Evolution - Speciation finally observed in the wild?

[tas8831]

No, Mendel also incorrectly used simple genetic not matching the reality we understand.

Myths of Human Genetics: Eye Color

You are simply confused and don’t understand anything about ainheritance and genetic mixing.

“One of the oldest myths in human genetics is that having blue eyes is determined by a single gene, with the allele for blue eyes recessive to the allele for non-blue eyes (green, brown, or hazel). Many people who know nothing else about genetics think that two blue-eyed parents cannot have a brown-eyed child.”

“Eye color is not an example of a simple genetic trait, and blue eyes are not determined by a recessive allele at one gene. Instead, eye color is determined by variation at several different genes and the interactions between them, and this makes it possible for two blue-eyed parents to have brown-eyed children.”

If Mendel had been correct in his belief that one allele is what controlled traits, blue eyed parents would never be able to have brown eyed children. But it’s not a simple 4 possibility choice, but a in reality multi allele choice of more than your simple choices you want it to be.

Blah blah blah.


Apparently, in your quest to save face, you didn't notice that all of that is only about the alleles for eye color. That is, they all deal with a continuously varying trait.

This is interesting and all, but 100% irrelevant to the point I had made (and lost on you):

"You truly seem to think that any allele can recombine or mix and match with any other allele, no matter what the alleles are - that is the ONLY way your fantasy could even hope to have merit.

But reality does not operate that way."
​

Your own link indicates:


"A number of groups surveyed associations of single-nucleotide polymorphisms with eye color, with fairly consistent results: variation in the HERC2 and OCA2 genes, which are next to each other on chromosome 15, plays a major role in determining eye color."

Tell us all, won't you, what is meant by "single-nucleotide polymorphisms "?

And your link also mentions this paper:

"Genetics of human iris colour and patterns"
Richard A. Sturm and Mats Larsson

in which we see:


"Nevertheless, it has been estimated that 74% of the variance in human eye colour can be explained by one interval on chromosome 15 that contains the OCA2 gene. Fine mapping of this region has identified a single base change rs12913832 T ⁄C within intron 86 of the
upstream HERC2 locus that explains almost all of this association with blue-brown eye colour. A model is presented whereby this SNP, serving as a target site for the SWI ⁄SNF family member HLTF, acts as part of a highly evolutionary conserved regulatory element required for OCA2 gene activation through chromatin remodelling. "

and one can also note the paper's Table 1. Human pigmentation gene polymorphisms associated with eye colour -

tell us all what is meant by "gene polymorphisms", won't you?

And tell us all, with your amazing genetics expertise (bolstered by keyword searches to find quotes that can be taken out of context to try to save face), HOW such things as "gene polymorphisms" and SNPs come to be?

Must be by interbreeding and hybridization, right?

Yes, continuing [sic] varying traits are traits that are never the same

LOL!!!


My gosh...

No, a continuously variable trait is something like height. There is HEIGHT, then within that trait, we have short, medium, tall, etc. I know of many people that are my exact same height. Don't you?

So, in your Grant paper, where they talk about these sorts of traits being influenced more by hybridization than mutation, it is because different combinations of alleles play a greater role than individual birds experiencing mutations and - wait for it - generating new alleles, since these would be of lower frequency in the population. Mixing and matching the relevant associated alleles that already exist (and already exist due to mutation) via hybridization has a greater short-term impact than new allele generation and waiting for them to increase in frequency sufficiently to have an impact on phenotype.

I think you confuse alleles with phenotype?

Do you still think they are called "allies"?

which falsifies your belief there are only 4 choices for each two allies inherited from parents.

Not at all.

You continue to look at these issues like a middle schooler.

Let us say for the sake of argument that height at the shoulders for wolves is governed by 10 loci.

A breeding pair will possess a maximum of a total of 40 possible alleles at these 10 loci.

Why a maximum? Because some could be identical, right?

So if we mix and match 40 alleles (4 per locus, 10 possible combinations per locus - remember? ABCD = AA,AB,AC,AD,etc.?), we can get a maximum of 100 unique combinations (or is it 400? My head hurts...).

Other factors influence height, such as nutritional status, etc. - we will ignore that for simplicity.
Wow! Justa population genetics is saved!


Or is it -


With 400 possible allele combination at 10 loci at which both member of a breeding pair had different alleles - we just populated a continuum with individuals of differing height.

We did NOT get a Mastiff and a Chihuahua - we just got wolves of differing heights.



But wait - you say that Adam and Eve had "perfect" genomes, that is, no mutation, so all of their alleles at these 10 loci had to have been identical (since that is how alleles arise - mutation).

That is right - creationists seem to believe that mutation was the result of the Fall - a curse. A punishment. So genetic variation - new alleles - is a punishment, if we accept creationist logic.

Creationist urologist Barney Maddox writes:

"The perpetuation of the Darwin myth clashes with reality--the God-created reality--where living things and their genomes were created "very good" and have degenerated from there."


Creationist John Mackay has a GREAT totally sciencey take on mutations - a must read. He demolishes the 'all hybridization all the time' model of Justa is seconds flat.

"So did God invent mutations? An analogy will help. God did invent gravity without which life would not be possible. Your bits wouldn’t stick and we wouldn’t have a planet to live on. But once gravity is invented, you can choose to jump out of a plane at 30,000 feet, but don’t you dare argue God pushed you! Obey the law of gravity and live, but the default setting of the law of gravity will kill you, specially when de-fault is yours. Likewise God did invent genes, but disobey his law and the default settings which do involve gene degeneration will bring about your death."


And this Bible and genetics expert writes:

"...explains all the phenomena and genetic mutations in species we see today and can be traced back to our roots and the fall of man in the Garden of Eden."


Amazing insights.
So no new alleles in Adam and Eve - all loci =A (AA,AA,AA,AA).

Thus, no Africans, Asians, etc. to hybridize to get Afro-Asians.

Just following Justa's scientific model's logic here, folks.

I notice you don’t object when they claim a mutation creates a variation in a trait, only when interbreeding creates a variation in the same trait, right?

Right - because I understand where 'interbreeding' gets its raw material from.

You refuse to.

Hmm, so a mutation that affected the allies [sic - my gosh! can you NOT learn at all????] of the genes that control height, would create a variation in, umm, height? Your explanations are laughable and so easily shown for what they are.... excuses.....

