A test for claimed knowledge of how macroevolution occurs

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Not only do I think this idea of millions of years is nutz, I think the idea that mutations create healthy alleles is also nutz.

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Millions of years is a fact. And if mutations are random the only thing stopping them from creating “healthy alleles” is probability. Thus it is at least possible in principle - unless you assume a non-random mechanism that prevents it - and even to say it is too unlikely requires evidence.

Plus it is important to use the applicable probability model.I'm more than a few decades rusty on proper terminology. Most of us are familiar with the problem of finding the probability, P(), of multiple independent events all succeeding: A classic example is a coin toss (P = 0.5) in which you figure the probability of tossing 5 heads in a row: But that does not model this problem. You have a population all mutating simultaneously and in parallel with each other and all you need is for one, just one, of them to succeed; ie, P(A or B or C or D). How would you do that?I encountered that problem when calculating the probabilities for my version of Dawkins' WEASEL, which I named MONKEY -- read my MONKEY PROBABILITIES (MPROBS) page for that analysis. I ended up applying De Morgan's Theorem from Boolean Algebra (streamlining it a bit here): Now for example, let's assume that the probability of each event is one in 10, 0.1. And let's assume 4 events: Notice that it is more likely, 3.5 times more likely, for at least one event to succeed than for any single event to succeed. Now let's test for 100 events: Now that rather low individual probability yields virtual certainty that at least one of 100 unlikely events will succeed.In my MONKEY, to probability for a single individual mutated string to advance towards the target is rather low. But since I was working with a population of 100 strings, the probability of at least one of them advancing is high. To put it in other words, the only way for the system to fail to advance would be if every single string were to fail every single time and that event was so unlikely as to be virtually impossible.

Sorry, ignore this postEdited by Dredge, : No reason given.

I understand your point now ... I was playing by my rules and not those of ToE.

I get it now. Okay, I understand that now.Edited by Dredge, : No reason given.

Thanks for that explanation. I take your point.

Okay, thanks; I get that now.

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?

You may well think that but it doesn't prevent it being true does it?The example of the mutation in the peppered moth changing its colour is a perfect example of a beneficial mutation - but only when the environment that they lived in changed. The mutation got the moth killed by predators in the wrong environment.

That's exactly what is illustrated in the post on meiosis.

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.

Just a bit on eye color for Faith:

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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.

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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.

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Is eye color determined by genetics?: MedlinePlus Genetics

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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:

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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.
Genotype—phenotype associations and human eye color | Journal of Human Genetics

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Edited by Taq, : No reason given.Edited by Taq, : No reason given.Edited by Taq, : No reason given.

And so, as usual, it's a little more complex than the comic-book version of evolution that anti-evos frequently peddle.

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?Edited by Taq, : No reason given.Edited by Taq, : No reason given.

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.So I gather genetics is getting more complicated, which is as it should be I'm sure. 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.I've been trying to find the best book on basic genetics for some time and none of them seem to cover enough of what I want to learn, or they add a whole bunch of stuff about human inheritance which I'm not interested in at the moment, and so on. And I'd suppose it doesn't explain enough of the things you are talking about to be useful in this discussion either. Yes????I did get Genetics for Dummies for the PC Kindle but now I can't open that page for some reason. If it isn't one thing it's another....