The mutations need to be guided. In evolutionary theory, the guiding is done by natural selection.
So I am curious to know where you place the limits on the “unguided” part.
The mutations need to be guided. In evolutionary theory, the guiding is done by natural selection.
So I am curious to know where you place the limits on the “unguided” part.
Natural selection does not affect which mutations occur. Natural selection only affects which mutations are passed on to future generations.
I don’t place any limits on the unguided part. What I do is test hypotheses using observations.
Two of the most famous experiments related to random mutations are the plate replica experiment first published by the Lederbergs and the fluctuation experiment first publised by Luria and Delbruck. In these experiments they were able to determine that beneficial mutations appeared in the population before they were needed by the organisms. For example, mutations which conferred antibiotic resistance occurred in environments where there was no antibiotic. There was no connection between the mutations an organism needed in a given environment and the mutations it got.
We find this same situation throughout most of biology. There are no pervasive cellular mechanisms whereby organisms can sense something in their environment and then mutate a specific stretch of DNA in their genome in response to that environmental cue. There are only a small handful of very limited mechanisms known which could possibly be considered to fall into the guided category, such as the CRISPR system in bacteria that specifically mutates a section of their genome by inserting viral DNA between DNA spacers.
Also, un-guided mutations (again, in the scientific sense) is probably a better solution than guided mutations. If you are relying on a set response to a specific stimulus then you have a limited number of responses. For example, if a host only has a limited number of responses to a virus then a randomly mutating virus can quickly produce features that they host has never seen and has no response to. A random mutating host can produce new solutions continuously and isn’t limited in how it can respond.
Is the Biologos paper measuring differences in the gene coding regions or is it over the entire genome?
This is weird. Do you believe all traits emerge fully formed through “unguided mutations” and selection only helps in fixing these traits?
I just gave you a link demonstrating that it isn’t an assumption. The evidence demonstrates that mutations are responsible for the differences between humans and other apes.
Let me explain how this works. First, here is a picture of the DNA/RNA bases
Notice how T and C are a single ring structure while G and A are a two ring structure. This means that due to simple biochemistry a DNA polymerase will tend to replace a one ring nucleotide with the other one ring nucleotide when mutations occur. The same applies for the two ring nucleotides. Mutations that switch between similar bases (e.g. C–>T) are called transitions while mutations that switch between dissimilar bases (e.g. C–>A) are called transversions.
Another special case are CpG mutations which change the C to a T at a high rate wherever there is a 5’-CG-3’ sequence. The C in a CpG can be methylated by other enzymes and this makes the C vulnerable to deamination which turns it into a uracil. When the DNA with a U is copied that U is copied as an A on the complementary strand and then into a T when that complementary strand is copied again. A bit complicated, but that is the biochemistry behind substitution mutations.
We can also confirm these processes by looking at the human population in real time. Genome sequencing has become much less expensive and much faster which has allowed scientists to directly measure the mutation rate in humans by sequencing the genomes of parents and their offspring. One such study looked at 283 family trios, and the mutations are broken down in this chart:
Non-CpG transitions happen at a higher rate than non-CpG transverisons, and CpG mutations occur at a much higher rate than the non-CpG mutations (rates are determined by the available bases where such a mutation can occur). Again, this is what we observe happening in real time.
Steve Schaffner (aka @glipsnort) did a wonderful job of outlining the types of differences within the human population which fits this same pattern (Biologos). Dr. Schaffner also details the differences between humans and other apes, between different ape species, and between different mammals. They all follow this same pattern. Transitions occur at a higher rate than transversions and CpG mutations occur at the highest rate. This is the fingerprint of mutation, and it is found throughout these genomes. Mutations aren’t assumed. they are evidenced.
Are the mutations measured here based on genes or the entire genome?
We observe that traits emerge fully formed through mutations that are statistically random with respect to fitness. Again, this is an observation. This was observed in the experiments done by the Lederbergs with the plate replica experiment and in by Luria and Delbruck in the fluctuation experiment.
Since their work in the 40’s and 50’s we have discovered the genetic basis for these adaptations and further confirmed their work.
The entire genome, including genes.
Are you claiming this for more than antibiotic resistance?.
Say eyes… these also emerged fully formed (each intermediate version that is)?
Or complex functions Ike photosynthesis?
As to mutations being “statistically random”; that’s just a big word to say, you don’t know how they arise… and can’t find any pattern to it.
Ok. I can see why you find this evidence is convincing given differences follow a mutational pattern. What does not make sense to me is we can get very defined morphological benefits like increased intelligence and speech capability mostly from neutral changes.
Yes. It applies to all mutations that have been observed (with a few exceptions like the CRISPR system). Mutations cause deleterious, neutral, and beneficial changes, all through the same mechanisms.
The changes that each individual mutation produces will emerge fully formed. If a feature is due to multiple mutations then the end product will not have emerged all at once.
We do know how they arise and we know what the pattern is. See my posts above.
That doesn’t make sense to me, either. I tend to think that those changes are due to beneficial mutations, not neutral ones.
Aren’t you contradicting yourself here? If most mutations are neutral, then it’s highly likely that features involving multiple mutations emerge all at once.i.e a one or more neutral mutations are added to by a new mutation that leads to a trait dependent on all the mutations.
Beneficial mutations happening by chance… adding up sequentially will need natural selection to play the role of compiler.
Which is dominant in the process? If it’s the latter, then what you are proposing is not essentially different from pan adaptionism.
A few points:
If most mutations are neutral then some are beneficial and some are detrimental.
Some anatomical or physiological changes are going to be neutral changes. For example, mutations that slightly change the shape of your nose are probably neutral.
Mutations present in the gametes that conceived you are immediately expressed. Therefore, any changes that a mutation may cause will be there from the moment that gene is first expressed.
I don’t know what you mean by compiler, but I would agree that natural selection will be needed to fix beneficial mutations in a population and help its transmission to subsequent generations. There is also interplay between mutations, which is called epistasis. A neutral mutation at one point in a species history may become beneficial later on if it interacts with a new mutation in a way that benefits the organism.
Neither is dominant over the other since they work in different areas of biology. Mutations occur at the individual level while natural selection occurs at the level of the population.
Was written by @glipsnort, and he used the entire genome.
So it’s basically chance all the way through.
No wonder you are fixated on lotteries…
Selection is not chance.
To what extent does selection influence the process? You skipped my question claiming selection is a population level phenomenon and is not directly related to molecular level phenomenon. This is fair enough as a set of genes in a population is selected for…
In what way does selection improve the probability?
Influence which process? Selection doesn’t influence which mutations occur in each individual in each generation, but it does influence population level changes in a species over time.
Improve the probability of what? Improve the probability of a beneficial mutation become fixed over time? Improve the probability of a neutral mutation becoming fixed in a population? Improve the probability of a deleterious mutation becoming less common in a population over time?
What probability are you interested in?
Perhaps an analogy would help. Start with a shuffled deck of cards and draw 5 cards. Draw one additional card. If that card improves your hand (rules of Poker) then keep it and discard another card from your hand. Keep doing this through the whole deck. What you will find is that your hand steadily improves over time. There is a chance process involved in the form of the shuffled deck, but there is also an element of selection that keeps the beneficial changes.
Poker has fixed rules… try the same in game of poker where the rules change abruptly in a random manner…
Natural selection is not static. A trait that is selected for in a couple of generations, can be selected against as the situation changes.
What you described is a process dependent in chance + contingency. Why deny it?