chicken or egg- i argue egg came first

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#61
mustardness
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The root/core of the question is not truly about chickens or dinosaurs. You guys are not getting to root/core of the question ergo your lost in superficiality, and not the more cosmic considerations.  You guys are like ants, crawling around in a sphere or tube, looking for a corner to crap in, when no corner exists.

You to digger deeper and think it much larger more comprehensive terms or just go along with abiogensis in hopes it will someday appear in the lab.

Chickens poofing into existence are not very likely, except in ways of taking a chicken apart here and then transmitting via ELMagnetics to be reassemble else where ex beam this chicken from here to there.  That my come happen on Earth if it does not already exist elsewhere.

What came first is the RNA-DNA coding for the egg.

There is evidence that more complex molecules come from less complex molecules via high pressures.

We know the 4-fold cubo-octahedron transforms into  double set of Euclidean sine-waves, at 90 degrees to each other, however, we also know that these same 2 peaks 2 troughs can configure as;

1} parrallel to each other and define the quadra-pedic side arms and tail flukes of cetacceans,

2} perpendicular to each other as side fins and tail fin at 90 degrees with fish.

We know that the area of the four internal bisecting planes of a spherical cubo-octahedron eguals the outer surface area of that spherical cubo-octahedron ---thank you Archimedes---.

This latter part is very similar what is inside a black hole is expressed on its event horizon --thank you Jacob Bekenstien.

The cubo-octahedron has 8 surface triangles and water is composed of 8 electrons. Biologics are 70 - 85% water.

I can envision parts and pieces of most complex RNA-DNA coding coming from black holes as evaporation of some other means and carried by celestrial phenomena within a galaxy, if not beyond.

We know there appears to be a black hole at center of every galaxy that has been observed.

#62
ethang5
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@Stronn
Chickens today were once dinosaurs having no feathers and no beaks.

More accurately, chickens today are descended from dinosaurs. 
Fair enough.

1. did the changes making them into chickens over time occur because of genetic mutations?

Yes.
Thank you. We will refer back to this later.

2. Did these mutations occur in an individual at a time, all individuals in the whole group, or many individuals within the group coincidentally at the same time?

The mutations occur at an even lower level than individuals. They occur in individual cells.
They can, but that was not the question. Cells are found in individuals. Please address the question.

Most mutations, however, are not passed to offspring. It is only when a mutation occurs in a gamete (sperm or ovum) that it can be passed on to offspring.
Thanks. So then we will limit our question only to mutations that occur in gametes and zygotes.

If a mutation occurs in a gamete, then it can be passed down to offspring, who then possess the mutation in every cell, including gametes, which is how it passes the mutation along to its own offspring. (A mutation can also occur during cell division in the zygote, in which case the offspring will possess the mutation in only some cells.)
Thank you for the lesson. Teach if you feel inclined to, but please include answers to the questions asked too.

So, I'm going to re-phrase question #2.

2A. Did these mutations that can be passed down to offspring occur only in individuals at a time, the whole group at once, or many individuals within the group coincidentally at the same time?

3. If this/these proto-chicken(s) mated with an earlier generation that did not have the mutation, would that not hinder or stop the propagation of the mutation within the gene pool?
Nope, makes no difference.

I find this answer surprising, so I must ask some questions to understand better. I will use eye color as a placeholder example.

3A. Was the blue eye color in humans caused by a mutation?
3B. If yes, is the gene for blue eyes recessive?
3C. If an individual and successive offspring of that individual keep mating with individuals that lack the gene for blue eyes, will the rate of blue eyed offspring resulting from these matings rise, stay the same, or fall within the population?

A mutation spreads through a population by its carrier(s) producing offspring.
This does not reflect reality. For example, the gene for dark skin among blacks in America is almost gone. Hardly any black is dark anymore, though blacks brought to America during the years of slavery were very dark.

If mutations spread through populations only by its carrier(s) producing offspring, where are all the very dark black offspring? Perhaps  factors other than just having offspring affect a mutation's spread (and expression) through a population.

This is, in fact, the simplest definition of evolution: the change in frequency of alleles (gene variants) in a population over time. 
We are trying to stay specific, because that is where one sees the illogic of evolution, so please let's leave the general for now.

In summery, you did not answer question 2, so it was rephrased for you.

And your answer for question 3 appears to be, at best, incomplete, and at worse, wrong. Comments?

Thanks.
#63
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People who refuse to avail themselves of a rudimentary education concerning the Theory of Evolution and instead believe what an ignorant middle eastern savage fabricated as the origin of life forms on this planet are proponents of the creationist version of "evolution".
In this version a dinosaur mated with another dinosaur and because of evolution the egg laid as a consequence of that union actually contained a chicken, go figure.
It's rather informative that these people are more than happy to expose this level of ignorance of the subject they are purporting to be discussing.
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They can, but that was not the question. Cells are found in individuals. Please address the question.
I thought I did. If a mutation occurs in a single cell in an individual, then it follows that it occurs in a single individual. While occasionally the same mutation might appear independently in different individuals, it happens so rarely that it is probably not a significant driver of evolution.

2A. Did these mutations that can be passed down to offspring occur only in individuals at a time, the whole group at once, or many individuals within the group coincidentally at the same time?
Individuals (aside from very rare events which we need not consider here).

I find this answer surprising, so I must ask some questions to understand better. I will use eye color as a placeholder example.

3A. Was the blue eye color in humans caused by a mutation?
Yes. A recent analysis found that all blue-eyed people are descended from a common ancestor, whose OCA2 gene mutated between 6,000 and 10,000 years ago.