Ummm... OK - so you DON'T think that mutations producing new alleles that affect height will influence height?

So what DOES affect height? Mixing up the "allies" that affect height via hybridization.

OK - where did those new "allies" come from?

Interesting.

Shortsighted brainwashed evolutionary PR trash......

From the fellow that STILL thinks alleles are called "allies", and who simultaneously declares - without evidence - that Adam and Eve had "perfect" genomes, but through the 'interbreeding' of their inbred, perfect-genome-having offspring, we get NEW combinations of alleles (that arose via???) producing all extant phenotypes (only to be washed away in a big flood (for which there is also no evidence) leaving only 4 inbreeding pairs to, yet again, re-populate and re-diversify all of humanity in only a couple hundred generations)...


I stand totally refuted.... A dude on the internet, who thinks alleles are called "allies", has totally refuted not only all of population genetics, but all of standard classical and transmission genetics as well!

LOL!!

 

[Justatruthseeker]

So you are unfamiliar with the fact that nearly all pathogens are species-specific? Typical.

Typical you regurgitate evolutionary PR trash.

Diseases Affecting Multiple Animal Species

Cross-species transmission - Wikipedia

http://www.cs.unm.edu/~melaniem/pdfs/DobsonAmnat.pdf

Is that how that works?

Do tell!

Right.

Well, according to this paper:

New bioinformatic tool for quick identification of functionally relevant endogenous retroviral inserts in human genome


there are ~700,000 identified sites in the human genome where ERVs/LRs are found.

Yah so? Just shows past infection multiple times.

In another paper, this figure is very nice - it shows the known integration sites in the human genome for 3 ERVs. There are a lot of them. This is the case for all ERVs - they integrate at specific DNA sequence sites which are all over the genome.

This means that when we see integration sites in 2 taxa at the same locus (as determined by the surrounding DNA sequence), it is a rare event.

Only in evolutionary PR trash. In reality virus cross species lines all the time. They are used in genetic to affect specific sites for genetic alteration.

And when we see the majority of such integration sites being shared by any 2 taxa, the data speaks for itself.

Yes it does. It says both species were affected by the same virus when they shared geographical location, not ancestry.

So if we just look at 1 ERV integrating at one specific site (1 in ~700000 = probability of 0.0000014 in one specimen), we get the probability that an ERV will integrate at the same site in 2 different specimens being 1.96E-12 = 0.00000000000196

For 2 specimens to share, at random, just 2 ERVs at specific loci, p= 3.8416E-24 = 0.00000000000000000000000384 (if we can trust calculator.net)

And so on.

If ya'll want to chalk it all up to chance alone, then ya'll have more confidence in mere chance than anyone I know.

Except we have already seen your belief that virus are specific to specific animals has shown to be in error, which changes the entire equation, not that you’ll bother with the truth....


“We have sequenced and characterized an endogenous type D retrovirus, which we have named TvERV(D), from the genome of an Australian marsupial, the common brushtail possum (Trichosurus vulpecula). Intact TvERV(D) gag, pro, pol, and env open reading frames were detected in the possum genome. TvERV(D) was classified as a type D retrovirus, most closely related to those of Old World monkeys, New World monkeys, and mice, based on phylogenetic analyses and genetic organization.” Gregory J. Baillie and Richard J. Wilkins, “Endogenous Type D Retrovirus in a Marsupial, the Common Brushtail Possum (Trichosurus vulpecula),” Journal of Virology, March 2001 vol. 75 no. 5 2499-2507. Endogenous Type D Retrovirus in a Marsupial, the Common Brushtail Possum (Trichosurus vulpecula)

“For instance gamma-retrovirus was isolated from trophoblastic cells of the baboon placenta. This virus was found to be very closely related antigenically and by sequence homology to the endogenous RD114 virus in cats (which is itself unrelated to endogenous FeLV). Benveniste and Todaro observed, like we did for jungle fowl, that only certain species of the cat genus, Felis, possessed this endogenous genome related to the baboon ERV. In contrast, all species of baboons carry this virus so it would appear to have been present in the germ line of primates much longer than in cats. Thus it seems evident that a horizontal, infectious event occurred to transfer the virus from baboons to cats, whereupon it became endogenous in the new species.” Robin A Weiss, “The discovery of endogenous retroviruses,” Retrovirology, 2006; 3: 67. Published online 2006 October 3. doi: 10.1186/1742-4690-3-67. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120

 

[Justatruthseeker]

blah, blah, blah

Here I’ll highlight your own quote.

“So, in your Grant paper, where they talk about these sorts of traits being influenced more by hybridization than mutation, it is because different combinations of alleles play a greater role than individual birds experiencing mutations and - wait for it - generating new alleles, since these would be of lower frequency in the population. Mixing and matching the relevant associated alleles that already exist (and already exist due to mutation) via hybridization has a greater short-term impact than new allele generation and waiting for them to increase in frequency sufficiently to have an impact on phenotype.“

Do you still think they are called "allies"?

No, I just think complaining about a spelling error is your only argument.

Not at all.

You continue to look at these issues like a middle schooler.

Let us say for the sake of argument that height at the shoulders for wolves is governed by 10 loci.

A breeding pair will possess a maximum of a total of 40 possible alleles at these 10 loci.

Why a maximum? Because some could be identical, right?

So if we mix and match 40 alleles (4 per locus, 10 possible combinations per locus - remember? ABCD = AA,AB,AC,AD,etc.?), we can get a maximum of 100 unique combinations (or is it 400? My head hurts...).

Other factors influence height, such as nutritional status, etc. - we will ignore that for simplicity.
Wow! Justa population genetics is saved!


Or is it -


With 400 possible allele combination at 10 loci at which both member of a breeding pair had different alleles - we just populated a continuum with individuals of differing height.

We did NOT get a Mastiff and a Chihuahua - we just got wolves of differing heights.



But wait - you say that Adam and Eve had "perfect" genomes, that is, no mutation, so all of their alleles at these 10 loci had to have been identical (since that is how alleles arise - mutation).

That is right - creationists seem to believe that mutation was the result of the Fall - a curse. A punishment. So genetic variation - new alleles - is a punishment, if we accept creationist logic.

Creationist urologist Barney Maddox writes:

"The perpetuation of the Darwin myth clashes with reality--the God-created reality--where living things and their genomes were created "very good" and have degenerated from there."


