The End of Evolution By Means of Natural Selection

You need to study up on the Luria-Delbruck fluctuation assay and the Plate Replica experiment. Both experiments start with a single bacterium and through mutations you get all kinds of mutations that can lead to bacteriophage resistance and antibiotic resistance. These mutations occur BEFORE selection of the traits. It's occuring across the entire genome and across the entire population. Yep. So if you look back in time you have an entire population with no blue fur, and then later in time you have a population with blue fur. That is change over time, and it requires mutation and then selection. Why not all alleles at all times?

And my response described a scientist's view of how mutation and selection work. The Luria-Delbruck fluctuation experiment and the Plate Replica experiment (google is your friend) are the foundation of that view. Both experiments demonstrate that mutations arise independently of selection and the needs of the organism. That is, the mechanisms that produce mutations do not sense which mutations are beneficial or detrimental to the organisms. In the L-D experiment, mutations that confer bacteriophage resistance occur in the absence of bacteriophage. In the Plate Replica experiment you are actually able to produce a population of antibiotic resistant bacteria without that population ever coming into contact with antibiotics.I strongly suggest you read up on these two experiments. The Wiki page for each would be a good start.

Not really. The plate replica experiment uses indirect selection to arrive at a population that is made up of antibiotic resistant bacteria. This involves several rounds of indirect selection, but the result is a resistant population where none of the ancestors or descendants have ever came into contact with antibiotic.When you replicate a master plate onto antibiotic plates using a "stamp" you still have the master plate. When you observe resistant mutants on the replica plates you can know where they originated from on the master plate. You can use something like a toothpick to sample the bacteria from that area. You grow these bacteria up for a few generations and then replate them making on an antibiotic free plate which is a new master plate. By repeating this process 2-3 times you can end up with a population that is >99% antibiotic resistant.

That's not what you said in the previous post. You said, "I'm asking: is this how evolutionists think mutations work?". That was your question. If you want to know what Dr. A thinks without anyone commenting then send him a personal message. Mutations create alleles that have never existed in the population before. Your genome probably contains between 1 and 3 alleles that are not found in anyone else in the population, and were not present in either of your parents. The average bacterial genome is 2-4 million bases. The human genome is 3 billion bases. Can you please explain how a genome with 1,000th of the DNA has more "potential" (whatever that means)? Also, please explain why it requires mutations to unlock this potential, and why these mutations occur before they are useful. And before that you have to increase the genetic diversity, and this occurs through mutation.Edited by Taq, : No reason given.

I would disagree with anyone who states the above. I would disagree because of the mountains of experimental evidence which demonstrate that mutations arise independently of the needs of the organism. Projection much? Your posts are a lesson in obsfucation and gobblygook. You have such phrases as "blurring the character of a species" and other notable nonsense terms.

Why? They are much less mystifying than eukaryotes, actually. You don't even have to keep track of diploid traits and recombination. Just asexual reproduction. Their DNA mutates just like ours, and given their short generation time and the ease with which they can be grown they make for the perfect model organism in genetics. If you want to learn the basics of genetics then you must understand genetics in bacteria. Again, it is known that mutations lead to antibiotic and bacteriophage resistance. These "possibilities" didn't exist in the original parent population. They only came about through mutation. For example, mutations in the tonB gene lead to bacteriophage resistance in E. coli. This bacteriophage resistance was not functioning in the original bacterium that was used to supply the population for the experiment.Even more, you claim that mutations do away with function. Now you are claiming just the opposite.

This focus is keeping you from seeing the big picture. You can't see the forest for the trees.You claim that this reduction is permanent even in growing populations. I have genomes that are different, and those differences are beneficial in each species. Obviously, changing DNA can result in a benefit otherwise there would be only one species with a very specific genome. No such assumption is needed for what I am saying. It doesn't matter how those differences got there, be it special creation or evolution from a common ancestor. The question at hand is whether a different DNA sequence of a specific gene can be beneficial. That's it. Obviously, you can change millions of bases and still have a very healthy species no matter if that is through mutation or design. Do you agree or not? How did you determine that the human and chimp lineages have hit that end? What genetic evidence shows this? What genetic evidence demonstrates that humans and chimps are not two varieties of apes just as tigers and house cats are two varieties of cat? You claim that DNA can not be different without causing disease. So how do you explain DNA that is different but doesn't cause disease? It's a very simple question. So it doesn't matter how much water the Sun evaporates into the air, we will still run out of water in the atmosphere because rain causes a reduction. This is what you are arguing, correct? Common ancestry is considered a fact within science, and for good reason. If you want to discuss common ancestry between humans and other apes it would probably be best to start another thread at a later time. Let's just ignore the possibility of common ancestry for now.What I want is an explanation for why DNA sequence can be different without causing disease, and even beneficial to the species. This is a fact. It is a fact that utterly destroys your argument.

