The advantage of sexual reproduction is that multiple mutations in different genes can be combined into the same genetic background. That doesn’t happen in asexual reproduction.
I am saying that plasmids are passed between bacteria through sex pili.
How are these multiple selective mutations accumulated and passed down to each generation? All 17 bases are in a single gene (allele). Did they accumulate by recombination? If not by recombination, what genetic mechanism do you think caused this? Here’s a more fundamental question, are these mutations random occurrences?
How do sexual replicators accumulate multiple selective mutations in a single allele?
Don’t sexual replicators have multiple selective mutations in a single gene (allele)? I understand that there is a possibility that multiple selective mutations can be recombined in an offspring if they occur in different genes but how do multiple different selective mutations accumulate in a single gene (allele)?
What determines the genetic material transmitted by a plasmid?
Recombination is the shuffling of genes. If you are considering multiple selective mutations in a single gene, how would shuffling genes add additional mutations to a particular gene?
When you say “mutation and inheritance”, how is that different than descent with modification?
If mutations are random occurrences, how would you compute the joint probability of two or more (or 17) random occurrences in a single gene?
You tell me. You are the only one who seems to think it can.
Descent with modification was coined before genetics was understood. “Mutation and inheritance” is more specific in that it details the actual mechanisms.
The human mutation rate is about 50 to 100 substitutions per person per generation. If we start with one person, they are born with 50 mutations. Their offspring will inherit about half of those mutations along with half of the new mutations from their other parent. The new offspring will also have 50 new mutations of their own, bringing us to 100 mutations. This keeps happening generation after generation.
A plasmid is genetic material. It is DNA. Whatever DNA sequence is in the plasmid is what is transmitted.
Recombination can’t do this. Multiple selective mutations can not be combined in a single allele by recombination (shuffling of genes). Where have I said that it could happen?
Explain to us your understanding of mutation and inheritance and how does it differ from descent with modification when applied to DNA evolution?
Show us how you would compute these joint probabilities using your mutation and inheritance mechanism for the 17 selective mutations in that gene.
Which of those 50 to 100 substitutions are the 17 selective mutations found in the gene you reference? Or are you claiming that all mutations are selective mutations?
Under what circumstances does the genetic material transmitted by a plasmid is a drug-resistant allele?
I’m not your puppet. If you have something to say, then say it.
The probabilities would depend on the genetic background in which the mutations are occurring. You would need the genomes of all of the human ancestors in order to calculate this. If 1 mutation is already present in 50% of the population, then a second mutation in that same gene will be quite common, as one example.
We could also look at population genetics. The rate of fixation for neutral mutations:
The mutation rate is about 50 to 100 per individual per generation. This means about 50 to 100 neutral mutations reach fixation in the human population per generation. Over 5 million years, that’s about 200,000 generations since sharing common ancestry with chimps which gives us 10 to 20 million mutations that reach fixation in both lineages. This is in line with the approximately 35 million mutations that separate humans and chimps. This is just for neutral mutations. Beneficial mutations would reach fixation even faster. The number of mutations that separate chimps and humans is entirely in line with what we would expect to see.
You only need a few hundred million births to get every possible mutation.
When the plasmid contains a gene for drug-resistance the drug resistance is transmitted with the plasmid because it is a gene on the plasmid. What are you not getting here?
Is it now clear to you that recombination has no effect on multiple selective mutations accumulating in a single gene?
Is that your way of saying that you cannot explain the difference between mutation and inheritance and descent with modification?
Are you saying that the joint probability of two mutations depends on the population size? Are all 17 of those selective mutations for that gene in 50% of the population?
You have said that there are 20,000-30,000 genes. Are there about 17 selective mutations in each of those genes. Are all those hundreds of thousands of selective mutation fixed by neutral fixation? What happens to the other variants in the population.
Are all those possible mutations selective mutations? How does every member of the population end up with the same 17 selective mutations in the same genetic locus as other members of the population? Then consider a different genetic locus and its set of selective mutations, how does every member of the population get the same selective mutations at that locus as well as the same set of 17 selective mutations at the genetic locus you have suggested?
It is clear to me that recombination has a large effect on multiple mutations accumulating over the entire genome. There is more than one gene in a genome, and an organism is the product of the whole genome, not a single gene.
I already explained it, and here you are asking the same question.
Read what I said.
“The probabilities would depend on the genetic background in which the mutations are occurring.”
I haven’t looked. Why don’t you if you are so curious about it? Why ask me to look up stuff for you?
If all of them are fixed and a new mutation happens in the same gene, what are the probabilities for all 18 mutations? It’s just the probability of one mutation, is it not?
I also showed you that the differences between the chimp and human genome are consistent with what we would expect from the probabilities of neutral drift.