For some time I have been trying to figure out on an alternative theory to neo-darwinism to explain evolution. The background to this study is that neo-darwinism does seem to have a serious problem in creating new species.
The problem can be described in a simple way as follows. A gene has protein coding parts, called exons, and non-protein coding parts, called introns. Introns often control the way exons work and a mutation in an intron can easily cause a large difference in the phenotype. This kind of evolution is possible via mutations and natural selection. As an example, in order to grow a bigger brain, ancestors of humans only needed a mutation in some intron causing brains to grow a longer time. So, the brain grew larger.
Single mutations in exons are also easy. As a concrete example, let us take the eye color.
The eye color in humans is mostly affected by chromosome 15. According to recent research human blue eyes appeared 6,000-10,000 years ago and all blue-eyed people share a common ancestor. Two genes influence the human eye color and blue eyes are created by a single mutation in the OCA2 gene. The brown-eyes OCA2 gene is exactly the same in mice, horses, cows, rats, dogs, cats, monkeys, chimpanzees and humans with brown eyes. Humans got blue eyes through a single mutation in an exon of the OCA2 gene.
Siberian huskies and Siamese cats also often have blue eyes. Blue eyes of Siberian husky seems to be caused by an allele of chromosome 18 (CFA18).
https://www.biorxiv.org/content/biorxiv/early/2018/01/15/247973.full.pdf
This is not the same gene that causes blue-eyes in humans. In dogs the DNA segment LOC100855460 corresponds to the first two exons of the human OCA2 gene, as shown in:
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0185944
In dog genome LOC100855460 is in chromosome 3, not in cromosome 18, so it is not the reason for husky’s eyes.
Husky’s blue eyes are also caused by a single mutation in an exon. Such mutations are not especially rare and different species can have different mutations with about the same result. That was mutations in exons. Only a single mutation is usually needed.
But there is a problem with mutations getting many mutations to exons. Exons code proteins and a particular protein is needed in some particular task. It cannot be much modified and still expected to perform the task it is supposed to do. One, or even two, mutations can be allowed. Then we have alleles of a gene. The gene still works as it should, but a bit differently. If we want many mutations to the exon in order to change the protein to a very different one, like if we want to create an animal which has feathers or hair instead of a reptilian skin, then the exon will stop working after very few mutations. The only way I see is that the exon first gets duplicated. One duplicate performs the original function and does not get many mutations. The other duplicate is not needed. It can mutate as far as it wants. Often some intron stops the mutated exon from working, so it becomes pseudo-code. The problem here is that as the mutated exon does not work, it is not under selection pressure. Nothing is guiding the mutations. If the exon would be working, there would be the fittest survive mechanism, but as it does not work, there is no such mechanism. Mutations are completely random. It is extremely unlikely that such completely random mutations could ever produce anything working.
Let us look at an example.
Proteins, and thus protein-coding segments, exons, are mostly quite similar in all mammals, but cats have a special protein Fel d 1 coded by CH1 and CH2 genes. Fel d 1 is the major allergen in domestic cats. Fel d 1 seems to be related to uterogobulin and to belong to protein family secretoglobulins found only in mammals. Fel d 1 belongs to the SCGB superfamily of proteins. Fel d 1 has two forms, the short one has 90 amino acids and the long form has 92 amino acids:
https://www.sciencedirect.com/science/article/pii/037811199290405E
As 3 nucleotides are needed for coding one amino acid, I conclude that CH2 has 270 base pairs.
A mouse has many proteins from this superfamily of proteins:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251818/
Fortunately someone has looked at this problem from an evolutionary point of view:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5957422/
It seems that cat Fed d 1 is similar to mouse ABP (androgen-binding proteine), but proteins differ by at least 50% of aminoacids. That is by some 45 amino acids. I will consider a triplet of base pairs as an unit, thus there are 90 units and 45 changes to the units.
Humans do not have Fel d 1 but many mammalian groups have it to some extent, including non-human primates. It seems that SCGB diversified in placental mammals in the time from 66 million years ago to 56 million years ago. The article derives an evolutionary tree and shows how SCGB superfamily has developed. We can trace SCGB back to the beginning of the Cenozoic Era, but the superfamily is absent from all other animals of the Mesozoic Era. In the beginning of the Cenozoic Era mammals diverged in 10 million years. As different families of SCGB (Fel 1 d, uteroglobulus etc.) can be found in many mammalian subclasses (rodents, bats, ruminants, cats) and they are similar in all subclasses, the time for the SCGB groups to diverge from each other is not more than 10 million years, assuming that evolution proceeds by mutations, not by getting genes from other species.
The question is how probable is to get 45 changes by mutations in 10 million years to 90 units assuming some population size?