3B. If yes, is the gene for blue eyes recessive?
Yes, although there is more to it than that. Eye color is influenced by at least 12 different genes. So it is actually possible for brown-eyed parents to have a blue-eyed child and vice versa.

3C. If an individual and successive offspring of that individual keep mating with individuals that lack the gene for blue eyes, will the rate of blue eyed offspring resulting from these matings rise, stay the same, or fall within the population?
If blue-eyed individuals only  produce offspring with brown-eyed individuals, then the rate of blue-eyed offspring will tend to decrease.

This does not reflect reality. For example, the gene for dark skin among blacks in America is almost gone. Hardly any black is dark anymore, though blacks brought to America during the years of slavery were very dark.

If mutations spread through populations only by its carrier(s) producing offspring, where are all the very dark black offspring? Perhaps  factors other than just having offspring affect a mutation's spread (and expression) through a population.
Skin color is actually a good example of the process. But first, realize that there is no "black gene" or "white gene." Skin color is determined by a combination of at least eight different genes, each with two or more alleles. Some alleles tend to promote darker skin, some lighter skin, depending on what other alleles they are combined with.

Africans who were brought to America have lighter skin because they produced offspring with people of European descent. Their offspring inherited some of the white-skin-promoting alleles from the European parent and some of the dark-skin-promoting alleles from the African parent. The result was skin that was darker than the typical European but lighter than the typical African. Genetic studies, in fact, have shown that blacks in some parts of the south are as much as 30% European on average.


#65
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@Stronn
Some molecule cause frequency of yellow light to be reflected/. Genes are compose of molecules.  It many cases teh gene that causes yellowm black or blue light to be reflected is the same in many differrent biologics.

You and others are still stuck in more superficial surface of a much larger and more comprehensive, cosmic scenario. 

The root/core of the question is not truly about chickens or dinosaurs. The disscussion is not getting to root/core of the question ergo dssscussion is lost in superficiality, and not the more cosmic considerations. 

This disscussion so so far is  like ants, crawling around in a sphere or tube, looking for a corner to crap in, when no corner exists.

When we dig deeper and think it much larger more comprehensive terms or just go along with abiogensis in hopes it will someday appear in the lab.

Chickens poofing into existence are not very likely, except in ways of taking a chicken apart here and then transmitting via ELMagnetics to be reassembled else where ex beam this chicken from here to there.  That my come happen on Earth if it does not already exist elsewhere.

What came first is the RNA-DNA coding for the egg.

There is evidence that more complex molecules come from less complex molecules via high pressures.

We know the 4-fold cubo-octahedron transforms into  double set of Euclidean sine-waves, at 90 degrees to each other, however, we also know that these same 2 peaks 2 troughs can configure as;

1} parrallel to each other and define the quadra-pedic side arms and tail flukes of cetacceans,

2} perpendicular to each other as side fins and tail fin at 90 degrees with fish.

We know that the area of the four internal bisecting planes of a spherical cubo-octahedron eguals the outer surface area of that spherical cubo-octahedron ---thank you Archimedes---.

This latter part is very similar what is inside a black hole is expressed on its event horizon --thank you Jacob Bekenstien.

The cubo-octahedron has 8 surface triangles and water is composed of 8 electrons. Biologics are 70 - 85% water.

I can envision parts and pieces of most complex RNA-DNA coding coming from black holes as evaporation of some other means and carried by celestrial phenomena within a galaxy, if not beyond.

We know there appears to be a black hole at center of every galaxy that has been observed.

#66
ethang5
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@Stronn

They can, but that was not the question. Cells are found in individuals. Please address the question.
I thought I did.
No, you didn't.

If a mutation occurs....
We are talking hereditery genetics and it is a precise science. If I know the gene makeup of the parents, the rate of expression of the gene in offspring can be calculated. Let's forget the "ifs".

While occasionally the same mutation might appear independently in different individuals, it happens so rarely that it is probably not a significant driver of evolution.
So we can eliminate the single proto-chicken theory. A single individual could not have been the answer.

Thus the mutation you say created the proto-chicken must have occurred in multiple individuals at the same time!  The odds of this are astronomical. Ultra astronomical. Do you have a mechanism for how the same random mutation would occur in multiple individuals at the same time?

I find this answer surprising, so I must ask some questions to understand better. I will use eye color as a placeholder example.

3A. Was the blue eye color in humans caused by a mutation?
Yes.

3B. If yes, is the gene for blue eyes recessive?
Yes,....

3C. If an individual and successive offspring of that individual keep mating with individuals that lack the gene for blue eyes, will the rate of blue eyed offspring resulting from these matings rise, stay the same, or fall within the population?

If blue-eyed individuals only  produce offspring with brown-eyed individuals, then the rate of blue-eyed offspring will tend to decrease.
Then your proto-chicken genes would quickly die out in the gene pool, as there would be no mates with the gene. Each 1st gen offspring would be less likely to carry the gene by a quarter, 2nd gen by 50% less, 3rd gen by 75% and so on.

But when I asked you, 

If this/these proto-chicken(s) mated with an earlier generation that did not have the mutation, would that not hinder or stop the propagation of the mutation within the gene pool?

You answered, 

Nope, makes no difference. 
Now you are admitting that it does make a difference.

Skin color is actually a good example of the process. But first, realize that there is no "black gene" or "white gene."
Nice misdirection, but I mentioned no "black gene" or "white gene".

If mutations spread through populations only by its carrier(s) producing offspring, where are all the very dark black offspring?