Creationist John Mackay has a GREAT totally sciencey take on mutations - a must read. He demolishes the 'all hybridization all the time' model of Justa is seconds flat.

"So did God invent mutations? An analogy will help. God did invent gravity without which life would not be possible. Your bits wouldn’t stick and we wouldn’t have a planet to live on. But once gravity is invented, you can choose to jump out of a plane at 30,000 feet, but don’t you dare argue God pushed you! Obey the law of gravity and live, but the default setting of the law of gravity will kill you, specially when de-fault is yours. Likewise God did invent genes, but disobey his law and the default settings which do involve gene degeneration will bring about your death."


And this Bible and genetics expert writes:

"...explains all the phenomena and genetic mutations in species we see today and can be traced back to our roots and the fall of man in the Garden of Eden."


Amazing insights.
So no new alleles in Adam and Eve - all loci =A (AA,AA,AA,AA).

Thus, no Africans, Asians, etc. to hybridize to get Afro-Asians.

Just following Justa's scientific model's logic here, folks.




Right - because I understand where 'interbreeding' gets its raw material from.

You refuse to.



Ummm... OK - so you DON'T think that mutations producing new alleles that affect height will influence height?

So what DOES affect height? Mixing up the "allies" that affect height via hybridization.

OK - where did those new "allies" come from?

Interesting.



From the fellow that STILL thinks alleles are called "allies", and who simultaneously declares - without evidence - that Adam and Eve had "perfect" genomes, but through the 'interbreeding' of their inbred, perfect-genome-having offspring, we get NEW combinations of alleles (that arose via???) producing all extant phenotypes (only to be washed away in a big flood (for which there is also no evidence) leaving only 4 inbreeding pairs to, yet again, re-populate and re-diversify all of humanity in only a couple hundred generations)...


I stand totally refuted.... A dude on the internet, who thinks alleles are called "allies", has totally refuted not only all of population genetics, but all of standard classical and transmission genetics as well!

LOL!!

Or is it as you recognized.... when they interact through interbreeding they are generating new alleles, and now want to ignore those interactions among the different alleles? Your math is shown to again be flawed. If new alleles are generated with interbreeding as they interact, then the possible interactions are unlimited, since interbreeding will generate new allele combinations that did not exist before. So that a mutation that does the same thing over 100 million years is virtually insignificant, compared to interbreeding doing it continuously. I mean I waited for it. It just seems your conclusion of continuously generating new alleles is flawed, even if you recognize its continually generating new alleles. Then want to claim a mutation that generates a new allele every 100 million years or so is somehow more important than a process that is doing it continuously.

Standard evolutionary PR trash.....

 

[tas8831]

Typical you regurgitate evolutionary PR trash.

Projection.

Diseases Affecting Multiple Animal Species

Cross-species transmission - Wikipedia

http://www.cs.unm.edu/~melaniem/pdfs/DobsonAmnat.pdf

So the phrase "nearly all " is lost on you...

In reality virus cross species lines all the time. They are used in genetic to affect specific sites for genetic alteration.

How often? Which viruses are used in genetics?

It must be any old virus, if your implications have merit.

Yes it does. It says both species were affected by the same virus when they shared geographical location, not ancestry.

Sure, no problem.

I will remember that when your fellow creationists insist that probability is against evolution and disproves abiogenesis - I will say "Nope - ask Justa - he KNOWS that low probabilities, such as the probability of just 2 taxa sharing just 2 ERVs at identical loci is 0.00000000000000000000000384, is not biggie! Happens all the time, just by chance."

Except we have already seen your belief that virus are specific to specific animals has shown to be in error, which changes the entire equation, not that you’ll bother with the truth....

So you have taken "nearly all" to mean "all"? That is, you have misrepresented me.

Of course, there is species resistance (aka species immunity) which should not exist according to your implication, but whatever.

“We have sequenced and characterized an endogenous type D retrovirus, which we have named TvERV(D), from the genome of an Australian marsupial, the common brushtail possum (Trichosurus vulpecula). Intact TvERV(D) gag, pro, pol, and env open reading frames were detected in the possum genome. TvERV(D) was classified as a type D retrovirus, most closely related to those of Old World monkeys, New World monkeys, and mice, based on phylogenetic analyses and genetic organization.” Gregory J. Baillie and Richard J. Wilkins, “Endogenous Type D Retrovirus in a Marsupial, the Common Brushtail Possum (Trichosurus vulpecula),” Journal of Virology, March 2001 vol. 75 no. 5 2499-2507. Endogenous Type D Retrovirus in a Marsupial, the Common Brushtail Possum (Trichosurus vulpecula)

“For instance gamma-retrovirus was isolated from trophoblastic cells of the baboon placenta. This virus was found to be very closely related antigenically and by sequence homology to the endogenous RD114 virus in cats (which is itself unrelated to endogenous FeLV). Benveniste and Todaro observed, like we did for jungle fowl, that only certain species of the cat genus, Felis, possessed this endogenous genome related to the baboon ERV. In contrast, all species of baboons carry this virus so it would appear to have been present in the germ line of primates much longer than in cats. Thus it seems evident that a horizontal, infectious event occurred to transfer the virus from baboons to cats, whereupon it became endogenous in the new species.” Robin A Weiss, “The discovery of endogenous retroviruses,” Retrovirology, 2006; 3: 67. Published online 2006 October 3. doi: 10.1186/1742-4690-3-67. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1617120

Cool.

Still not sure where I said there is no inter-species transmission at all.

You have a distinct tendency to go off the rails like this, with a misrepresentation/misinterpretation leading to a full blown act of silliness.

Keep it up - I find it entertaining.

 

[tas8831]

Here I’ll highlight your own quote.

Ok, great!

“So, in your Grant paper, where they talk about these sorts of traits being influenced more by hybridization than mutation, it is because different combinations of alleles play a greater role than individual birds experiencing mutations and - wait for it - generating new alleles, since these would be of lower frequency in the population. Mixing and matching the relevant associated alleles that already exist (and already exist due to mutation) via hybridization has a greater short-term impact than new allele generation and waiting for them to increase in frequency sufficiently to have an impact on phenotype.“

Not sure why you highlighted that - it contradicted your dopey claims.

