Not necessarily. "In just 26 generations, we managed to create relationships between the shape and size of (fruit) fly wings that were more extreme than those resulting from more than 50 million years of evolution." - Geir H. Bolstad, researcher at the Norwegian for Nature Research. (sciencedaily.com, "58,000 fruit flies shed light on 100-year old evolutionary question", 2015)
Yes, necessarily. What was the genetic diversity in that population? Did they differ by 2% like chimps and humans do?
Well, I don't think those are mutations, you see, . . .
They sequenced the genomes of the father, mother, and child to measure the de novo mutation rate. Those are mutations. You can hold the parent's DNA up to the child's DNA and see where the mutations happened. How can you say that these are not mutations when we can observe them happening in real time?
When we compare the rate of mutations happening right now they exactly mimic the genetic differences between people in the human population. How is this not evidence for mutations producing human genetic diversity?
Actually, rather than that I don't understand what you consider to be the basics of genetics, it's that I reject the whole idea that you consider to be those basics, that mutations are the cause of any of this.
I would agree that you have to reject everything in genetics in order to hold on to your fantasies, including the most basic concepts of Mendelian genetics.
Just a little context for my previous posts. Here is a chart for transition and transversion substitutions:
Transition mutations are substitutions for bases that are structurally similar. Adenine and guanine have two rings while thymine and cytosine have one ring. Therefore, it is more likely for the protein that is copying DNA to substitute similar bases than dissimilar bases. Due to biochemistry, we would expect naturally caused substitution mutations to be biased towards transitions over transversions.
There is also a second major mechanism. If there is a two base sequence CG (called CpG because of the phosphate between them on the DNA backbone) then the C can be methylated by proteins in the cell nucleus. A methylated C can be deaminated into a T.
The fingerprint of naturally occurring mutations is a high rate of CpG mutations and transitions outnumbering transversions. We know this is the natural process because we understand the biochemistry and also observe these same rates in new organisms. When we see this fingerprint in a comparison of genomes it is smoking gun evidence that those differences were produced by known and observable natural processes.
Well, but aren't you just talking about observed differences, and how do you know those differences are the result of mutations rather than the result of sexual recombination producing a new set of alleles?
If they were the result of recombination then the child's DNA would match one of the alleles carried by the parents. This isn't what they see. The child has a difference in its DNA not found in either parent, not in any of their alleles. This is a mutation by definition.
But wouldn't the substitution of one allele for another show the same kinds of differences?
No. The child's DNA sequence doesn't match any of the 4 alleles carried by the parents.
Here is a simple example. Each parent has two alleles, and the child gets one allele from each parent:
Mother: AAAAAAAAAAA AGAAAAAAAAA
Child: AAAAAAAACAA AAAAAAAAAAA
The child has two all A alleles, on from each parent. However, there was a C mutation that happened in one of those alleles. We know it is a mutation because none of the parents' alleles had that sequence. The child now has a new allele due to that mutation.
Are you now saying that mutations never happen? If so, that's just nuts.
Re: Can we back up for a basic genetics discussion?
What happens in the DNA when say a brown-eyed Bb father and a brown-eyed Bb mother produce children? The Mendelian formula is one BB, two Bb and one bb, right? How is this expressed in the DNA? Is the parents' B on one strand and b on the other?
What happens during the production of sperm and eggs is that the genome is split into two. Some sperm will have B and some sperm will have b. The same for eggs.
I'm sure there must be a different sequence of the four chemicals for a B versus a b, right?
Yes. There can also be new mutations that happen in either allele, making it different from the B and b alleles found in the parents.
Let's start with mitosis. This is how human cells multiply in your body. You start with 23 pairs of chromosomes, duplicate them, and then separate the duplicates into different cells. (I apologize if the background is black. I included blockcolor code, but apparently it doesn't work for everyone).
Meiosis is a bit more complicated. This is the process that creates egg and sperm, each of which only carries one copy of each chromosome instead of the pairs found in your other cells in your body.
In the first step the chromosomes have already replicated, so they are at the sister chromatids stage in the mitosis picture. This first step is the same as mitosis. However, things get a bit different from here. In meiosis I you get recombination between homologous chromosomes which is often called "crossing over". This usually happens about once per chromosome. After the chromosome pairs have swapped pieces, the pairs are separate from one another. After the pairs are separated, the sister chromatids are separated. What you end up with is sex cells with only half the number of chromosomes. When they combine they produce the usual 23 pairs of chromosomes.
Okay, but hypothetically speaking and according to ToE, given millions of years, wouldn't enough mutations occur that could eventually lead to the breeding of a new species?
If you are dealing with just a single population through time, how do you determine when they have become a new species? It's a bit like trying to determine when some goes from being skinny to being fat. It's easy to see the differences between the end points, but there isn't a single microsecond in time where they go from being skinny to fat.