Africans who were brought to America have lighter skin because they produced offspring with people of European descent.
Yes. Like your proto-chicken, black slaves had few mates with their genes, so the incidence of dark skin in the gene pool virtually dispeared in 10 generations. And 10 generations is nothing in evolutionary terms.

Your correct answer to 3C shows that your theory of a proto-chicken is incorrect. That cannot be how chickens descended from dinosaurs. Maybe, chickens did not descend from dinosaurs at all.

Without your proto-chicken idea, do you have an alternative? This is what I mean when I say if you examine evolution closely, it falls apart. Most people accept the proto-chicken illogic without any critical thinking. But there is no way it can work given the beliefs of evolution. It is illogical.

Genetic studies, in fact, have shown that blacks in some parts of the south are as much as 30% European on average.
As genetic studies on your proto-chicken would also quickly show that they were as much as 30% non-proto on average, and 100% given enough time.

Sorry. What you believe is not representative of reality.
#67
Stronn
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@ethang5

We are talking hereditery genetics and it is a precise science. If I know the gene makeup of the parents, the rate of expression of the gene in offspring can be calculated. Let's forget the "ifs".
I meant "if" in the formal, logical sense. If X, then Y. If a mutation occurs in a single cell, then it follows that it occurs in a single individual. In other words, occurring in a single cell implies occurring in a single individual. This was in answer to your question about whether mutations occur in multiple individuals at once. They do not.

I don't know what you mean by "rate of expression". Gene expression is the process of genes coding for (usually) proteins. Perhaps you mean genetic makeup? If so, you cannot predict it exactly.

So we can eliminate the single proto-chicken theory. A single individual could not have been the answer.
I don't know what you mean by "single proto chicken theory." Do you mean a mutation starting in a single individual? If so, you have no basis to eliminate it as an option.

Thus the mutation you say created the proto-chicken must have occurred in multiple individuals at the same time!  The odds of this are astronomical. Ultra astronomical. Do you have a mechanism for how the same random mutation would occur in multiple individuals at the same time?
No one mutation created the proto-chicken. I'm not sure where you got that idea. A proto-chicken was just your name for some species that was ancestors to modern chickens.

3C. If an individual and successive offspring of that individual keep mating with individuals that lack the gene for blue eyes, will the rate of blue eyed offspring resulting from these matings rise, stay the same, or fall within the population?

If blue-eyed individuals only  produce offspring with brown-eyed individuals, then the rate of blue-eyed offspring will tend to decrease.
Then your proto-chicken genes would quickly die out in the gene pool, as there would be no mates with the gene. Each 1st gen offspring would be less likely to carry the gene by a quarter, 2nd gen by 50% less, 3rd gen by 75% and so on.
See what you did here? You asked what would happen if X was true. I answered that Y would happen. You then assumed that Y would happen, without ever bothering to consider whether X was indeed true. It isn't. 

In other words, it is true that if every individual with allele A only produces offspring with individuals with allele B, then allele A becomes less frequent and eventually dies out. But that is a huge "if".

But when I asked you, 

If this/these proto-chicken(s) mated with an earlier generation that did not have the mutation, would that not hinder or stop the propagation of the mutation within the gene pool?

You answered, 

Nope, makes no difference. 
Now you are admitting that it does make a difference.
See how you asked the question (I bolded the relevant part). Since I answered one of your previous questions by saying a mutation starts in a single individual, I interpreted your question it to be asking whether it made a difference whether that individual mated with members of previous generations. Again, it doesn't, since no other individual in the population has the mutation yet.

Nice misdirection, but I mentioned no "black gene" or "white gene".
You said "gene for dark skin" which I unintentionally misquoted, although I don't think the meaning is much different. My point was that there is no one gene that controls skin color.

If mutations spread through populations only by its carrier(s) producing offspring, where are all the very dark black offspring?
Why would you expect there to be very dark offspring in American blacks? As I explained, they are lighter skinned because their genes have been mixed with those of Europeans. The lighter skin of U.S. blacks is, in fact, an example of genes that promote lighter skin spreading through the population over the generations. 

Yes. Like your proto-chicken, black slaves had few mates with their genes, so the incidence of dark skin in the gene pool virtually dispeared in 10 generations. And 10 generations is nothing in evolutionary terms.
Where do you get that black slaves had few mates with their genes? Most slaves had offspring with other slaves. Even today, most blacks have offspring with other blacks.
 
Your correct answer to 3C shows that your theory of a proto-chicken is incorrect. That cannot be how chickens descended from dinosaurs. Maybe, chickens did not descend from dinosaurs at all.

Without your proto-chicken idea, do you have an alternative? This is what I mean when I say if you examine evolution closely, it falls apart. Most people accept the proto-chicken illogic without any critical thinking. But there is no way it can work given the beliefs of evolution. It is illogical.
It only falls apart if you misunderstand one or more key concepts.

As genetic studies on your proto-chicken would also quickly show that they were as much as 30% non-proto on average, and 100% given enough time.
I have no idea what "30% non-proto" means, since every member of the population is a proto-chicken.


#68
ethang5
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@Stronn
We are talking hereditary genetics and it is a precise science. If I know the gene makeup of the parents, the rate of expression of the gene in offspring can be calculated. Let's forget the "ifs".

>I meant "if" in the formal, logical sense.

Uh huh.

>I don't know what you mean by "rate of expression". Gene expression is the process of genes coding for (usually) proteins. Perhaps you mean genetic makeup? If so, you cannot predict it exactly.

Check out the TYPES heading. Read and learn.

