Creation: Mutations Refutations Part III

You said this:
…”Since the Modern Evolutionary Synthesis, the philosophy of Neo-Darwinism has assumed that mutation accomplished ALL cross-species changes, and then natural selection afterward refined those changes. This, of course, assumes that mutations and natural selection are both beneficial and goal oriented. This means that Darwinists must be capable of keeping two contradictory notions in mind simultaneously — that of randomness and purpose and that of benificicent and deleterious.” (my bold)
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No, no, no!
I’ve said this so many times, Gregg! Evolutionary theory DOES NOT ASSUME that mutations are goal-oriented. It does NOT ASSUME that natural selection is goal-oriented. This is the opposite of what evolutionary theory says. Evolution is not goal-oriented or directed. Biologists do not think this! Biologists do not hold this contradictory idea you say they hold, so you are accusing them of something untrue, and this is not fair. I don’t understand why you keep saying things like this.
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Maybe you have a chain of logic in your mind which leads you to believe that biologists should think evolution is goal-oriented (but maybe are too blind or biased or stupid to recognize it?). If that’s what you think, then you could be explicit about your chain of thought rather than imputing ideas to other people which they do not hold!
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Nor is there an assumption that mutations or natural selection in general are beneficial.
To even talk about whether something is beneficial you have to define what you mean by beneficial and you have to specify the conditions under which you think something would be beneficial.
The wording of your first sentence above could be taken to suggest that evolutionary theory thinks that first a new species occurs as a result of some number of mutations and only THEN can natural selection act on the new species. Just to make it clear, that would not be a correct picture. Natural selection is the combination of all the factors in an organism’s environment which affect its ability to survive and produce offspring. These factors are always present, and include such obvious things as the climate and weather, the availability of food, actions by predators, mate choice by others in the same species that affect an individual’s chance to reproduce.

You said this:
…”The gene has to already exist (have been created) before it can mutate. Therefore, all mutation results in is a varied form of an already-existing (already created) gene. In other words, you get variation within kind, just as the Biblical account of creation predicts.”
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I don’t want to discuss abiogenesis right now. Let’s assume for the moment that the first bacterial populations appeared by divine or supernatural or alien or magical processes if you insist on keeping the ideas of abiogenesis off the table. What you have in that early stage is a very rich set of single-celled bacterial and archaeal organisms that are able to pass genetic information back and forth by horizontal transfer, and from which eukaryotic single cells develop (currently thought to be by endosymbiosis). Let’s start with the development of multi-cellular organisms from those single-celled eukaryotes, which have a good base of genes and cellular mechanisms in place.
In the single-celled eukaryotes there is a set of genes and genetic information and the mechanism for cellular reproduction. But not all genes that we find in, say, chordates or insects or mammals or primates etc. are present. For the genes that are present, not all the alleles we find in chordates or insects or mammals or primates etc. are present. There is genetic raw material that can be swapped around and mutated and transposed and duplicated. But the specific genetic material to make all the biblical kinds (such as rabbits and ravens) is NOT present at this point. All the genes and alleles and genetic information that exists in a raven are not present in a single-celled eukaryote. A long history of reproductions by these single-celled and early multicellular eukaryotes that did not include mutations could not result in the biblical kinds just by variation alone.
Mutations, including gene duplications, of the genes and genetic material of those early organisms IS thought to result in all the subsequent organisms. In the early organisms the basic genetic information for cellular processes and cellular division is already there. Mutations can duplicate and vary that material. Mutations can change the control of the expression of genes. Mutation can mix parts of existing genes in a way that produces different proteins.
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So in one sense the genetic material for multicellular organisms did already exist from the single-celled bacteria and archaea.
But mutation varied the genetic material,not just varying the already existing genes or alleles but also bringing new genes into existence as a result of mixing and changing bits of previously existing material. Because of gene duplication, a new gene could result from variation of a copy of a gene while leaving the original gene functional. So the possible result of mutations is not just varied forms of already existing genes but includes the origination of new genes. The result of some mutations is a change in the control of expression of genes.
The effect of mutations is not limited to just variation within biblical kinds.