Let me highlight it another way, to prove how laughable your attempted 'gotcha' was:


“So, in your Grant paper, where they talk about these sorts of traits being influenced more by hybridization than mutation, it is because different combinations of alleles play a greater role than individual birds experiencing mutations and - wait for it - generating new alleles, since these would be of lower frequency in the population. Mixing and matching the relevant associated alleles that already exist (and already exist due to mutation) via hybridization has a greater short-term impact than new allele generation and waiting for them to increase in frequency sufficiently to have an impact on phenotype."

Clearer now?

Doubt it.

You still refuse to learn that the new alleles came about VIA MUTATION.

No, I just think complaining about a spelling error is your only argument.

Repeatedly misspelling a key term even after being corrected numerous times is very informative.

However, I note that you ignore via omission nearly all of my actual argument - an argument that did not rely on your lousy spelling and instead laid bare you near total lack of understanding of the subject matter, and your tendency to do keyword searches and declare victory rather than actually learning about the material:

Apparently, in your quest to save face, you didn't notice that all of that is only about the alleles for eye color. That is, they all deal with a continuously varying trait.

This is interesting and all, but 100% irrelevant to the point I had made (and lost on you):



"You truly seem to think that any allele can recombine or mix and match with any other allele, no matter what the alleles are - that is the ONLY way your fantasy could even hope to have merit.

But reality does not operate that way."



Your own link indicates:


"A number of groups surveyed associations of single-nucleotide polymorphisms with eye color, with fairly consistent results: variation in the HERC2 and OCA2 genes, which are next to each other on chromosome 15, plays a major role in determining eye color."

Tell us all, won't you, what is meant by "single-nucleotide polymorphisms "?

And your link also mentions this paper:

"Genetics of human iris colour and patterns"
Richard A. Sturm and Mats Larsson

in which we see:


"Nevertheless, it has been estimated that 74% of the variance in human eye colour can be explained by one interval on chromosome 15 that contains the OCA2 gene. Fine mapping of this region has identified a single base change rs12913832 T ⁄C within intron 86 of the
upstream HERC2 locus that explains almost all of this association with blue-brown eye colour. A model is presented whereby this SNP, serving as a target site for the SWI ⁄SNF family member HLTF, acts as part of a highly evolutionary conserved regulatory element required for OCA2 gene activation through chromatin remodelling. "

and one can also note the paper's Table 1. Human pigmentation gene polymorphisms associated with eye colour -

tell us all what is meant by "gene polymorphisms", won't you?

And tell us all, with your amazing genetics expertise (bolstered by keyword searches to find quotes that can be taken out of context to try to save face), HOW such things as "gene polymorphisms" and SNPs come to be?

Must be by interbreeding and hybridization, right?

Yes, continuing [sic] varying traits are traits that are never the same

LOL!!!


My gosh...

No, a continuously variable trait is something like height. There is HEIGHT, then within that trait, we have short, medium, tall, etc. I know of many people that are my exact same height. Don't you?

So, in your Grant paper, where they talk about these sorts of traits being influenced more by hybridization than mutation, it is because different combinations of alleles play a greater role than individual birds experiencing mutations and - wait for it - generating new alleles, since these would be of lower frequency in the population. Mixing and matching the relevant associated alleles that already exist (and already exist due to mutation) via hybridization has a greater short-term impact than new allele generation and waiting for them to increase in frequency sufficiently to have an impact on phenotype.

I think you confuse alleles with phenotype?
​

Or is it as you recognized.... when they interact through interbreeding they are generating new alleles,

That is the OPPOSITE of what I wrote - truly, you cannot be this dense? This is an act, right?


Yet again:

“So, in your Grant paper, where they talk about these sorts of traits being influenced more by hybridization than mutation, it is because different combinations of alleles play a greater role than individual birds experiencing mutations and - wait for it - generating new alleles, ...“


It is painfully obvious to the non-malicious and sensible that I clearly indicated that the generation of new alleles is via MUTATION, and NOT hybridization - and that the mixing of alleles was 'quicker' than having to wait for 'new alleles arising via mutation'.


I know you will not acknowledge this obvious and laughable error on your part, because you are a creationist, but anyone else reading this will see.

 

[Justatruthseeker]

Here’s another flawed evolutionary belief.

“A number of groups surveyed associations of single-nucleotide polymorphisms with eye color, with fairly consistent results: variation in the HERC2 and OCA2 genes, which are next to each other on chromosome 15, plays a major role in determining eye color."

Tell us all, won't you, what is meant by "single-nucleotide polymorphisms "?”

Why variation of a single letter or nucleotide which makes two alleles at a senile genetic loci.

Which when combined by interbreeding, generates new single-nucleotide polymorphism.

“Three mechanisms may cause polymorphism:[3]

• Genetic polymorphism – where the phenotype of each individual is genetically determined
• A conditional development strategy, where the phenotype of each individual is set by environmental cues
• A mixed development strategy, where the phenotype is randomly assigned during development”

So in reality we find these polymorphism are randomly assigned during development. I.e. during interbreeding and the combining of these alleles to generate new alleles.

But notice evolutionary supporters recognize new alleles are being generated, then refuse to accept they are randomly being generated during interbreeding, even when they recognize new alleles are being generated during interbreeding.

Do you see their inherent illogic? That new alleles are beings randomly generated during development from interbreeding, but somehow these new random polymorphism are irrelevant, and only the ones that randomly change them over millions of years are important.

I’ll say it again. Pure evolutionary PR trash....

 

[Justatruthseeker]

Ok, great!


Not sure why you highlighted that - it contradicted your dopey claims.

Let me highlight it another way, to prove how laughable your attempted 'gotcha' was:


“So, in your Grant paper, where they talk about these sorts of traits being influenced more by hybridization than mutation, it is because different combinations of alleles play a greater role than individual birds experiencing mutations and - wait for it - generating new alleles, since these would be of lower frequency in the population. Mixing and matching the relevant associated alleles that already exist (and already exist due to mutation) via hybridization has a greater short-term impact than new allele generation and waiting for them to increase in frequency sufficiently to have an impact on phenotype."

Clearer now?

Doubt it.

You still refuse to learn that the new alleles came about VIA MUTATION.

Oh no, I accept new random mutations come about by mutation once in a blue moon. It’s you that refuses to accept those polymorphism create new random variations of alleles with every birth during development.