So we can eliminate the single proto-chicken theory. A single individual could not have been the answer.

>I don't know what you mean by "single proto chicken theory." Do you mean a mutation starting in a single individual? If so, you have no basis to eliminate it as an option.

You said...
>While occasionally the same mutation might appear independently in different individuals, it happens so rarely that it is probably not a significant driver of evolution.

>This was in answer to your question about whether mutations occur in multiple individuals at once. They do not.

And…

>…since no other individual in the population has the mutation yet.

The single proto-chicken theory is dead Stronn. Mutations are not spread by single individuals. Thus you must explain how multiple individuals can carry the same mutation at the same time. The odds of this are astronomical. Ultra astronomical. Do you have a mechanism for how the same random mutation would occur in multiple individuals at the same time?

>No one mutation created the proto-chicken. I'm not sure where you got that idea. A proto-chicken was just your name for some species that was ancestors to modern chickens.

It wasn't my name. When I asked, “All I want to know is who did your proto-chicken mate with?”

You answered, “It mated with other proto-chickens.”

Whether its one mutation or not, the principle is the same. Please tell us how animals change species. By your own admittal, It cannot begin by a single animal, and multiple animals cannot carry the same mutation at the same time. Can you explain the mechanics?

3C. If an individual and successive offspring of that individual keep mating with individuals that lack the gene for blue eyes, will the rate of blue eyed offspring resulting from these matings rise, stay the same, or fall within the population?

>If blue-eyed individuals only  produce offspring with brown-eyed individuals, then the rate of blue-eyed offspring will tend to decrease.

Then your proto-chicken genes would quickly die out in the gene pool, as there would be no mates with the gene. Each 1st gen offspring would be less likely to carry the gene by a quarter, 2nd gen by 50% less, 3rd gen by 75% and so on.

>See what you did here?

I see what you did. You are trying to be dishonest. Watch.

>You asked what would happen if X was true. I answered that Y would happen. You then assumed that Y would happen, without ever bothering to consider whether X was indeed true. It isn't.

>In other words, it is true that if every individual with allele A only produces offspring with individuals with allele B, then allele A becomes less frequent and eventually dies out. But that is a huge "if".

Yet, in reality, as with even the imperfect example of blacks in America, we see its not a big if.

If this/these proto-chicken(s) mated with an earlier generation that did not have the mutation, would that not hinder or stop the propagation of the mutation within the gene pool?

You answered,
>Nope, makes no difference.

Now you are admitting that it does make a difference.

>See how you asked the question (I bolded the relevant part). Since I answered one of your previous questions by saying a mutation starts in a single individual, I interpreted your question it to be asking whether it made a difference whether that individual mated with members of previous generations. Again, it doesn't, since no other individual in the population has the mutation yet.

Exactly! So if speciation begins with mutated genes, it cannot begin with single individuals. It MUST begin with multiple individuals. But multiple individuals having the same random mutation at the same time is mathematically impossible. So how does speciation begin?
#69
ethang5
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@Stronn
Nice misdirection, but I mentioned no "black gene" or "white gene".

>You said "gene for dark skin" which I unintentionally misquoted,….

Uh huh.

If mutations spread through populations only by its carrier(s) producing offspring, where are all the very dark black offspring?

>Why would you expect there to be very dark offspring in American blacks?

I don't. Just as I don't expect there to be any proto-chicken offspring.

>As I explained, they are lighter skinned because their genes have been mixed with those of Europeans.

As would happen with your proto-chicken. Its genes would have been mixed with those of non proto-chickens .….since no other individual in the population has the mutation yet. Just using your words buddy.

>The lighter skin of U.S. blacks is, in fact, an example of genes that promote lighter skin spreading through the population over the generations.

Yes. Like your proto-chicken, black slaves had few mates with their genes, so the incidence of dark skin in the gene pool virtually dispeared in 10 generations. And 10 generations is nothing in evolutionary terms.

>Where do you get that black slaves had few mates with their genes?

From the fact that 2 African blacks back then could not have had a fair offspring. There must have been mixing.

>Most slaves had offspring with other slaves. Even today, most blacks have offspring with other blacks.

But they did mate enough with others who did not share their genes for dark skin to begin to fade away. It isn't a perfect example, but it is telling. Imagine how much more it happened when there was only one individual with the mutation.

Your correct answer to 3C shows that your theory of a proto-chicken is incorrect. That cannot be how chickens descended from dinosaurs. Maybe, chickens did not descend from dinosaurs at all.

Without your proto-chicken idea, do you have an alternative? This is what I mean when I say if you examine evolution closely, it falls apart. Most people accept the proto-chicken illogic without any critical thinking. But there is no way it can work given the beliefs of evolution. It is illogical.

>It only falls apart if you misunderstand one or more key concepts.

We are all ears. I have asked you questions and used your answers. Which key concept do you misunderstand?

As genetic studies on your proto-chicken would also quickly show that they were as much as 30% non-proto on average, and 100% given enough time.

>I have no idea what "30% non-proto" means, since every member of the population is a proto-chicken.

How did they come about? By a single individual with a mutation, or many individuals with the same mutation? Can you say?
#70
Stronn
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@ethang5
Uh huh.
I have noticed a pattern where, when you misunderstand something, and someone tries to clarify, rather than attempting to understand their explanation, you question their honesty. It doesn't foster a productive discussion.

>Check out the TYPES heading. Read and learn.
So you meant expression of phenotypes. Are you really asserting that phenotypes can be predicted exactly? It should be evident to anyone that that is not the case, from the simple observation that two children with the same parents can look quite different.