You said this:
…”Tossing a single mutation into a living organism is like tossing a solid oak tree in front of a speeding automobile so that they collide.”
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No it’s not.
It completely depends on what the mutation is and where in the genome it takes place. Some mutations are lethal. Others – most of them – have no effect, or little effect. A mutation in a noncoding non-control region or in most parts of introns would not have an effect. A mutation in a coding region which causes a synonymous change in an amino acid codon would have virtually no effect. Some amino acids in some protein regions can be exchanged for others with similar properties with hardly any effect. etc.
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Maybe your analogy would make more sense if the oak tree were dropped randomly from a helicopter somewhere in eastern Nevada. There’s some chance it would land on a highway but a much greater chance it would land in some empty stretch of sagebrush or playa.

You said this:
…”Scientifically, the number of times mutations not deemed beneficial would not carry through to subsequent generations would vastly outnumber the times it would propigate into major lineages.”
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Is that what you meant to say? I think one of the ‘not’s might be a typo.
Either way, it’s irrelevant. It doesn’t matter if something is less likely than some other thing as long as it is likely enough to happen.

…”Only mutational changes within the male or female reproductive (gametic) cells could affect oncoming generations. Mutational changes in the reproductive cells occur far less frequently than in the cells throughout the rest of the body.”
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I don’t know if it is true that mutations happen less frequently in reproductive cells, but either way, it’s irrelevant as presented. What matters is that mutations do happen in reproductive cells; what happens in the other cells doesn’t matter for this argument.
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…”the reality is that mutations are exponentially more often likely to weaken or even terminate the life process or an organism’s ability to successfully reporoduce. The very sound reason we all fear radiation and (if we have any sense) high concentrations of industrial grade chemicals is because these are a powerful means of producing mutations which will irreparably damage our bodies and can cause birth defects or raise infant mortality rates.”
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But mutations DO happen naturally – you agreed with that. They do happen at some general rate from natural causes. I think you agreed with that. Some mutations are harmful – we agree on that. This is an ongoing fact of life for all species.
(This is a fact of the world, and it seems to me that the fact that mutations occur and some are damaging to individuals is a function of the design that you attribute to God. Even if the original world was perfect and had no mutations, and mutations only began to happen after Adam’s fall, it still must have been God’s choice to cause that to happen.)
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There are a variety of types of mutations from a variety of causes including effects of copying mistakes and transposons as well as mild environmental effects. To subject an individual to a high level of radiation or mutagens is to unnaturally increase the damage to the whole genome all at once from just one particular type of mutation. This is likely to cause negative effects on that individual. But it is irrelevant to the idea that mutations at a natural rate are the source of genetic variation for evolution over time.

(Evolution looks back in history, over millions of individuals and millions of years. Each mutation does happen in an individual, but that mutation does not affect the species unless it is spread by reproduction throughout the population in which that organism lives. In the course of the history of a species, there will have been many mutations as a result of natural causes and some of them will have been harmful to the individual organism in which they occurred.
Many mutations will have been essentially neutral. Some mutations may have turned out to be beneficial but only in certain contexts, and the context in which the mutation is ‘beneficial’ (tricky word) might not exist for the individual in which the mutation first occurs. The mutation might spread through the population as a more or less neutral change (maybe even somewhat negative) and only have a beneficial effect in a totally different environmental or genomic context thousands of year later.}