The standard figure given for the average mutation rate in all life forms on the Earth is λ=0.5*10-9 mutations per base pair per year. The mutation rate is not constant, but for calculating evolution in the large scale this number is quite fine. In 10 million years we expect 0.5*10-2 mutations per base pair. Unit his 3 base pairs, so the change probability is 3/200. As there are 90 units in this exon, we expect a bit less than 1.35 changes. To get two changes it is (3/200)2 times all possible places for these two changes, which is binomial coefficient (90 over 2)=4005. The probability of getting 45 mutations is (3/200) to 45 times binomial coefficient (90 over 45). It is 2-273283=2-190. The size of the population does not help, unless the population is really, really large. In order to get a realistic probability, the population should be on the range of 2-190.
It does not help if we assume that pseudogene has a much higher mutation rate as corrections mechanims of the cell are not in force, because then we assume the exon developed as pseudogene. Then it was not under any selection pressure and it is totally unbelievable that the mutations led to anything useful.
So, that is the problem.
New exons differing by many mutations cannot be produced by mutations and selection. This is why I ended up to viruses and bacteria. Though even 2-190 is far too high even for viruses, it is possible that the SCGB superfamily developed much earlier in viruses or in bacteria and only moved to mammals in the beginning of the Cenozoic Era. If the time for mutations is increased from 10 million years to, say 0.5 billion years, the problem disappears.
Virus transfer can solve this mathematical problem in neo-darwinism, so I suggest that viruses move a working gene or a part of it from one species to another. The new gene works already rather well when it is obtained. Natural selection can improve it, but there is no stage with the intermediate steps.
It is indeed possible for viruses to transfer genes. It is called horizontal gene transfer:
https://en.wikipedia.org/wiki/Horizontal_gene_transfer
The following link states that viruses can transfer genes between organisms that belong to totally different places in the evolutionary tree
https://www.sciencedaily.com/releases/2017/12/171218120248.htm
It also says that viruses have genes that are needed in cell-based organisms. The authors suggest that this can mean that viruses once were cell-like. I think differently: as viruses can transfer DNA from their genome to the host, so can hosts transfer DNA to viruses, this cell-oriented DNA in viruses has been obtained from hosts that were cell-oriented. The conclusion is that there is a mechanims, via viruses, how different species can transfer genes without interspecies sex.
This is a mechanism that can create a new species and it avoids the problem of mutations: with mutations there is always the problem that even if one individual would get new mutations, how can it find another individual with the same mutations in order to start a new species. It does not help much if the new mutations are recessive, because then the problem is how these recessive mutations get a high enough penetration in the population. With viruses passing the new gene it is much simpler: the whole population gets infected and more than one individual will get the new gene. Then there is only needed the behavior pattern that the like draw each other and those with the new gene can create a new species.
I finish this post with a not-so-serious though examples. I hope nobody gets offended by jokes.
Let us assume there was a mass extinction event, like at the end of the Mesozoic Era 66 million years ago when the dinosauri got extinct. Many animals went extinct at that time, for instance pterosauri, sauri who could fly. Viruses remained and had genes of pterosauri in their DNA. Then placential mammals multiplied. Some population of them got the virus and developed a kind of a wing. Had there bee pterosauri, these flying mammals had not survived as the ecological niche was already taken, but as the niche was empty, bats developed to fill it. But bats did not gradually develop a wing, they got rather good genes from pterosauri.
Humans turn out to have shared genes with cats, cows and mice. I read from the Web that: “Cats have 90% of homologous genes with humans, 82% with dogs, 80% with cows, 79% with chimpanzees, 69% with rats and 67% with mice.” Cats should be closer to dogs than to humans and about as far from humans and chimps, but it is not so. It is like cats have got human genes and the only way would be by microbes moving them between species.
Humans living near some animal species can obtain genes from these animals to their genome. Let us remember that the Old Testament is strongly against pigs and also as strongly against infanticide. Nobody has explained the tabu of pork meat in a satisfactory way. There were people raising pig in the Levant before Israelis. Domestic pigs are one of the species that savage: the mother treats the offspring aggressively and may kill the offspring. There is some genetic component in savaging. Biblical people did not think of viruses transferring genes. They may have thought that your company makes you similar to them. However, there theoretically could be transfer of genes from pigs to humans and some genes affect behavior.
Quite many animals are cannibals. In abnormal conditions pigs can become cannibals. People in New Guinean high-lands kept pigs as pets. These peoples were also cannibals. They have Denisovan genes as well as Neandertalen’s genes. It is currently believed that they got the genes through interspecies sex, but it is not necessarily so.
What would we expect if genes from sheep were transferred to humans? Maybe the population would have thicker and curly hair and strong beards? Or would they behave sheepishly and believe all their priests tell them? Or maybe they would eat all that there is and move to the next place, as sheep do?
Then what would we expect from people who keep cows? If they got cow genes, would the sheep breeders call them cattle? Cows are quite peaceful. Worse may be people, who got genes from mice. Those would be the city dwellers. And one better stay far from hunter-gatherers, who tried hard to get the properties of their totem animans: bears and jaguars. Maybe they succeeded by gene transfer.
Naturally, we must never make such politically highly incorrect speculations about different peoples, but somebody ought to make a study of allele frequencies in different populations and compare them to homologues in domestic animals.
I guess I will put this post to religion. I still cannot see the evolution theory as science.