>The single proto-chicken theory is dead Stronn. Mutations are not spread by single individuals.
Sure they are. Maybe you are not considering that an individual with the mutation can have more than one offspring, and each of those offspring can in turn have more than one offspring. In this way a mutation can increase in a population, potentially at an exponential rate.

Whether its one mutation or not, the principle is the same. Please tell us how animals change species. By your own admittal, It cannot begin by a single animal, and multiple animals cannot carry the same mutation at the same time. Can you explain the mechanics?
First, animals don't change species, populations do.

Speciation occurs when one segment of a population becomes isolated. Over a long period of time, two things happens. First, new mutations arise and spread through the isolated population, and second, the frequency of existing alleles changes in the population, with some alleles dying out. 
Meanwhile, the same things happen in the population that is not isolated.  Over time, the changes accumulate and the two populations become more and more genetically dissimilar. Once they become dissimilar enough that individuals of one population can no longer produce viable offspring with
individuals of the other population, we have two different species. (It is worth noting that neither one is the same as the original species.)

I see what you did. You are trying to be dishonest. Watch.
Again with the dishonesty accusation, when you did exactly what I described. Read it again..

Yet, in reality, as with even the imperfect example of blacks in America, we see its not a big if.
Seriously? Are you asserting that blue-eyed people only mate with brown-eyed people, or that blacks only mate with non-blacks? If not, then how can you possibly disagree that assuming either one is a big if?

Nice misdirection, but I mentioned no "black gene" or "white gene".

>You said "gene for dark skin" which I unintentionally misquoted,….

Uh huh.
Again with the dishonesty insinuation. No reasonable person would conclude that I changed "gene for dark skin" to "black gene" on purpose as some sort of misdirection tactic. They mean the same thing, and the only point I was making was that there is not just one gene controlling the trait.

As would happen with your proto-chicken. Its genes would have been mixed with those of non proto-chickens .….since no other individual in the population has the mutation yet. Just using your words buddy.
I addressed this above.

>Where do you get that black slaves had few mates with their genes?

From the fact that 2 African blacks back then could not have had a fair offspring. There must have been mixing.
Yes, there must have been some mixing. But you are making an unjustified leap from "some" to "most." In fact, most blacks have two black parents, then and now.

But they did mate enough with others who did not share their genes for dark skin to begin to fade away. It isn't a perfect example, but it is telling. Imagine how much more it happened when there was only one individual with the mutation.
Yes, they mated enough with Europeans to spread genes for lighter skin throughout the population. Certainly nowhere near a majority of black offspring had a European parent, however.

Your correct answer to 3C shows that your theory of a proto-chicken is incorrect. That cannot behow chickens descended from dinosaurs. Maybe, chickens did not descend from dinosaurs at all.
Again, I think you did not take into account that individuals can have more than one offspring.

Without your proto-chicken idea, do you have an alternative?
By the "proto-chicken idea," I assume you mean mutations arising in single individuals. Now that I've explained it, I hope you understand how it works.

If not, consider this simplified example. Mutation A occurs in one individual. That individual produces two offspring with the mutation. There are now two individuals in the population with the mutation (not counting the parent). Each of these then produces two offspring with the mutation. There are now four individuals with the mutation. Each of these produces two offspring with the mutation....see where this is going?

Of course it is more complicated than that, since the number of offspring varies, and other individuals in the population are producing offspring too. But that is a synopsis of how a single individual with a mutation can spread it over successive generations.



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@Stronn
>I have noticed a pattern where, when you misunderstand something, and someone tries to clarify, rather than attempting to understand their explanation, you question their honesty. It doesn't foster a productive discussion.

Do you know what I've noticed? When you misstate something, and someone tries to clarify, rather than attempting to understand their explanation, you question their understanding. It doesn't foster a productive discussion.

Check out the TYPES heading. Read and learn.

>So you meant expression of phenotypes. Are you really asserting that phenotypes can be predicted exactly?

The rate which individuals will have the mutation will follow a ratio. Don't worry if you don't get it right away.

>It should be evident to anyone that that is not the case, from the simple observation that two children with the same parents can look quite different.

But the ratio of children who carry a certain gene will follow a pattern that can be predicted. Maybe you never got to do those simple charts in high school of hereditary science.

The single proto-chicken theory is dead Stronn. Mutations are not spread by single individuals.

>Sure they are. Maybe you are not considering that an individual with the mutation can have more than one offspring, and each of those offspring can in turn have more than one offspring. In this way a mutation can increase in a population, potentially at an exponential rate.

Untrue. Each time the individual with the mutation mates with an individual without the mutation, only one out of 4 of the offspring will carry the gene. And the 1 in 4 offspring from that mating that carries the mutation, only 1 out of 8 of his offspring will carry the mutated gene, if he mates with another individual that does not have the gene.

Mutated genes in a single individual are extremely unlikely to spread throughout the gene pool.

When one adds in that other mutations can erase the original one, and that the dominance or recessiveness of the gene can affect it's expression, the idea is ludicrous.

Whether its one mutation or not, the principle is the same. Please tell us how animals change species. By your own admittal, It cannot begin by a single animal, and multiple animals cannot carry the same mutation at the same time. Can you explain the mechanics?

>First, animals don't change species, populations do.

Again, this is evolution doublespeak. Populations are comprised of individuals, and we are speaking mostly to laymen, we should not try to use jargon to obfuscate.

>Speciation occurs when one segment of a population becomes isolated. Over a long period of time, two things happens. First, new mutations arise and spread through the isolated population, and second, the frequency of existing alleles changes in the population, with some alleles dying out.