Here’s a question.
There’s a subspecies of a mouse species which lives on beach areas and islands on the Gulf coast of Florida. It is lighter in color than the mice that live farther inland. Presumably the mice on the beach that are lighter in color are harder for a predator to spot against the sand than darker mice (and vice versa inland). The difference in the colors of these mice is not a difference in genes but a difference in alleles. The allele for the lighter mouse gene is a single base pair different from the darker mice. and it is assumed that it is the result of a mutation which became established in the beach population and not in the inland mice because of natural selection.
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You said there could conceivably be beneficial mutations, and you said there could be changes in alleles but not genes as a result of mutations. This is an example of an allele change and it does not result in a new species, let alone a new ‘kind’ of mice.
So my questions are, first, would you call this a beneficial mutation?
I’d say it was not beneficial in a mouse in the inland, but it is beneficial in a mouse on the beach; it depends on the environment.
And second, do you see this mutation as a loss of information or a degradation? In one sense it changes the molecule away from its original function, makes it less active. But on the other hand, there are now two versions of that gene instead of one, which result in two colors of mouse instead of one, and they can survive better in two different places. Both alleles exist so the mutation in one version of that gene did not eliminate that original information. So it seems to me that it could be considered an increase in information.
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(There are light-colored mice in this species also on the Atlantic side of the Florida which do not have this allele. It seems like they have another allele but it was not clear from the article I read whether that allele was responsible for the light color.)
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Also it seems worth pointing out that this same set of genes that produce mouse color hair are active in all the other mammals, and versions of them are active in birds and reptiles. The same genes were used over and over in all these different animals; there was not a requirement for new genes in each type of animal. I think it is possible to make new genes by mutations, although they would most often be adaptations of existing genetic material. But different ‘kinds’ do not have to have different genes.

In the vampire bat article it says that fruit bats, closely related to vampire bats, also have the short section of DNA to make the second channel splice variant, but they make it as a very low percent of the normal splice variant. So the mutation in the channel gene happened before there were vampire bats. The vampire bat makes the mostly normal splice variant in other nerve cells and only makes the half and half mixture in the cells for detecting prey in the nose. It seems like it’s not yet known what the switch is to make the higher percent of the second variant in the neurons that have heat receptors in the nose. Maybe there’s another mutation in a region outside the gene that activates this.
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A whole lot of questions in case you’re bored:
So do you think vampire bats are a separate ‘kind’? If so, were they flying around Eden biting cows?
Or were they in Eden eating fruit but preprogrammed for the Fall? (I’ve seen this idea on some website, not about bats but about organisms in general.)
Or were there only fruit bats (or a more generic bat) in Eden but after the Fall some of those fruit bats mutated into vampire bats? In these cases, I could wonder why all fruit bats have the genetic sequence to make the second splice variant if they aren’t going to use it.
If they mutated before the Flood, were there vampire bats on the Ark? Did Noah let them bite the sacrificial cows during the journey for food?
Or did they mutate from fruit bats – microevolution – after the Flood? Maybe the mutation for the second splice variant happened in fruit bats after the flood but before vampire bats had diverged from fruit bats. And a hypothetical mutation to express the second splice variant happened some time later. (The vampire bats wouldn’t require this ability to survive; it would just make their lives easier.)
Would you consider a mutation which makes it easier for vampire bats to find good places to bite their prey a beneficial mutation? Or is anything relating to vampire bats a degradation because of their lifestyle?
Is the ability to make this second splice variant an increase in information, a decrease, or no change? How does one decide? For vampire bats, they now have an extra protein isoform made in the infrared neurons; they now make two versions of the protein instead of one, and apparently the two protein molecule types act together (maybe it will turn out that the channel protein is assembled from a combination of both proteins in those neurons, to give it its different heat sensitivity). Those neurons have a new function – maybe you could call it a trait – that other mammals don’t have. (This is only one of the differences between vampire bats and other bats though; by itself it doesn’t create a new species.)
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The bats have the info for the second splice variant, and it makes the mRNA longer than the normal splice variant. Is this an increase in info because it is longer? But because it introduces a stop codon, the actual protein molecule is shorter. Is that a decrease in information? A corruption in function? The new protein is different from the original protein in that it is sensitive to a lower temperature. Is this a loss or a gain?
Humans and rats (etc.) don’t have the sequence for making that particular second splice variant. Does that mean they have less information? Cows (and dogs etc.) can make a similar second splice variant but the sequence is different from the bats. It doesn’t contain the stop codon, so it makes a longer protein instead of a shorter one. (I don’t know how much of the longer protein is made in cows, or what it does if anything; that wasn’t in the paper.) Does that means cows have more information?
The whole TRP channel family has a variety of functions; it is interesting.

