Understanding through Discussion


Welcome! You are not logged in. [ Login ]
EvC Forum active members: 64 (9038 total)
212 online now:
Phat (AdminPhat), Pollux (2 members, 210 visitors)
Newest Member: Barry Deaborough
Post Volume: Total: 885,690 Year: 3,336/14,102 Month: 277/724 Week: 35/91 Day: 3/17 Hour: 0/0


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   Y.E.C. Model: Was there rapid evolution and speciation post flood?
Tanypteryx
Member
Posts: 2499
From: Oregon, USA
Joined: 08-27-2006
Member Rating: 6.9


Message 151 of 518 (808832)
05-13-2017 2:18 PM
Reply to: Message 149 by Tangle
05-13-2017 2:12 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
She can't, Adam and Eve didn't have parents to donate the extra alleles :-)

(Insert miracle here)

That reminds me of something I have always wondered, did Adam and Eve have belly buttons?


What if Eleanor Roosevelt had wings? -- Monty Python

One important characteristic of a theory is that is has survived repeated attempts to falsify it. Contrary to your understanding, all available evidence confirms it. --Subbie

If evolution is shown to be false, it will be at the hands of things that are true, not made up. --percy

The reason that we have the scientific method is because common sense isn't reliable. -- Taq


This message is a reply to:
 Message 149 by Tangle, posted 05-13-2017 2:12 PM Tangle has not yet responded

Replies to this message:
 Message 152 by Porosity, posted 05-13-2017 2:31 PM Tanypteryx has not yet responded

  
Porosity
Member (Idle past 995 days)
Posts: 158
From: MT, USA
Joined: 06-15-2013


Message 152 of 518 (808835)
05-13-2017 2:31 PM
Reply to: Message 151 by Tanypteryx
05-13-2017 2:18 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
That reminds me of something I have always wondered, did Adam and Eve have belly buttons?

Why would they if they're magicked into existence? They are the original snow flakes, predating all modern primates.


This message is a reply to:
 Message 151 by Tanypteryx, posted 05-13-2017 2:18 PM Tanypteryx has not yet responded

  
Percy
Member
Posts: 20113
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.2


Message 153 of 518 (808837)
05-13-2017 2:50 PM
Reply to: Message 144 by bluegenes
05-13-2017 9:48 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
bluegenes writes:

I don't think so. Her posts here certainly seem to accept "neutral". But I'm sure she'll clarify.

Yes, you're right, I should have said that Faith accepts non-beneficial alleles, or deleterious and neutral alleles.

--Percy


This message is a reply to:
 Message 144 by bluegenes, posted 05-13-2017 9:48 AM bluegenes has not yet responded

  
Faith 
Suspended Member (Idle past 345 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 154 of 518 (808839)
05-13-2017 3:08 PM
Reply to: Message 148 by PaulK
05-13-2017 2:08 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
Two

Given that heterozygosity is an advantage in these genes I think you should go for four in this case.

One gene made up of the two alleles B and b, possessed by both parents, produces both blue and brown eyes in the offspring, most of them brown heterozygous Bb's like the parents. Even with no more genes with their two alleles contributing to eye color, subsequent generations will continue to have more Bb heterozygous brown eye color than the homozygous bb and BB.

Even when you get populations that become completely homozygous BB or bb there is no disadvantage over many generations. What eventually can threaten the genetic makeup is mutations that kill one of the alleles and therefore kill the trait in an individual. This would have to be a seriously lethal change in the sequence, and I don't know what it would do to the trait itself, do you? In reality the other genes for the trait would probably kick in anyway, but I'm trying to stick to the example of the one gene Bb. (If the mutations are neutral the trait will continue as always of course).

The point is that it takes a lot to kill a gene and a trait, it can take a long time of deleterious mutations attacking genes for a disease process to result and then be passed on. Homozygous genes are most vulnerable, could even be completely disabled by one lethal mutation, but unless it's lethal to the organism, to the individual, it can get passed on but while that would be a disease process spreading through the population it won't threaten the population itself. It would take a lot of these occurrences in a lot of genes to do that. That has happened in heavily inbreeding populations like the Amish and the Inuit. But unless a lot of genetic disease occurs frequently throughout the population it won't take a toll on the species itself for a long time. Of course since each individual has -- what? -- hundreds of mutations of his/her/its own, the odds aren't negligible, and they get more problematic with each generation, and not being lethal, get passed on to the next.

