspot.com/2010/08/if-youre-going-to-quote-dawkins-do-it.html
As pointed out therein:
And the specific passage:
“Thus, what natural selection does is to consolidate particular random mutations into a more stable, adaptive adjustment – governed by deterministic factors and inputs.Thus, that while the selected trait often appears at random, its preservation in the gene structure cannot be relegated to randomness”
In other words, once the trait – say ligand recognition by a protein- is incorporated, and gene frequencies (see previous blog on evolution misconceptions) increase, the process ceases to be random. While the emergence of an original operator or structure gene - say in the case of E. Coli. (above) was random (say from a mutation incepted by absorption of a cosmic ray) the incorporation, retention and direction into interactive, teleonomic processes resulting in protein synthesis is not. The failure of the critic is being unable to recognize the distinctions between the condition leading to the initial mutation and the subsequent natural selection consolidating it into higher gene frequencies!
As I also noted in the previous blog:
“In quantitative genetics we actually have indices and markers to show how strong the selection survival effects are. We refer these as preferential alleles and they appear by virtue of their relative increase in gene frequency”
He also gets into more trouble;
“ Moreover , because many such proteins are required to co-exist simultaneously , it is impossible for the sequences to have evolved , as only a full system of proteins has a function . This is the basis of the argument of irreducible complexity . “
Of course, this is nonsense – since I already showed how many “such proteins” CAN exist simultaneously purely on the basis of bio-chemical cybernetics – wherein each protein recognizes (chemically) a binding ligand or "operator gene" - say for E. coli. - and which can lead to the synthesis of many proteins! Thus, the “complexity” which is only apparent, is easily reducible to the chemicals -molecules governing the processes for specific activation, say in enzymes. All such protein interactions to deliver protein sequences are thus interpretable in terms of specific chemical interactions “chosen” by regulatory proteins – as opposed to some innominate “designer”.
As Richard Dawkins points out the fallacy in all ID reasoning:
“This kind of default reasoning leaves completely open the possibility that, if the biological structure or organism is too complex to have evolved, it might also be too complex to have been created.”
Now, solely for amusement purposes, the final bit of dreck:
“Lastly , let's compare evolution and the Bible . According to the theory of evolution , all living things on Earth have descended from common ancestors and thus all creatures are physically related to all others . Such a view is inconsistent with the account of creation in Genesis , which states God created different types of creatures on different days of the creation week . Plants were made on day three , fish and birds on day five , and man and land animals on day six”
Let’s parse this idiocy. First, if the common ancestry concept is not accurate, then how explain the presence of the SAME DNA molecule in all organisms? The very existence of DNA in cell nuclei of all terrestrial organisms points to their common ancestry at least in the distant past. If all were created “differently” surely there’d be different DNA molecules, not the same. But, of course, he’s unable to explain that!
Second, asserting a scientifically tested and proven theory is “inconsistent with Genesis” is like putting the cart before the house, or saying something equally dense like “Astronomer’s discovery of two Plutonian moons is inconsistent with astrology”. Or, the nuclear fusion to obtain gold is “inconsistent with alchemy”. Sorry, but science stands on its own merits, and isn’t expected to be “consistent” with any ideations formulated of balderdash, bunkum and baloney! It is the balderdash claims which must be consistent with science, or consigned to the realm of….balderdash!
His last sentence is also daft since he seems to be confusing the fact all organisms are physically related to others, with all appearing at the same time (else, why would he so solemnly set out his different species, groups on different “days”?) In fact, the course of evolution more or less follows his sequence, except we use half billion year blocks for “days”. The only adjustment we’d make is to insert the emergence of methanotrphic bacteria on his mythical Genesis“day one” – since around 3.8 billion years ago the atmosphere was largely methane and consumed by methane-eating (methanotrophic) bacteria. So, at least in a limited sense his Genesis story is consistent with the evolutionary emergence timeline. And in that very limited sense he's accurate, but not at all to do with his presumed "irreducible complexity" - which basically commits the fallacy of ignotium per ignotius./
Stay tuned - there's more amusement to come when I examine the incomparable Lee Strobel's five tropes on atheism- naturalism!