“Three mechanisms may cause polymorphism:[3]

• Genetic polymorphism – where the phenotype of each individual is genetically determined
• A conditional development strategy, where the phenotype of each individual is set by environmental cues
• A mixed development strategy, where the phenotype is randomly assigned during development

Repeatedly misspelling a key term even after being corrected numerous times is very informative.

Yes, it shows I’m dyslexic and often type words incorrectly and have to retype them, and that all you have is spelling errors.

However, I note that you ignore via omission nearly all of my actual argument - an argument that did not rely on your lousy spelling and instead laid bare you near total lack of understanding of the subject matter, and your tendency to do keyword searches and declare victory rather than actually learning about the material:

Apparently, in your quest to save face, you didn't notice that all of that is only about the alleles for eye color. That is, they all deal with a continuously varying trait.

This is interesting and all, but 100% irrelevant to the point I had made (and lost on you):



"You truly seem to think that any allele can recombine or mix and match with any other allele, no matter what the alleles are - that is the ONLY way your fantasy could even hope to have merit.

But reality does not operate that way."



Your own link indicates:


"A number of groups surveyed associations of single-nucleotide polymorphisms with eye color, with fairly consistent results: variation in the HERC2 and OCA2 genes, which are next to each other on chromosome 15, plays a major role in determining eye color."

Tell us all, won't you, what is meant by "single-nucleotide polymorphisms "?

And your link also mentions this paper:

"Genetics of human iris colour and patterns"
Richard A. Sturm and Mats Larsson

in which we see:


"Nevertheless, it has been estimated that 74% of the variance in human eye colour can be explained by one interval on chromosome 15 that contains the OCA2 gene. Fine mapping of this region has identified a single base change rs12913832 T ⁄C within intron 86 of the
upstream HERC2 locus that explains almost all of this association with blue-brown eye colour. A model is presented whereby this SNP, serving as a target site for the SWI ⁄SNF family member HLTF, acts as part of a highly evolutionary conserved regulatory element required for OCA2 gene activation through chromatin remodelling. "

and one can also note the paper's Table 1. Human pigmentation gene polymorphisms associated with eye colour -

tell us all what is meant by "gene polymorphisms", won't you?

And tell us all, with your amazing genetics expertise (bolstered by keyword searches to find quotes that can be taken out of context to try to save face), HOW such things as "gene polymorphisms" and SNPs come to be?

Must be by interbreeding and hybridization, right?



LOL!!!


My gosh...

No, a continuously variable trait is something like height. There is HEIGHT, then within that trait, we have short, medium, tall, etc. I know of many people that are my exact same height. Don't you?

So, in your Grant paper, where they talk about these sorts of traits being influenced more by hybridization than mutation, it is because different combinations of alleles play a greater role than individual birds experiencing mutations and - wait for it - generating new alleles, since these would be of lower frequency in the population. Mixing and matching the relevant associated alleles that already exist (and already exist due to mutation) via hybridization has a greater short-term impact than new allele generation and waiting for them to increase in frequency sufficiently to have an impact on phenotype.

I think you confuse alleles with phenotype?
​

That is the OPPOSITE of what I wrote - truly, you cannot be this dense? This is an act, right?


Yet again:

“So, in your Grant paper, where they talk about these sorts of traits being influenced more by hybridization than mutation, it is because different combinations of alleles play a greater role than individual birds experiencing mutations and - wait for it - generating new alleles, ...“


It is painfully obvious to the non-malicious and sensible that I clearly indicated that the generation of new alleles is via MUTATION, and NOT hybridization - and that the mixing of alleles was 'quicker' than having to wait for 'new alleles arising via mutation'.


I know you will not acknowledge this obvious and laughable error on your part, because you are a creationist, but anyone else reading this will see.

And yet your mutations only affect one allele. If one affects the trait for eye color, it only affects the trait for eye color, not for leg size. If one affects the trait for leg size, it likewise does not affect the trait for eye color.

Your mutations do less than interbreeding, since interbreeding affects numerous genetic loci simultaneously, not only for leg size, but eye color at the same time. While mutations only work on one at a time.

It’s that quick change that is your falsification. That’s why every fossil remains the same for every type, and then suddenly, becomes a new form that remains the same for that distinct type. Not gradually, suddenly.

It is not only quicker, but does the exact same thing as mutation, except it affects numerous genetic loci simultaneously. Your mutation only affects a single allele. Again, if it affects the gene for eye color, it does not affect leg size. If it affects the allele for leg size, it does not affect eye color. Only in your dreams does mutation affect alleles it doesn’t affect, while interbreeding affects several genetic loci simultaneously.

Mutations are insignificant to the overall process. They create random change, just as all polymorphism do to development create random change, and do it to several loci simultaneously, not just one.

Keep regurgitating that rediculous standard evolutionary PR trash..... we have already seen your reasoning is flawed. That random polymorphism happen in every developmental episode, affecting several genetic loci simultaneously, yet you claim a single random mutation that does the exact same thing over millions of years is somehow more important.

Standard evolutionary brainwashed PR trash....

Now wait for it.....

“Three mechanisms may cause polymorphism:[3]

• Genetic polymorphism – where the phenotype of each individual is genetically determined
• A conditional development strategy, where the phenotype of each individual is set by environmental cues
• A mixed development strategy, where the phenotype is randomly assigned during development

Oh my, look, during development new alleles are created. Can we say variation kids?

And let’s not forget the first either.

“Genetic polymorphism
Since all polymorphism has a genetic basis, genetic polymorphism has a particular meaning:

• Genetic polymorphism is the simultaneous occurrence in the same locality of two or more discontinuous forms in such proportions that the rarest of them cannot be maintained just by recurrent mutation or immigration, originally defined by Ford (1940).[8][15]:11 The later definition by Cavalli-Sforza & Bodmer (1971) is currently used: "Genetic polymorphism is the occurrence in the same population of two or more alleles at one locus, each with appreciable frequency", where the minimum frequency is typically taken as 1%.[16]

The definition has three parts: a) sympatry: one interbreeding population; b) discrete forms; and c) not maintained just by mutation.”

 

[xianghua]

I agree that a robot penguin is a robot.



Not even close.

One penguin is not identical to another.

You only get identical with human-made things.

Not even identical twins are truly identical.

You should learn some biology and can the inapt analogies and tortured argument-via-definition.

sure. a two ferarri f40 cars arent identical too. but they are still a ferarri f40 cars. so a penguin is also a robot.