This is a bit different for two populations of sexually reproducing organisms that split off from one another. In this case, we can determine if they are different species by looking at gene flow and divergence. If there isn't any significant interbreeding between the two populations resulting in the genes of the two populations diverging then they are separate species. Obviously, we can't see if fossils can interbreed with other fossils or with living populations.
quote: A particular region on chromosome 15 plays a major role in eye color. Within this region, there are two genes located very close together: OCA2 and HERC2. The protein produced from the OCA2 gene, known as the P protein, is involved in the maturation of melanosomes, which are cellular structures that produce and store melanin. The P protein therefore plays a crucial role in the amount and quality of melanin that is present in the iris. Several common variations (polymorphisms) in the OCA2 gene reduce the amount of functional P protein that is produced. Less P protein means that less melanin is present in the iris, leading to blue eyes instead of brown in people with a polymorphism in this gene.
A region of the nearby HERC2 gene known as intron 86 contains a segment of DNA that controls the activity (expression) of the OCA2 gene, turning it on or off as needed. At least one polymorphism in this area of the HERC2 gene has been shown to reduce the expression of OCA2, which leads to less melanin in the iris and lighter-colored eyes.
These are the two genes that affect eye color the most, and they are right next to each other. OCA2 produces a protein that affects how much melanin is produced in the iris. Different variations in the OCA2 gene sequence affect how much melanin is produced in the iris. The HERC2 gene just upstream of OCA2 controls how strongly the OCA2 gene is turned on. This also affects the amount of melanin produced in the iris. Having one allele that causes higher levels of melanin to be produced can result in darker eyes which makes that allele a dominant allele. If you have two alleles for low melanin production then you have low melanin in the iris which results in blue eyes.
If little to no melanin is produced then light scatters in the iris without being absorbed by melanin, and the result of this diffraction is the color blue. People with blue eyes don't have a blue colored protein or dye in their eyes. Instead, the blue comes from light scattering in the iris. The same thing happens in some birds. For example, the bluebird isn't actually blue. The color you see is due to the scattering of light in its feathers.
added in edit:
Another great resource for the genotype-phenotype relationships for eye color:
quote: The OCA2 gene also contains numerous regions for eye color expression. Over 300 [single nucleotide polymorphisms] (SNP) for eye color have been identified on the gene, but classification of their results proved too arduous. The gene contains a main coding region for brown eyes (BEY2 15q11-15) and hazel eyes (BEY1).3, 5 Other SNPs result in blue and green eyes. One SNP has been studied to show a large significance for eye color. Before the revelation of the effect of HERC2, rs1800407 in exon nine was thought to be the main factor for eye color. The change of this base from a C to a T causes a change from brown eyes to non-brown eyes (usually blue). In the P protein, the mutation causes residue 419 to change from an arginine to a glutamine. The possible changes in the DNA sequence are GCT to GTT and GCC to GTC. Although the crystal structure has not been published for the P protein coded by OCA2, residue 419 is predicted to face the cytoplasmic portion of the lipid bilayer in one of the several transmembrane domains.14 Therefore, the SNP change that results in R419Q most likely affects the P protein in conformation. https://www.nature.com/articles/jhg2010126
I would expect it to alter it, but not in any beneficial way.
Reality doesn't care about your expectations. What you need to do is show how mutations could not result in beneficial changes using actual evidence and facts instead of your expectations.
Let's do a bit of math. There are 6 billion bases in the human genome if we are considering both pairs of chromosomes. There are 3 possible substitution mutations at each position in the human genome since there are 3 other bases that can be substituted. This means there are 18 billion possible substitution mutations in the human genome.
Each human is born with ~100 substitution mutations. This would mean that in 10 births there are 1,000 mutations. In 1 million births there are 100 million mutations total. In 180 million births there are 18 billion mutations.
This would mean that we only need 180 million births to have an even chance of creating all possible substitution mutations at every position in the human genome. There are about 7 billion humans alive right now. This means that every possible substitution mutation has happened about 40 times over in the current population.
So can you please tell me why random mutations could not produce beneficial changes in the human genome when every possible mutation has happened 40 times over in the current population?
What I "expect" isn't about my own guesses, it's about what I've picked up from YOU GUYS by reading various web sites and so on.
That's a bit strange since I have stated over and over that random mutations can produce beneficial mutations. Obviously, you are ignoring what we are saying.
Where I used to think a single trait such as eye color was probably governed by many genes, it seems now that it's governed by different regions of a single gene?????? How that works I don't yet grasp since I thought a whole gene made a particular protein, which protein is what brought about the trait.
There are multiple genes that can affect eye color, but most variation in eye color is affected by two genes. One of those genes is for the protein, and different mutations will affect the function of that protein. The other gene controls how much of that protein is made.