Trouble is we know now that the “ID- too complex to have evolved” meme is essentially an intellectual ‘rope a dope’ or better, a convenient trope for those who lack an extensive science background (which means more than reading a couple of books by Dawkins – when one hasn’t even read Origin of Species) . But never mind, these blabbering, blustering Babbits will continue using it so long as they are convinced most people can’t call them on it.
Let’s consider assorted claims made by a wannabe “specialist” in biological complexity who himself has never taken a single biology course, even in high school. He scribbles on his blog:
“Complex molecular systems in organisms pose a considerable challenge to Darwinian evolution . Many of the proteins within the cell need to interact together for a particular function . “
Here, the concept of “ligand” escapes him. This is defined as a compound structured in terms of it ability to bind with other compounds. Their role is particularly critical for the allosteric proteins. Key to this is “allosteric transition” wherein a molecule shifts from one to the other and back again, such as illustrated in Fig. 1. Since we know the shape-changing properties of a protein depend on the shape of its binding sites, then we know stereospecific properties are modified by the transition.
To fix ideas, in state P1 the protein will be able to recognize and therefore bind ligand L1 at one site (but not ligand, L2) whereas in state P2 it will recognize and bind ligand L2, but not Ligand L1. From this we see either ligand, L1 or L2, will have the effect of stabilizing the protein in one of two states, P1 or P2, and that L1 and L2 will be mutually antagonistic.
All of this is critical, because it shows exactly HOW proteins within a cell can interact with each other to enable a particular function. The emergence of the function arrives when one includes a third ligand, call it L(3)s which we denote as a substrate (E.g. L(3)s allows binding in some other site of the molecule than the one L1 binds). Thus the role of L(3)s is cooperative in stabilizing the protein in its active state (which recognizes the substrate)
In this guise, we see that ligands L1 and L(3)s act as activators, while L2 acts as an inhibitor. It is important to note here that the activity of a population of molecules will be proportional to the fraction of them that are in state P1, say, a fraction which will be larger or smaller depending on the relative concentrations of the ligands as well as intrinsic equilibrium between P1 and P2.
The point to be emphasized in the foregoing is that there are no direct interactions between the 3 ligands identified, all interactions occur exclusively between the protein and each ligand separately. These sort of indirect interactions are the very thing that enables biochemists to account for the subtle adaptations shown in the protein’s nonlinear response to variations in the concentration of effector agents. To wit, all known allosteric proteins are oligometric or made up of a noncovalent assembly of a few chemically identical sub-units called protonomers. Each protonomer bears a receptor for each of the ligands the protein recognizes.
The upshot of all this points to a microscopic, cybernetic system which also has arisen purely from Darwinian adaptations. For example, the synthesis of three key proteins (P1, P2, P3) is seen most clearly in the simple lactose system of Escherichia coli bacteria. This is illustrated in Fig. 2. In the diagram R is a repressor protein acting in association with a galactoside -inducer BG. T is also a repressor protein but acting in association with an operator (o) segment of DNA. Three other gene segments, G, G2 and G3 govern the the synthesis of the three proteins: P1, P2, and P3 (bottom). It is these "structure" genes that have appeared via natural selection - and makes them no longer "random", as evidenced by their gene frequencies relative to more primitive ancestors of E. coli. (See below). Meanwhile, the 'p' designated segment initiates the synthesis of messenger RNA (mRNA) while the 'i' segment embodies the "regulator" gene governing the synthesis of the repressor R. The key idea to take away here is that the repressor gene specifically recognizes the operator segment (o) to which it binds forming a very stable complex with a binding energy of ~ 15kCal. Because the processes and interactions are “teleonomic” (long distance-interactive) the synthesis can proceed without external additions.