This again is the general picture where you breeze over the illogic with a flippant, “new mutations arise and spread through the isolated population”. You are being asked to break this down. How do new mutations arise and spread? It cannot be by a single individual.

Yet, in reality, as with even the imperfect example of blacks in America, we see its not a big if.

>Seriously? Are you asserting that blue-eyed people only mate with brown-eyed people, or that blacks only mate with non-blacks?

No. But even the low rate of mixing in the US with multiple individuals was enough to begin to erase the genes for dark skin. If a single black had been brought to the US, do you think dark skin would have spread at an exponential rate?

>If not, then how can you possibly disagree that assuming either one is a big if?

I know science.

Nice misdirection, but I mentioned no "black gene" or "white gene".

>You said "gene for dark skin" which I unintentionally misquoted,….

Uh huh.

>Again with the dishonesty insinuation.

This is America. Language has more than just the dry meaning of words. Gene for dark skin is not race specific, black gene is. You intended a negative connotation about my understanding of genes. Plus, it was not necessary to specify genes over gene. There is no need to be anal. We are posting for a general science board, not the National Academy of Sciences.

>No reasonable person would conclude that I changed "gene for dark skin" to "black gene" on purpose as some sort of misdirection tactic.

One wonders then what “reasonable person” means to you.

>…..the only point I was making was that there is not just one gene controlling the trait.

What trait is that? The one for darker skin or the one for black skin?
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As would happen with your proto-chicken. Its genes would have been mixed with those of non proto-chickens .….since no other individual in the population has the mutation yet. Just using your words buddy.

Even with multiple individuals with the genes, it did not expand at an exponential rate, but is disappearing. Yet you think a single individual could change an entire gene pool.

>Yes, they mated enough with Europeans to spread genes for lighter skin throughout the population. Certainly nowhere near a majority of black offspring had a European parent, however.

But that supports my point. In your proto-chicken scenario, there were no other individuals with the mutation. The majority of offspring would have parents without the mutation. If the low rate of mixing as with blacks in America could not sustain black skin, why would you think the high rate of mixing with your proto-chicken could sustain the mutation? It doesn't make sense.

Your correct answer to 3C shows that your theory of a proto-chicken is incorrect. That cannot be how chickens descended from dinosaurs. Maybe, chickens did not descend from dinosaurs at all.

>Again, I think you did not take into account that individuals can have more than one offspring.

I did. The laws of heredity kick in. Only ¼ of its offspring would carry the mutation regardless of how many offspring it had. And most of those offspring would mate with individuals not carrying the mutation. In this way gene pools are protected from random bad mutations in single individual.

>By the "proto-chicken idea," I assume you mean mutations arising in single individuals. Now that I've explained it, I hope you understand how it works.

If you think, “mutations arise and spread into the gene pool” is an explanation of how it works, then it's no wonder you believe evolution.

>If not, consider this simplified example. Mutation A occurs in one individual. That individual produces two offspring with the mutation.

Odds are, it would have to produce 8 offspring to get 2 with the mutation. And those two would have to happen to be male and female to be able to mate. But siblings generally do not mate. Neither do mothers and sons.

Each of those 2 individuals would only have offspring at the rate of 1 to 8 with the mutation. The mutation would quickly die away.

>There are now two individuals in the population with the mutation (not counting the parent). Each of these then produces two offspring with the mutation.

For this to happen, they would Have to have 16 offspring on average to get 2 with the mutation, because they would likely be mating with individuals that do not carry the gene.

>There are now four individuals with the mutation. Each of these produces two offspring with the mutation....

And they would have to have 32 offspring on average to get 2 with the mutation.

>see where this is going?

Do you?

>Of course it is more complicated than that, since the number of offspring varies, and other individuals in the population are producing offspring too. But that is a synopsis of how a single individual with a mutation can spread it over successive generations.

Sorry, it is unrealistic in nature, and it flies against mathematical odds. This is why evolutionists like to keep it general and vague. Examining the details shows that evolution just doesn't make sense.
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Our fundamental disagreement thus far is whether a mutation arising in individuals can spread through a population, so why don't we concentrate on that point for now.

I assume you accept that mutations can and do occur in individuals. But you assert that such mutations must always die out within a few generations.

One thing that may help to convince you is that the rate of inheritance is 1/2, not the 1/4 that you are using. That is because each parent has two copies of a gene. A child gets exactly one of those copies. If one of the parents copies has a mutation, there is a 50% chance a child will inherit it (assuming the other parent does not have the mutation).

All it takes for a mutation to begin spreading is for the first individual with the mutation to have more than one offspring with the mutation. If the first individual has two offspring, then there is a 25% change both will have the mutation. Three offspring, and there is 50% chance at least two will have the mutation (and 12.5% of the time three will).

For a mutation to increase, all it takes is for the average number of offspring produced by each individual with the mutation to be greater than 1. Fewer than 1 and the mutation decreases.

Does anything about this not seem plausible?


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@Stronn
The Punnett square is a square diagram that is used to predict the genotypes of a particular cross or breeding experiment. It is named after Reginald C. Punnett, who devised the approach. The diagram is used by biologists to determine the probability of an offspring having a particular genotype.

The Punnett square is a tabular summary of possible combinations of maternal alleles with paternal alleles. These tables can be used to examine the genotypical outcome probabilities of the offspring of a single trait (allele), or when crossing multiple traits from the parents.

The Punnett Square is a visual representation of Mendelian inheritance. It is important to understand the terms "heterozygous", "homozygous", "double heterozygote" (or homozygote), "dominant allele" and "recessive allele" when using the Punnett square method.