Homozygosity for one gene is likely to be accompanied by homozygosity for many, since it's usually the result of reduced numbers of individuals in the founding population, the Amish, the Inuit, being cases in point for human beings. The larger the population grows from that point the safer it will be from a genetic problem due to the homoygosity, but once it is established it's going to be passed on unless it actually kills the organism. I may not be saying this as well as I'd like, but I think I'm in the ballpark.

If they don't change the function of the original allele they would continue to occur in the population as the original allele would.

You haven't even bothered to find out what these genes do, have you ?

I don't even know how to find this out, I have to rely on whatever comes up here.

See above. If they do what the original allele did this whole line of reasoning does not apply. They would "spread" according to the circumstances under which the original allele would spread.

If they don't offer any advantage then - on average - they won't increase in frequency at all. That is pretty basic.

"Advantage" is a ToE concept that doesn't have much to do with the YEC model, some perhaps but not much. In the YEC model variation is a random thing that follows the principles of the Mendelian square. Some traits may proliferate over others for many reasons but the "advantage" in each case is mostly a random thing too. Random selection such as by migration and geographic isolation of a portion of the larger population is more common than natural selection.

I still don't get what is "highly unlikely" about this

How do the extra alleles spread so quickly ?

The same way the original allele would spread, nothing unusual, just according to the principles of the Mendelian square.

Edited by Faith, : No reason given.


This message is a reply to:
 Message 148 by PaulK, posted 05-13-2017 2:08 PM PaulK has responded

Replies to this message:
 Message 155 by PaulK, posted 05-13-2017 3:34 PM Faith has responded

  
PaulK
Member
Posts: 16861
Joined: 01-10-2003
Member Rating: 4.0


(1)
Message 155 of 518 (808840)
05-13-2017 3:34 PM
Reply to: Message 154 by Faith
05-13-2017 3:08 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
quote:

One gene made up of the two alleles B and b, possessed by both parents, produces both blue and brown eyes in the offspring, most of them brown heterozygous Bb's like the parents.

Instead of rambling on about other genes perhaps you could deal with the specific genes under discussion ?

quote:

I don't even know how to find this out, I have to rely on whatever comes up here

You could have read the link provided in Message 52

quote:

"Advantage" is a ToE concept that doesn't have much to do with the YEC model, some perhaps but not much. In the YEC model variation is a random thing that follows the principles of the Mendelian square. Some traits may proliferate over others for many reasons but the "advantage" in each case is mostly a random thing too. Random selection such as by migration and geographic isolation of a portion of the larger population is more common than natural selection

So the YECs don't allow alleles to increase in frequency? Isn't that a bit awkward when you have to explain how these alleles very quickly increased in frequency ?

quote:

The same way the original allele would spread, nothing unusual, just according to the principles of the Mendelian square.

The Mendelian square doesn't include increases in frequency.

This is why it pays to understand what you are talking about.


This message is a reply to:
 Message 154 by Faith, posted 05-13-2017 3:08 PM Faith has responded

Replies to this message:
 Message 156 by Faith, posted 05-13-2017 6:16 PM PaulK has responded

  
Faith 
Suspended Member (Idle past 345 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 156 of 518 (808842)
05-13-2017 6:16 PM
Reply to: Message 155 by PaulK
05-13-2017 3:34 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
I've responded a few times to the message you suggest I respond to.

Please answer this question: WHAT exactly has "increased in frequency?"

and how can you know when (how long ago) a particular mutation occurred and how "quickly" it spread?

Edited by Faith, : No reason given.


This message is a reply to:
 Message 155 by PaulK, posted 05-13-2017 3:34 PM PaulK has responded

Replies to this message:
 Message 157 by PaulK, posted 05-14-2017 3:46 AM Faith has responded

  
PaulK
Member
Posts: 16861
Joined: 01-10-2003
Member Rating: 4.0


Message 157 of 518 (808845)
05-14-2017 3:46 AM
Reply to: Message 156 by Faith
05-13-2017 6:16 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
quote:

I've responded a few times to the message you suggest I respond to

I didn't suggest that you respond to any message. I suggested that you read a link to understand the function of the genes and why heterozygosity is an advantage.

quote:

Please answer this question: WHAT exactly has "increased in frequency?"