 

[xianghua]

Natural penguin:

View attachment 215451

Robot penguin:

View attachment 215452


Call me when you find a natural penguin that is "identical" to a robot penguin.

but the robo-penguin in the image isnt an artificial penguin. is just a robo-penguin made from plastic. we talked about an artificial penguin and you already agree that such apenguin will be a robot. so according to this criteria an artificial penguin is a robot were a natural penguin isnt.

 

[xianghua]

If what YOU imply is correct, then you should have no problems finding any 2 creatures that share more ERV's then with a creature that is more closely related according to evolution.

If you find such a thing, you'ld single handedly succeed where just about every creationist (and biologist) has failed: debunking evolution.

so what about this case?:

Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans

"We performed two analyses to determine whether these 12 shared map intervals might indeed be orthologous. First, we examined the distribution of shared sites between species (Table S3). We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates"

 

[Justatruthseeker]

I suggest you inform yourself a bit on what ERV's are.

Endogenous retrovirus - Wikipedia

quote from the opening paragraph:

When integration of viral DNA occurs in the germ-line, it can give rise to an ERV, which can later become fixed in the gene pool of the host population.[1][7]

Let’s look at that, “when integration of viral DNA occurs in the germ-line” in other words when the two species in shared proximity from living in the same geographical area become infected...... “it can give rise to an ERV, which can later become fixed in the gene pool of the host population.” So what you believe shows common descent is merely time of infection of both humans and apes, which was then fixed in both populations which you mistake as common descent... a mistake based on shared DNA at these sites.

http://emerald.tufts.edu/med/apua/about_issue/about_antibioticres.shtml

“Viruses are another mechanism for passing resistance traits between bacteria. The resistance traits from one bacterium are packaged into the head portion of the virus. The virus then injects the resistance traits into any new bacteria it attacks.”

Likewise with both chimps and man. Those viruses passed DNA from one host to another.

That they share the same cites or inserted cross species DNA is not remarkable at all.

How are viruses used in genetic engineering (recombinant DNA technology)? | eNotes

“One of the qualities viruses have that makes them attractive to genetic engineering scientists is their ability to attach to and invade specific cells, and incorporate the DNA (and/or RNA) they are carrying into the host cell, where it combines with the host cell's DNA.“

You only confuse time of infection of both species to those specific sites, as meaning shared ancestry. When it simply means the time when both species were infected and DNA was transferred from one to the other, which then combined with both hosts DNA and was at that point fixed into both populations. You interpret from the incorrect starting point. A different starting point leads to the same observed results.

 

[Justatruthseeker]

Projection.

Yes, you are good at that, we agree.

So the phrase "nearly all " is lost on you...

Oh no, it means many do.

How often? Which viruses are used in genetics?

Why retrovirus of course.

Gene Therapy Retrovirus Vectors Explained

“A retrovirus is any virus belonging to the viral family Retroviridae. All The genetic material in retroviruses is in the form of RNA molecules, while the genetic material of their hosts is in the form of DNA. When a retrovirus infects a host cell, it will introduce its RNA together with some enzymes into the cell.”

It must be any old virus, if your implications have merit.

Just retrovirus that have adapted over time. Like the HIV virus is a relatively new virus capable of cross species infection.

Sure, no problem.

I know, cause you ignore answering. That’s never a problem.

I will remember that when your fellow creationists insist that probability is against evolution and disproves abiogenesis - I will say "Nope - ask Justa - he KNOWS that low probabilities, such as the probability of just 2 taxa sharing just 2 ERVs at identical loci is 0.00000000000000000000000384, is not biggie! Happens all the time, just by chance."

Go ahead, won’t affect my argument, just theirs.

So you have taken "nearly all" to mean "all"? That is, you have misrepresented me.

No, just showing your claims to not be as sure as you like to make them sound.

Of course, there is species resistance (aka species immunity) which should not exist according to your implication, but whatever.

Of course their is. Interbreeding causes multiple changes simultaneously and resistance can be random.

Cool.

It was. But you won’t mind if I use your response to other evolutionists since that seems acceptable to you.

Still not sure where I said there is no inter-species transmission at all.

Nothing at all except your trying to imply those retrovirus found in human and apes can’t cross species.

You have a distinct tendency to go off the rails like this, with a misrepresentation/misinterpretation leading to a full blown act of silliness.

Keep it up - I find it entertaining.

In other words you have no valid response. Understood.

 

[Jimmy D]

Since DNA tests shows they are of mixed ancestory, they were never reproductively isolated and speciation never occurred. We are talking about different subspecies here of the same species, not separate species.

The very point of the entire thread, which you seem to be missing.

The point of the thread is that speciation has been observed, which it has.

The variety of finches we're discussing descended from the single ancestral population of about 20 or 30 finches that arrived on the islands several million years ago. Of course it's speciation in action.

One (sub) species diverging into more than a dozen (sub) species = speciation.

(No, I don't deny that some have hybridized along the way)

 

[Justatruthseeker]

The point of the thread is that speciation has been observed, which it has.

The variety of finches we're discussing descended from the single ancestral population of about 20 or 30 finches that arrived on the islands several million years ago. Of course it's speciation in action.

One (sub) species diverging into more than a dozen (sub) species = speciation.

(No, I don't deny that some have hybridized along the way)

One species making 20 or 30 or even 100 subspecies is NOT Speciation.

Speciation - Wikipedia

“Speciation is the evolutionary process by which populations evolve to become distinct species.”

I see no evidence something becoming a subspecies is doing anything but remaining the same species, being they are of mixed ancestory to the point of being virtually indistinguishable.

But please, support your claim. Which of the processes of Speciation did they undergo?

Was it allopatric, peripatric, parapatric, or sympatric. Speciation? I mean surely if you have observed it you can tell me which of the processes they underwent?

Or would you like to claim at this time it is those mutations to the ALX1 gene that caused their Speciation? It’s what your experts claim, but for some reason I can’t get any of you to make a stand and side with your experts.

DNA Reveals How Darwin's Finches Evolved

I’m curious as to why none of you seem to want to claim it’s those mutations of the ALX1 gene when it’s the reason the biologists do?

 

[Jimmy D]

One species making 20 or 30 or even 100 subspecies is NOT Speciation.