Example table here

>Our fundamental disagreement thus far is whether a mutation arising in individuals can spread through a population, so why don't we concentrate on that point for now.

OK, but that isn't our fundamental disagreement.

>I assume you accept that mutations can and do occur in individuals. But you assert that such mutations must always die out within a few generations.

In cases where a single individual enters the population with no other individuals carrying the mutation, and no external gene manipulation occurs, yes.

>One thing that may help to convince you is that the rate of inheritance is 1/2, not the 1/4 that you are using.

No sir. Please study the link at the beginning of this post. It is ¼ for the 1st generation. 1/8th  for the second, 1/16th for the third, and so on.

>That is because each parent has two copies of a gene.

No. Only one parent has the mutated gene, and only onePlease look up Mendelian inheritance, it will help you.

>A child gets exactly one of those copies. If one of the parents copies has a mutation, there is a 50% chance a child will inherit it (assuming the other parent does not have the mutation).

Incorrect. It is only 25% chance and only for the 1st generation.

>All it takes for a mutation to begin spreading is for the first individual with the mutation to have more than one offspring with the mutation. If the first individual has two offspring, then there is a 25% change both will have the mutation.

This is untrue. You must be unfamiliar with hereditary science. You are also incorrectly assuming that the two siblings will mate and will be the right genders. Neither is likely.

>Three offspring, and there is 50% chance at least two will have the mutation (and 12.5% of the time three will).

This is incorrect. Until you learn how heredity works, it will be silly to continue along this track.

>For a mutation to increase, all it takes is for the average number of offspring produced by each individual with the mutation to be greater than 1. Fewer than 1 and the mutation decreases.

>Does anything about this not seem plausible?

Yes. It is incorrect and not representative of what happens in reality.

Here is the math on it from the site.

The probability of an individual offspring's having the genotype BB is 25%, Bb is 50%, and bb is 25%. The ratio of the phenotypes is 3:1, typical for a monohybrid cross. When assessing phenotype from this, "3" of the offspring have "Brown" eyes and only one offspring has "green" eyes. (3 are "B_" and 1 is "bb")

Please, I asked you to look at this 2 posts ago.
#75
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The RNA-DNA code for biologic eggs came before any adult biologics.

Read my lips/text;

RNA-DNA  coding > egg > progeny

Cosmic coding or abiogenesis.  Neither have any laboratory evidence.

However, we do find left-handed amino-acids in celestial phenomena.  How did they get there?

We have evidence of  more complex molecules being created from less complex molecules via high pressures.

Another thing we find being formed from high pressures is diamonds if not also buckminster fullerenes.
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Please study the link at the beginning of this post. It is ¼ for the 1st generation. 1/8th  for the second, 1/16th for the third, and so on.
You are the one misunderstanding Mendelian inheritance.

Each individual has two copies of each gene (it's called being diploid). A mutation occurs in only one copy. That is why a gene in an individual is represented by two letters. If both letters are identical, both copies of the gene are identical. If the letters are different, the two copies are different.

We can use the Punnet Square you linked to determine what happens when only one parent has the mutation in only one copy of the gene. To do this, we use uppercase Y to represent the mutated gene and lowercase y the original gene. One parent is said to have genotype Yy and the other parent yy.

Now look at the cells in the table. Of the four possibilities, how many inherit the mutated Y gene? Two. That is 1/2.

Incorrect. It is only 25% chance and only for the 1st generation.
Do you see how it is 50% now?

You are also incorrectly assuming that the two siblings will mate and will be the right genders. Neither is likely.
I make no such assumption, because the inheritance rate is 50%.

This is incorrect. Until you learn how heredity works, it will be silly to continue along this track.
Replace "you" with "one of us" and I would agree.

Here is the math on it from the site.

The probability of an individual offspring's having the genotype BB is 25%, Bb is 50%, and bb is 25%.
That example applies only when both parents carry the mutation in one copy of the gene, meaning both parents have genotype Bb, where b is the mutated gene and B is the original. In that case, 3/4 offspring carry the mutation.

So a) this is the wrong example to use for the case where only one parent has the mutation, and b)  you have the math backwards: 25% is the chance that an offspring won't have the mutation.

The ratio of the phenotypes is 3:1, typical for a monohybrid cross. When assessing phenotype from this, "3" of the offspring have "Brown" eyes and only one offspring has "green" eyes. (3 are "B_" and 1 is "bb")
You are conflating carrying the mutation with having blue eyes.  Of the 3 offspring with "B_", two are "Bb". They carry the mutation for blue eyes, even though they have brown eyes, because the gene for brown eyes is dominant.


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Dinosaurs laid eggs. chickens did not exist,  enter evolution, speciation, the egg. 
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Replace "you" with "one of us" and I would agree.
Eh. If you need to appear smart that bad. I don't care as I don't need your agreement. You are wrong whether you know it or not.

You are conflating carrying the mutation with having blue eyes.
No sir. The principle works with any similar example. The particular configuration of the genes doesn't matter.

To do this, we use uppercase Y to represent the mutated gene and lowercase y the original gene.
Funny then that when experts do it, the mutation is represented with the lowercase letter. Do you know why? Because mutations are almost never dominant.
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The choice of labels has absolutely nothing to do with the correctness of the example. I chose the labels to so the example would match your lined Punnet square.  Otherwise it would be the wrong Punnet square for the case where one parent has the mutation in one copy of the gene.
 