The mutant alleles of course. As I said.

quote:

and how can you know when (how long ago) a particular mutation occurred and how "quickly" it spread?

I'm not claiming to know any such thing. Only that in your model the mutations can't occur much more than 6000 years ago, and that they would have to spread very quickly to reach the observed frequencies.


This message is a reply to:
 Message 156 by Faith, posted 05-13-2017 6:16 PM Faith has responded

Replies to this message:
 Message 158 by Faith, posted 05-14-2017 7:16 AM PaulK has responded

  
Faith 
Suspended Member (Idle past 345 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 158 of 518 (808851)
05-14-2017 7:16 AM
Reply to: Message 157 by PaulK
05-14-2017 3:46 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
WHAT exactly has "increased in frequency?"

The mutant alleles of course. As I said.

this should really be answered by bluegenes who posted that information. He might be more informative.

So far I don't have any good reason to think they are something other than neutral mutations that didn't alter the function of the original allele, in which case an increase in frequency means nothing.

I don't know what link you were talking about so I seem to have missed it. And if it's a link that goes to a long white page I won't be able to read it carefully anyway.


This message is a reply to:
 Message 157 by PaulK, posted 05-14-2017 3:46 AM PaulK has responded

Replies to this message:
 Message 162 by PaulK, posted 05-14-2017 7:58 AM Faith has responded

  
Faith 
Suspended Member (Idle past 345 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 159 of 518 (808852)
05-14-2017 7:46 AM
Reply to: Message 132 by Taq
05-12-2017 3:32 PM


Re: Multiple Alleles of OCA2 Produce a Wide Variety of Human Eye Colors
[qs]
Taq writes:

Ran across this paper:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1785344/?too...

It lists multiple alleles for the OCA2 gene, and those alleles are not equal in function. Different combinations of alleles produces different eye colors. This is an example of more than 2 alleles for the same gene

1) I can't read the paper, it's too technical and it's hard on my eyes as well, and your summary is nothing but an assertion.

Different combinations of alleles at one locus? What do you mean? What's combining with what? How many different eye colors?


This message is a reply to:
 Message 132 by Taq, posted 05-12-2017 3:32 PM Taq has responded

Replies to this message:
 Message 190 by Taq, posted 05-15-2017 1:43 PM Faith has responded

  
Faith 
Suspended Member (Idle past 345 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 160 of 518 (808853)
05-14-2017 7:48 AM
Reply to: Message 132 by Taq
05-12-2017 3:32 PM


Re: Multiple Alleles of OCA2 Produce a Wide Variety of Human Eye Colors
Taq writes:

Ran across this paper:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1785344/?too...

It lists multiple alleles for the OCA2 gene, and those alleles are not equal in function. Different combinations of alleles produces different eye colors. This is an example of more than 2 alleles for the same gene

1) I can't read the paper, it's too technical and it's hard on my eyes as well, and your summary is nothing but an assertion.

Different combinations of alleles at one locus? What do you mean? What's combining with what? How many different eye colors?


This message is a reply to:
 Message 132 by Taq, posted 05-12-2017 3:32 PM Taq has not yet responded

  
Faith 
Suspended Member (Idle past 345 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 161 of 518 (808854)
05-14-2017 7:54 AM
Reply to: Message 131 by Taq
05-12-2017 3:15 PM


Re: The model in more detail
You say I can't extrapolate from one gene to the entire genome. Seems to me if one gene can be understood in terms of a Mendel square many others ought to be as well. Even more complicated situations such as codominance can be expressed in those terms.

The problem with standard genetics seems to be that mutations are treated as normal events and that's why it's all so complicated. A bunch of random accidents of replication complicates things enormously if you're trying to discover a lawful pattern there, and explain things like variation in eye color as in the previous post.

And it's so unnecessary if eye color is governed simply by some number of genes with two alleles each. Extra alleles are redundant at best in such a system.


This message is a reply to:
 Message 131 by Taq, posted 05-12-2017 3:15 PM Taq has not yet responded

Replies to this message:
 Message 163 by PaulK, posted 05-14-2017 8:02 AM Faith has responded

  
PaulK
Member
Posts: 16861
Joined: 01-10-2003
Member Rating: 4.0


Message 162 of 518 (808855)
05-14-2017 7:58 AM
Reply to: Message 158 by Faith
05-14-2017 7:16 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
quote:

this should really be answered by bluegenes who posted that information. He might be more informative.