LOL. Of course it is. You do realize that speciation is a gradual process right?

I had to laugh when I read the paper you linked to..

"The most important take-home message may be that species are not fixed, shut off from other species by inability to interbreed. On the contrary, for a long time, millions of years in some cases, they are capable of exchanging genes," the Grants wrote in an e-mail.

I see no evidence something becoming a subspecies is doing anything but remaining the same species, being they are of mixed ancestory to the point of being virtually indistinguishable.

But please, support your claim. Which of the processes of Speciation did they undergo?

Was it allopatric, peripatric, parapatric, or sympatric. Speciation? I mean surely if you have observed it you can tell me which of the processes they underwent?

Even bigger LOL, did you bother reading the page you linked to, try looking at the "allopatric" paragraph ....

"Though the finches were less important for Darwin, more recent research has shown the birds now known as Darwin's finches to be a classic case of adaptive evolutionary radiation."

Or would you like to claim at this time it is those mutations to the ALX1 gene that caused their Speciation? It’s what your experts claim, but for some reason I can’t get any of you to make a stand and side with your experts.

I made no such claim.

 

[Justatruthseeker]

LOL. Of course it is. You do realize that speciation is a gradual process right?

That’s what you all keep claiming without being able to support that claim.

I had to laugh when I read the paper you linked to..

"The most important take-home message may be that species are not fixed, shut off from other species by inability to interbreed. On the contrary, for a long time, millions of years in some cases, they are capable of exchanging genes," the Grants wrote in an e-mail.

And they have observed this million year process? Or in reality have finches remained finches for as far back as finches go?

Is this another one of those evolutionary claims that can never be observed like missing common ancestors?

Even bigger LOL, did you bother reading the page you linked to, try looking at the "allopatric" paragraph ....

"Though the finches were less important for Darwin, more recent research has shown the birds now known as Darwin's finches to be a classic case of adaptive evolutionary radiation."



I made no such claim.

Yah I know, we have already discussed evolutionists tendency to ignore scientific definitions, or do we need to go back to the definition of subspecies? That they are pseudo scientists is without a doubt. No radiation has occurred, because Speciation has never occurred.

I read it, did you?

“ is a mode of speciation that occurs when biological populations of the same species become isolated from each other to an extent that prevents or interferes with genetic interchange.“

So since they are interbreeding and are of mixed ancestory, they were never isolated to the point of preventing or interfering with genetic exchange. So again, Speciation never occurred and your unsupported claims have no merit at all.

So I’ll ask again, which mode of Speciation occurred? Clearly not the one you and they assert.

Evolution of Darwin’s finches and their beaks revealed by genome sequencing

“Here we report the results of whole-genome re-sequencing of 120 individuals representing all of the Darwin’s finch species and two close relatives. Phylogenetic analysis reveals important discrepancies with the phenotype-based taxonomy. We find extensive evidence for interspecific gene flow throughout the radiation. Hybridization has given rise to species of mixed ancestry.

So DNA evidence falsifies your pseudo scientists claims because they can’t follow definitions and admit Darwin made a mistake in calling them separate species because of his incorrect belief they were reproductively isolated.

 

[Jimmy D]

That’s what you all keep claiming without being able to support that claim.

Are you saying it's not a slow process? Or that speciation doesn't exist?

And they have observed this million year process? Or in reality have finches remained finches for as far back as finches go?

Is this another one of those evolutionary claims that can never be observed like missing common ancestors?

Dunno mate, one minute you're citing the Grant's research, next minute you're disagreeing with it, you tell me, you posted the link to back up your point.

Yah I know, we have already discussed evolutionists tendency to ignore scientific definitions, or do we need to go back to the definition of subspecies? That they are pseudo scientists is without a doubt. No radiation has occurred, because Speciation has never occurred.

I'll post this so you can read it again.

"The most important take-home message may be that species are not fixed, shut off from other species by inability to interbreed. On the contrary, for a long time, millions of years in some cases, they are capable of exchanging genes,"

The definition of species allows for interbreeding, I realize that you can't accept that as your whole sorry argument hangs on it but the rest of the world does.

I read it, did you?

“ is a mode of speciation that occurs when biological populations of the same species become isolated from each other to an extent that prevents or interferes with genetic interchange.“

So since they are interbreeding and are of mixed ancestory, they were never isolated to the point of preventing or interfering with genetic exchange. So again, Speciation never occurred and your unsupported claims have no merit at all.

Can't see the wood for the trees?

Where did the original population of finches that colonized the island come from?


How you can post links to articles to back up your arguments and then, in the very next post, dismiss those articles as pseudoscience just about sums this conversation up. It's quite bizarre.

 

[tas8831]

Speaking of trash...

Here’s another flawed evolutionary belief.

“A number of groups surveyed associations of single-nucleotide polymorphisms with eye color, with fairly consistent results: variation in the HERC2 and OCA2 genes, which are next to each other on chromosome 15, plays a major role in determining eye color."

Tell us all, won't you, what is meant by "single-nucleotide polymorphisms "?”

Why variation of a single letter or nucleotide which makes two alleles at a senile genetic loci.

"Senile"?

Did you mean "single"?

And is it a letter or a nucleotide?

And did you copy paste that from a PDF? Because sometimes when you copy from a PDF or save a PDF as a word doc the OCR software is screwy.

Or are you just as clueless as I suspect and did not even notice that "senile genetic loci" does not even make sense?

And where does that variation come from?

interbreeding? how?

Which when combined by interbreeding, generates new single-nucleotide polymorphism.

“Three mechanisms may cause polymorphism:[3]

• Genetic polymorphism – where the phenotype of each individual is genetically determined
• A conditional development strategy, where the phenotype of each individual is set by environmental cues
• A mixed development strategy, where the phenotype is randomly assigned during development”

So cute how you cannot tell the difference between "single nucleotide polymorphism" and "genetic polymorphism."


Why do you still pretend to understand any of this? You make these truly laughable, easily - trivially - proven false assertions, and you actually try to back them up with links, but you either do not read the links or do not understand them, and just post them because they showed up in your keyword search.

Single nucleotide polymorphism - from YOUR LINK, the title of citation 3 -

"The evolution of phenotypic polymorphism: randomized strategies versus evolutionary branching"."

So you don't know what phenotype is?

Or did you think that I wouldn't (dumb mistake)?