If you like, we can use B to represent a dominant brown-eyed allele and b to represent a recessive blue-eye mutation. One parent has one copy of the mutated gene (Bb) and the other has no mutated copy (BB). Both parents have brown eyes, because the brown-eyed gene is dominant. But look what happens with the offspring.

      B    b
B   BB  Bb
B   BB  Bb

All four children have brown eyes, yet two still inherit the inherit the mutation.



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@Stronn
Hey Darwin, 

The mutation is not eye color.

We can use y to represent the mutation, and 0 to represent the absence of the mutation. One parent has one copy of the mutated gene (By) and the other has no mutated copy (BO). 

Here it is corrected.
    
      B    y
B   BB  By
O  OB  Oy

Our mutation is not a change of an existing quality like brown eyes to blue, but a wholly new quality. There is no gene representing its absence.
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@ethang5
Ok, back to first principles.

Allele: one of two or more alternative forms of a gene.

In a Punnet square, each column represents one of a parent's two copies of a gene. Same with each row. If the two letters are different, that means the parent's  two copies are different alleles. Each parent contributes only one of their copies to each offspring.

So in your example "By" represents an individual's two copies of the gene, not just one, with one copy being allele "B" and the other allele "y". When talking about a specific mutation, the "B" allele either contains the mutation or does not. Same with the "y" allele.

In your Punnet square, you use "B", "y" and "O", three different alleles. If you want to use it to track a mutation, you need to specify for each allele whether it contains the mutation or not. In your example, if "O" is the only allele without the mutation, then both "B" and "y" must necessarily contain the mutation. In that case, all four offspring inherit the mutation  





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@ethang5
Here is an illustration where only one parent has the mutation in one gene copy. Observe that two of the four children have the mutation.



#83
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RNA-DNA { molecular } coding > egg > progeny

Abiogenesis follows the following way;

quantum > atoms > molecules > precursor to RNA-DNA > egg > progeny.

Occupied space  poofing into existence,  from where before all that existed  only macro-infinite non-occupied space is irrational, illogical and lacks common sense.

Full blown adult human{s} --ex adam and eve-- poofing into existence from where before, in sum-total, finite Universe, no non-biologic life existed, is irrational, illogical and lack of common sense.

The RNA-DNA coding does seem more feasibly possible in a finite Universe that contains exotic  black hole phenomena i.e. cosmic egg that contains RNA-DNA coding i.e. some specific, patterened set of occupied space, infomation bits { quanta }.

Which came first, black hole phenomena or RNA-DNA coding ?





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@Stronn
>Here is an illustration where only one parent has the mutation in one gene copy. Observe that two of the four children have the mutation.

You did not use the Punnet square. Wonder why? And we agreed that the mutation needed to occur in a zygote or gamete. You seem to have forgotten that in your misleading example.

Look. I don't care to convince you. Anyone who wants to know can look it up on the net. I will leave you to close unopposed.

Gentle Reader, here are some good credible links that do not try to hoodwink you.

The Top Ten Scientific Problems with Biological and Chemical Evolution

Seven fundamental, unsolved questions in molecular biology.

Cytochrome oxidase: some unsolved problems and controversial issues.

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@ethang5
I used an example to help you visualize that each parent has two copies of the gene and passes only one copy to offspring because you failed to grasp that basic concept from Punnet squares. But if you absolutely must have a Punnet square where one parent has one capital letter and one lowercase letter, and the other parent two capital letters, then look here.



Notice how two of the four offspring inherit the lowercase letter?

Yes the mutation must occur in a zygote or gamete. Guess what? Gametes (and only gametes) carry only one of an individual's two copies of each gene. That is, in fact, how one and only one copy from each parent is passed to each offspring.

Bow out if you want, but you are missing the chance to correct a misunderstanding you have of a basic concept in biology.

23 days later

#86
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MY established response to this question is STFU no one cares.
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@sadolite
MY established response to this question is STFU no one cares.
STFU?

RNA-DNA coding > egg > comes before dinosaur { progeny }

Still the Best Answer { SBA }

RNA-DNA { molecular } coding > egg > progeny

Abiogenesis follows the following way;

Occupied SPACE > quantum > atoms > molecules > precursor to RNA-DNA > egg > progeny.

Occupied space  poofing into existence,  from where before all that existed  only macro-infinite non-occupied space is irrational, illogical and lacks common sense.

Full blown adult human{s} --ex adam and eve-- poofing into existence from where before, in sum-total, finite Universe, no non-biologic life existed, is irrational, illogical and lack of common sense.

The RNA-DNA coding does seem more feasibly possible in a finite Universe that contains exotic  black hole phenomena i.e. cosmic egg that contains RNA-DNA coding i.e. some specific, patterened set of occupied space, infomation bits { quanta }.

Which came first, black hole phenomena or RNA-DNA coding ?

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Occupied SPACE > quantum > atoms > molecules > precursor to RNA-DNA > egg > progeny.

Biological life is 80% water?

See structure of water via 8 electrons in following link


6 oxygen + 2 hydrogen = 8 electrons

..."The result is a distorted tetrahedral arrangement in which the H—O—H angle is 104.5°."....


Seen  as 87 great tori   --at minimum-- via my four level/line presentation of each tori having three primary aspects;

1} ( ) positive shaped geodesic gravity SPACE,

2} \/\/\ or as ^v^v sine-wave patterning frequencies,

3} )( negative shaped geodesic dark energy SPACE.




#89
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Biological life is mostly atomic space.

In this respect life is just an illusion or a projection.
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@mustardness
STFU = shut the fuk up, no one cares