It's not exactly a difficult concept. As an allele becomes more common in the population it increases in frequency.

quote:

So far I don't have any good reason to think they are something other than neutral mutations that didn't alter the function of the original allele, in which case an increase in frequency means nothing.

You have been given reasons to think that they differ (although the basic function is the same there are important differences - that is part of the reason why heterozygosity is an advantage).

But the increase in frequency IS the big point. I'm still waiting for you to offer any explanation for it that is consistent with YEC.

quote:

I don't know what link you were talking about so I seem to have missed it

There are times when I think you are just playing at being obtuse. And even if your inability to understand the use of frequency - despite all the context - isn't one of them, being unable to find a link in a post is pretty bad.

The major histocompatibility complex (MHC) and its functions. NCBI

You might like to consider this part of the quoted section again


Expression of MHC alleles is codominant, with the protein products of both the alleles at a locus being expressed in the cell, and both gene products being able to present antigens to T cells. The extensive polymorphism at each locus thus has the potential to double the number of different MHC molecules expressed in an individual and thereby increases the diversity already available through polygeny

This message is a reply to:
 Message 158 by Faith, posted 05-14-2017 7:16 AM Faith has responded

Replies to this message:
 Message 164 by Faith, posted 05-14-2017 8:08 AM PaulK has responded

  
PaulK
Member
Posts: 16861
Joined: 01-10-2003
Member Rating: 4.0


Message 163 of 518 (808856)
05-14-2017 8:02 AM
Reply to: Message 161 by Faith
05-14-2017 7:54 AM


Re: The model in more detail
I think you mean that the "problem" is that scientists try to find out what is really going on rather than just settling for a simple theoretical model that you happen to like.

And that is just another example of your anti-scientific thinking.


This message is a reply to:
 Message 161 by Faith, posted 05-14-2017 7:54 AM Faith has responded

Replies to this message:
 Message 165 by Faith, posted 05-14-2017 8:12 AM PaulK has responded

  
Faith 
Suspended Member (Idle past 345 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 164 of 518 (808857)
05-14-2017 8:08 AM
Reply to: Message 162 by PaulK
05-14-2017 7:58 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
I can't offer an explanation for an increase in frequency I don't think even exists.

Expression of MHC alleles is codominant, with the protein products of both the alleles at a locus being expressed in the cell, and both gene products being able to present antigens to T cells. The extensive polymorphism at each locus thus has the potential to double the number of different MHC molecules expressed in an individual and thereby increases the diversity already available through polygeny

I already gave an answer to this. It's meaningless if the "new" alleles do not change the function of the original. That paper actually says that all the variations are a good thing because they vary the product. Not so if they are "neutral" mutations that DON'T vary the product despite the sequence variation. In fact the statement is a very strange assertion, even naïve.

Seems to me all the answers to my simple YEC model are nothing but unnecessary complications based on standard ToE assumptions that treat mutations as normal. Even assuming that a difference in DNA sequence -- produced by a mutation -- means a difference in product? That's really a sort of heresy.

Edited by Faith, : No reason given.


This message is a reply to:
 Message 162 by PaulK, posted 05-14-2017 7:58 AM PaulK has responded

Replies to this message:
 Message 166 by PaulK, posted 05-14-2017 8:31 AM Faith has responded
 Message 175 by NosyNed, posted 05-14-2017 10:39 AM Faith has not yet responded

  
Faith 
Suspended Member (Idle past 345 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 165 of 518 (808858)
05-14-2017 8:12 AM
Reply to: Message 163 by PaulK
05-14-2017 8:02 AM


Re: The model in more detail
I think you mean that the "problem" is that scientists try to find out what is really going on ...

No. what I mean is that scientists are operating under a false paradigm that won't tell them what is really going on because they have false assumptions to begin with. Treating what is really a disease process as if it were normal is not going to show you "what is really going on."


This message is a reply to:
 Message 163 by PaulK, posted 05-14-2017 8:02 AM PaulK has responded

Replies to this message:
 Message 168 by PaulK, posted 05-14-2017 8:41 AM Faith has responded

  
Newer Topic | Older Topic
Jump to:


Copyright 2001-2018 by EvC Forum, All Rights Reserved

™ Version 4.0 Beta
Innovative software from Qwixotic © 2021