I am laughing at your hubris and exceptionally prominant expression of the Dunning-Kruger effect.

You are so far out of the loop you cannot even tell how far out you are.

So in reality we find these polymorphism are randomly assigned during development. I.e. during interbreeding and the combining of these alleles to generate new alleles.

In reality, we see yet another creationist that lacks sufficient knowledge of basic genetics to understand how little they know.

Alleles are NOT generated by combining other alleles during reproduction.

A SNP is NOT a genetic polymorphism.

My gosh, did you not even bother to even TRY to understand the wiki page? The opening paragraph:

Polymorphism[1] in biology and zoology is the occurrence of two or more clearly different morphs or forms, also referred to as alternative phenotypes, in the population of a species. To be classified as such, morphs must occupy the same habitat at the same time and belong to a panmictic population (one with random mating).[2]

Three mechanisms may cause polymorphism:[3]

Genetic polymorphism – where the phenotype of each individual is genetically determined
A conditional development strategy, where the phenotype of each individual is set by environmental cues
A mixed development strategy, where the phenotype is randomly assigned during development
​

For crying out loud - you COPY-PASTED part of it! And you still didn't see any clues that SNP is NOT a genetic or phenotypic polymorphism?????

You HAVE to be a troll. I cannot believe that an adult human can be this clueless.

I can't even bring myself to go on dismantling this nonsense, but I will leave your silliness with a parting shot at your sad misrepresentation of me (bolstered by malice or ignorance, can't decide which):

Or is it as you recognized.... when they interact through interbreeding they are generating new alleles,

That is the OPPOSITE of what I wrote - truly, you cannot be this dense? This is an act, right?


Yet again:

“So, in your Grant paper, where they talk about these sorts of traits being influenced more by hybridization than mutation, it is because different combinations of alleles play a greater role than individual birds experiencing mutations and - wait for it - generating new alleles, ...“


It is painfully obvious to the non-malicious and sensible that I clearly indicated that the generation of new alleles is via MUTATION, and NOT hybridization - and that the mixing of alleles was 'quicker' than having to wait for 'new alleles arising via mutation'.

You don't know what an allele is! LOL!

 

[tas8831]

Yes, you are good at that, we agree.

SNP = genetic polymorphism = phenotypic polymorphism.

According to you, and nobody ever in the world, but you.

Oh no, it means many do.

Right - so why misrepresent me in the first palce?

Is it in your nature?

Why retrovirus of course.

Gene Therapy Retrovirus Vectors Explained

“A retrovirus is any virus belonging to the viral family Retroviridae. All The genetic material in retroviruses is in the form of RNA molecules, while the genetic material of their hosts is in the form of DNA. When a retrovirus infects a host cell, it will introduce its RNA together with some enzymes into the cell.”


Just retrovirus that have adapted over time. Like the HIV virus is a relatively new virus capable of cross species infection.

Just one page back from that one, we see that there are lots of other viral vectors, too.

I like how easy you make it to undermine your assertions and pretense to superior knowledge.

I know, cause you ignore answering. That’s never a problem.


Go ahead, won’t affect my argument, just theirs.

It affects both.

You creationists just love to argue AGAINST low-probability phenomena when it suits you, yet here you are embracing low-probability phenomena.

Hilarious.

So you have taken "nearly all" to mean "all"? That is, you have misrepresented me.

No, just showing your claims to not be as sure as you like to make them sound.

Via misrepresentation.

Got it. Jesus would be so proud!

Of course, there is species resistance (aka species immunity) which should not exist according to your implication, but whatever.

Of course their [sic] is. Interbreeding causes multiple changes simultaneously and resistance can be random.

Makes precisely zero sense.

You should have just omitted that part in your response, for your response shows that you do not understand how infection even occurs, do not understand what random means in this context.

But whatever.

It was. But you won’t mind if I use your response to other evolutionists since that seems acceptable to you.

What response - 'cool'? Yeah, what you posted was cool - it is also irrelevant. Like pretty much everything else you quote, paste, or paraphrase, your use of it was misdirected.

In other words you have no valid response. Understood.

It is like this.

A kid comes up and asks who my favorite baseball player is. I respond "Joe DiMaggio." He says "Mine is Flip Wilson." I say, "Flip Wilson was not a baseball player." The kid says "You are just mad because Wilson is better that DiMaggio!."

In my shock, I have no response.

Therefore, Flip Wilson is a better baseball player than DiMaggio?

According to the creationist logic, I guess so.

 

[Justatruthseeker]

Are you saying it's not a slow process? Or that speciation doesn't exist?

You have yet to show any Speciation, slow or otherwise, until you ignore those definitions.

Dunno mate, one minute you're citing the Grant's research, next minute you're disagreeing with it, you tell me, you posted the link to back up your point.

Their research data is not in question. That finches are interbreeding is not in question. What is in question is calling subspecies separate species due to reproductive isolation that never existed.

I'll post this so you can read it again.

"The most important take-home message may be that species are not fixed, shut off from other species by inability to interbreed. On the contrary, for a long time, millions of years in some cases, they are capable of exchanging genes,"

The definition of species allows for interbreeding, I realize that you can't accept that as your whole sorry argument hangs on it but the rest of the world does.

Then you would also agree that inability to breed is not a defining feature of separate species as well? If breeding doesn’t mean same species, then not breeding doesn’t mean separate.

But to accept your claims as well as theirs, we must ignore the very definitions they wrote.

Definition of SUBSPECIES

“a category in biological classification that ranks immediately below a species and designates a population of a particular geographic region genetically distinguishable from other such populations of the same species and capable of interbreeding successfully with them where its range overlaps theirs”

Exactly the situation with those finches. You have yet to provide one scientific reason to ignore the scientific definitions.

Can't see the wood for the trees?

They are your trees that blind you to the individual bushes underneath.

Where did the original population of finches that colonized the island come from?

From the mainland, which then through interbreeding, just as with dogs, produced separate subspecies. Shown to you already when the ground finch from the mainland flew over to the islands and mated with a tree finch that had ground finch genes.

How you can post links to articles to back up your arguments and then, in the very next post, dismiss those articles as pseudoscience just about sums this conversation up. It's quite bizarre.

The data is not being challenged. It’s your interpretation of the data and your ignoring the scientific definitions that is. Not sure if you can understand the difference in your brainwashed state.