The Lederbergs' plate replica experiment starts out with a single bacterium. Link.Either that first bacterium is resistant or it is not. If it is then 100% of the subsequent population is also resistant. This is not what the Lederbergs observed. They observed that a tiny percentage of the descendants of that single bacterium were resistant, and that this resistance was clonal in nature and inheritable. Therefore, the resistant phenotype had to arise due to a mutation sometime between the original common ancestor of the entire bacterial population in the study and the time when the descendants were exposed to antibiotics.

Quorum sensing in bacteria is well below what is seen in multicellular eukaryotes like ourselves. I wouldn't describe so much as intelligence but as an automaton. Bacteria have set reactions to a set of stimuli, but they don't really show an ability to improvise. Actually, bacteria are often the best type of life to use when testing the theory of evolution. Their generation times and ease of growth make them ideal for studying the theory.

Evolution solely by means of natural selection is controversial. The most famous of these experiments is the emergence of lactose metabolism due to metabolic stress. When the first studies came out they made a rather obvious mistake. They assumed that the mutation rate didn't change. It does. When DNA damage occurs due to metabolic stresss or antibiotic treatment this turns on the SOS response. This response includes the production of error prone polymerases which increase the background mutation rate. It also turns on recombinases which can copy a gene multiple times.So what about the lactose experiments? Well, it turned out that the presence of lactose did not cause the mutations to happen. Rather, the lactose rich environment SELECTED for the lactose mutations and lactase gene duplications. There was no mechanism that sensed the presence of lactose and then produced the needed mutations to metabolise lactose. These mutations occur at the same rate no matter if lactose is present or not. These mutations are random with respect to fitness. Show me the evidence and I will gladly do so.

This is more of what I would expect from an adaptive mutational response. Transposons are not your "classic" mutation, but they are a mutation nonetheless.However, these types of mechanisms are rare, at best. We can see bugs adapting to carbon sources, like nylon oligomers, that have never existed before. Also, the size of the bacterial genome (ca. 2-8 million bases) doesn't seem big enough to hold a specific mutational response to every possible carbon source or environmental challenge. A much more elegant system is random mutation which requires very few genes.

I agree that it runs contrary to random mutations as well. In order for this system to stay intact you would also need constant exposure to glycerol. Neutral drift could wipe out this system if the bugs were not exposed to glycerol over an extended period of time.But how could such a system come about? Well, I don't see why RM/NS could not produce this mechanism. Obviously, there is selection pressure on both the transposon insertion site and the sequence for the DNA binding protein. Transposon sites are not hard to come by, so the key to this whole system is the glycerol sensitive DNA binding protein. Once that evolved the system was in place.

The glycerol metabolism example is but a single example. We know from experimentation that the vast majority of mutations do come about through random mechanisms, and that those random mutations do pass through natural selection.What you need to show is that every single mutation occurs through a similar mechanism. Perhaps you can stick to real world observations instead of inventing fantasies to falsify the theory?

The proof is in our genomes and the genomes of other species. It is quite simple, really.Why are humans and chimps different? It is because our DNA is different.Mutations cause DNA to be different.It is an inescapable conclusion that changing DNA through mutations will result in different species. That is completely false. You might want to check out the Human Haplotype (or HapMap) Project:http://www.genome.gov/10001688We know of tons of neutral mutations. Most biologists use cladistics nowadays so the phyla designation really doesn't have that much pull. No matter what happens to the sea slug it will always be a member of its clade.

A mutation was a change in phenotype. Throughthe work done by Luria and Delbruck with their fluctuation assay and the Lederbergs' work with the plate replica experiment it was shown that these changes in phenotype preceded exposure to selection pressure. Specifically, Luria and Delbruck were able to show that mutations leading to bacteriophage resistance occurred prior to the bacteria being exposed to bacteriophage. Their conclusion was that mutations were random with respect to fitness, the same conclusion we hold today. This work was done before the structure of DNA was discovered.