I have so far written three posts about the problem in the evolution theory and not finally I think that I stumbled on some kind of an idea how to fix the problem. This is all speculative, as it must be if it is a question of evolution or anti-evolution theories. I have these posts in the religion topic as very clearly, the evolution theory is not science, it is religion or ideology. Certainly after writing of conspiracy theories, it is good to write some posts of Intelligent Design or problems in the evolution theory. It continues the same anti-everything-style, and this at least is not anti-Semitic like the historical truth too often is.
The problem in the evolution theory is that mutations are not so common to change the species fast enough. The mutation rate is usually estimated as 0.5*10-9 mutations per base pair (bp) per year. A typical gene has 1000 base pairs. We would expect that one such gene has a single mutation in 0.5 million years. Is this much or little in your opinion?
It depends. This mutation rate is quite sufficient for single bp mutations of single cell organism. If the population is 2 million, then one from the population has a single mutation every year. If the population is single cell organisms and the mutated cell has some advantage, then it multiplies by cell division exponentially and in a short time the whole population is of the mutated type.
A population of 2 million is not large. I remember having capsules of milk bacteria in the refrigerator stating that they contain 100 billion bacteria (1011). There was about 1 ml of liquid. This kind of a population could turn to a mutated one in a matter of days. This seems to be what happens when bacteria gain immunity to antibiotics. The medicine kills normal bacteria cells and new mutations have an advantage. This happens in the time scale of years and there are many bacteria strains that are resistant to most antibiotics.
An even faster adaptation happens in the immunological system. It learns to identify diseases in a matter of days or weeks and in the time frame of years. Identification of the disease is done based on its proteins, so the process probably requires developing new protein-coding parts through mutations.
These processes are fast, but the issue is that the protein-coding part of the gene is mutated only by a single, or very few, mutations, and it stays functional. If there are more mutations to the protein-coding part, it most probably will not stay functional. There most probably is no way to change a protein-coding part by single mutations to a very different one so that in all intermediate steps the gene is functional.
This is why I think that large changes to the protein-coding part must happen in a different way: first a gene, or a protein-coding section of it, gets multiplied. Mutations change one of these copies and it becomes non-functional, but these still is the functional copy and the organism gets the proteins it needs. The non-functional part becomes a part of Junk DNA, which is not active. Because Junk DNA is not active, selection does not work on it and mutations are fully random. We can calculate how many mutations can accumulate to the Junk DNA directly from the mutation rate. With active DNA this is not the case, as there is selection, which favors good mutations and purges out bad mutations. The junk DNA gathers mutations just with the mutation rate: the gene has 1000 base pairs and gets a single bp mutation in two million years. Thus, it gets 1000 bp mutations in 2 billion years. In two million years the gene in Junk DNA may have changed to any possible gene. Some of these new genes are functional. They get turned on and start producing proteins. This was evolution can create totally new functionalities to new species.
This is my basic theory how evolution could work and it is simply based in the observation that protein-coding parts of genes must change considerably in order to create totally new functionalities and that it is very unlikely that the gene stays functional on each intermediate step. Therefore the gene must be for most of the time in Junk DNA. The problem is the time, two billion years. Multicellular organism have been around only for 600 million years. Only single cell organisms have been evolving for longer than two billion years.
The gene size of 1000 bp may be too long to be used as the unit. Protein-coding parts can be shorter, say 100 bp. Then comes control parts. Making this change the evolution time scale shortens to 200 million years. This means a considerable fraction of 200 million years, as we do not know how many mutations are needed.
It still seems quite long. Humans and African apes have diverged about 20 million years ago, humans and chimpanzees maybe 7 million years ago. It is possible that this evolution did not require essentially new protein-coding parts but it happened through mutations in the control part of a gene. Single mutations in a control part can change the species quite much by turning on or off existing functionalities. They cannot create totally new functionalities; they only modify how existing functionalities are used. For instance, the growth time of the brain can be lengthened. Protein-coding parts in these relates species can be different, as there are mutations that keep the gene functional, but these differences should be minor and the gene has never changed totally in Junk DNA.
Maybe 200 million years time scale is not too long for this kind of evolution with the Junk DNA stage in multicellular organisms, but as multicellular organism have been in existence only for 600 million years, it certainly is not short. The proposal is that it only happened with single cell organisms. Multicellular organisms have lots of Junk DNA, but it has not had time to turn functional through mutations. But single cell organisms had the time, so they can have in their Junk DNA genes that can work in multicellular organisms, if we get them there.
It probably is a rare event, but DNA from bacteria and viruses can merge into the DNA of the host animal. I do not know of plants, but plants have plant diseases and probably the mechanism is the same. Even if it is rare for the DNA to become inserted, it still may be more probable than any other way for multicellular organisms to get essentially new protein-coding parts.
If a totally new gene gets into the genome, is it recessive or dominant? I figured it out like this: each individual has two copies of the gene, one from each parent. If the mutated copy does not do what it should do, but the original one does, then the task of the gene gets done. Thus, the mutated gene is recessive. If the mutated gene does something that the original gene does not do, then this task gets done. Thus, the gene is dominant. It is simply a mater of mutated genes lacking functionalities or having more of them.
A totally new gene can and does lack the functionality of the original gene, so this would make it recessive, but it also has new functionalities and it resides in the Junk DNA. So, the previous classification is not sufficient. This is a case of adding a new gene. It probably has to jump to some chromosome to a better place and it is dominant, as the original genome does not have this gene. Dominant properties spread easier than recessive ones, so the new gene would spread into the population quite fast.
Bacteria and viruses infect a large number of hosts and this increases the probability of the rare event of transferring DNA.