…From the quote from Parker: ” Mutations produce only alleles, which means they can produce only variation within kind (creation), not change from one kind to others (evolution).”
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When I think about different kinds of mammals, it’s hard for me to think of different genes in the different types, like genes in dogs that are not in cats, and vice versa. I’m not saying there aren’t any. But different mammals, in particular placental mammals, all have the same basic cell types and organs, so they have the same general genes.
But according to evolutionary biology, mammals developed from a line of ancestral reptiles, synapsids. Mammals have several differences from reptiles, and a main difference is lactation. There is a particular group of genes that are found in mammals but not other vertebrates: the casein genes that make casein proteins in milk. Those proteins are not enzymes or structural proteins; they are proteins secreted into milk to carry a mixture of amino acids, but also calcium and phosphate to growing mammal babies. So the casein genes, for instance the alpha casein genes, are thought to be part of the evolution of mammals, and they are new genes – not alleles of another gene.
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So do biologists think this gene come into being from a random assortment of nucleotides assembled by chance, starting from scratch? No.

A couple of quotes from a paper by Kawasaki, who has been researching this protein (lots of detail in the paper):
…”Kawasaki and Weiss (2003, 2006) previously reported that casein genes were found only in mammalian genomes and that all casein genes are members of the secretory calcium-binding phosphoprotein (SCPP) gene family. The SCPP gene family initially arose from SPARCL1 (SPARC-like 1) in an early vertebrate (Kawasaki et al. 2007), and, in modern vertebrates, many SCPPs are involved in mineralization of bone and teeth (Kawasaki et al. 2004; Kawasaki and Weiss 2008).”
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“All casein genes are among the P/Q-rich SCPP genes and
are closely related to two tooth enamel matrix genes, ameloblastin
(AMBN) and enamelin (ENAM) (Kawasaki and
Weiss 2003).”
from “The Evolution of Milk Casein Genes from Tooth Genes before
the Origin of Mammals”, Kazuhiko Kawasaki,*,1 Anne-Gaelle Lafont,2 and Jean-Yves Sire2, Mol. Biol. Evol. 28(7):2053–2061. 2011.
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This is not proof – it’s hard to prove something which is assumed to have happened 100 million years ago. But it shows that there is a reasonable pathway for the casein gene to have arisen, starting with gene duplication of an already present tooth enamel gene which would already contain the series of amino acids which bind calcium, followed by mutations and recombinations. Mutations of a duplicated tooth enamel gene, contrary to what Parker siad, could reasonably lead to a new gene (not a new allele), a new gene which was a part of the evolution of new kinds.
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There is a gene called vitellogenin which is involved in transporting nutrients to the yolk of eggs. In monotremes, like the platypus, mammals which still produce eggs, there is apparently a functioning copy of a vitellogenin gene. In marsupials and placental mammals, which have no need of yolk, there are inactive vitellogenin pseudogenes. It seems to me this is evidence of the evolutionary history of marsupials and placental mammals from egg-producing ancestors. If they were created separately, it seems to me difficult to explain the presence of an unnecessary, nonfunctional yolk pseudogene in placental mammals.
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Mammals have certain traits in common such as hair and lactation. Animals as different as whales, bats and lions have these traits and they are considered by biologists to share a common origin. If animal types were created separately, I wonder why we don’t see lactating birds or cats with feathers. Why weren’t these traits mixed between different kinds? Why only a couple of monotremes along with the huge numbers of placental mammal types?

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