The fundie critic goes on to write:
“Proteins are comprised of a specific sequence of building blocks , the order of which is encoded in DNA . According to evolution , such sequences can only be the result of random mutation , yet random processes cannot produce information “
Again, he misuses the term “random” here which we already explained in an earlier blog:
http://brane-space.blogspot.com/2010/08/if-youre-going-to-quote-dawkins-do-it.html
As pointed out therein:
And the specific passage:
“Thus, what natural selection does is to consolidate particular random mutations into a more stable, adaptive adjustment – governed by deterministic factors and inputs.Thus, that while the selected trait often appears at random, its preservation in the gene structure cannot be relegated to randomness”
In other words, once the trait – say ligand recognition by a protein- is incorporated, and gene frequencies (see previous blog on evolution misconceptions) increase, the process ceases to be random. While the emergence of an original operator or structure gene - say in the case of E. Coli. (above) was random (say from a mutation incepted by absorption of a cosmic ray) the incorporation, retention and direction into interactive, teleonomic processes resulting in protein synthesis is not. The failure of the critic is being unable to recognize the distinctions between the condition leading to the initial mutation and the subsequent natural selection consolidating it into higher gene frequencies!
As I also noted in the previous blog:
“In quantitative genetics we actually have indices and markers to show how strong the selection survival effects are. We refer these as preferential alleles and they appear by virtue of their relative increase in gene frequency”
He also gets into more trouble;
“ Moreover , because many such proteins are required to co-exist simultaneously , it is impossible for the sequences to have evolved , as only a full system of proteins has a function . This is the basis of the argument of irreducible complexity . “
Of course, this is nonsense – since I already showed how many “such proteins” CAN exist simultaneously purely on the basis of bio-chemical cybernetics – wherein each protein recognizes (chemically) a binding ligand or "operator gene" - say for E. coli. - and which can lead to the synthesis of many proteins! Thus, the “complexity” which is only apparent, is easily reducible to the chemicals -molecules governing the processes for specific activation, say in enzymes. All such protein interactions to deliver protein sequences are thus interpretable in terms of specific chemical interactions “chosen” by regulatory proteins – as opposed to some innominate “designer”.
As Richard Dawkins points out the fallacy in all ID reasoning:
“This kind of default reasoning leaves completely open the possibility that, if the biological structure or organism is too complex to have evolved, it might also be too complex to have been created.”
Now, solely for amusement purposes, the final bit of dreck:
“Lastly , let's compare evolution and the Bible . According to the theory of evolution , all living things on Earth have descended from common ancestors and thus all creatures are physically related to all others . Such a view is inconsistent with the account of creation in Genesis , which states God created different types of creatures on different days of the creation week . Plants were made on day three , fish and birds on day five , and man and land animals on day six”
Let’s parse this idiocy. First, if the common ancestry concept is not accurate, then how explain the presence of the SAME DNA molecule in all organisms? The very existence of DNA in cell nuclei of all terrestrial organisms points to their common ancestry at least in the distant past. If all were created “differently” surely there’d be different DNA molecules, not the same. But, of course, he’s unable to explain that!
Second, asserting a scientifically tested and proven theory is “inconsistent with Genesis” is like putting the cart before the house, or saying something equally dense like “Astronomer’s discovery of two Plutonian moons is inconsistent with astrology”. Or, the nuclear fusion to obtain gold is “inconsistent with alchemy”. Sorry, but science stands on its own merits, and isn’t expected to be “consistent” with any ideations formulated of balderdash, bunkum and baloney! It is the balderdash claims which must be consistent with science, or consigned to the realm of….balderdash!
His last sentence is also daft since he seems to be confusing the fact all organisms are physically related to others, with all appearing at the same time (else, why would he so solemnly set out his different species, groups on different “days”?) In fact, the course of evolution more or less follows his sequence, except we use half billion year blocks for “days”. The only adjustment we’d make is to insert the emergence of methanotrphic bacteria on his mythical Genesis“day one” – since around 3.8 billion years ago the atmosphere was largely methane and consumed by methane-eating (methanotrophic) bacteria. So, at least in a limited sense his Genesis story is consistent with the evolutionary emergence timeline. And in that very limited sense he's accurate, but not at all to do with his presumed "irreducible complexity" - which basically commits the fallacy of ignotium per ignotius./
Stay tuned - there's more amusement to come when I examine the incomparable Lee Strobel's five tropes on atheism- naturalism!
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