Understanding through Discussion


Welcome! You are not logged in. [ Login ]
EvC Forum active members: 123 (8774 total)
Current session began: 
Page Loaded: 07-23-2017 12:48 PM
379 online now:
Dr Jack, DrJones*, nwr, PaulK, Phat (AdminPhat), Tangle, vimesey (7 members, 372 visitors)
Chatting now:  Chat room empty
Newest Member: Tom Larkin
Happy Birthday: anglagard
Post Volume:
Total: 814,448 Year: 19,054/21,208 Month: 1,813/3,111 Week: 34/574 Day: 34/38 Hour: 1/2

Announcements: Reporting debate problems OR discussing moderation actions/inactions


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Prev1234
5
Author Topic:   A question about evolution
Pressie
Member
Posts: 1685
From: Pretoria, SA
Joined: 06-18-2010
Member Rating: 2.8


Message 61 of 70 (801084)
03-03-2017 7:05 AM
Reply to: Message 56 by CRR
03-03-2017 4:56 AM


CRR writes:

Generally the same. They have the same number of functional genes. However I have read that red hair is due to a defect in the MC1R gene so there would be a loss of genetic information in that case.

So, you still can't quantify genetic information.
This message is a reply to:
 Message 56 by CRR, posted 03-03-2017 4:56 AM CRR has not yet responded

    
AZPaul3
Member
Posts: 3428
From: Phoenix
Joined: 11-06-2006


Message 62 of 70 (801086)
03-03-2017 7:13 AM
Reply to: Message 60 by CRR
03-03-2017 7:01 AM


Re: Step 2
We all have the gene that is linked most strongly to red hair, MC1R. It is just that most red haired people have different versions of this gene compared to people without red hair.

And there are lots of different versions of MC1R out there.

Same source.

A different allele of the same gene. No information loss. An information difference. Different proteins resulting from the different nucleotide sequences.



This message is a reply to:
 Message 60 by CRR, posted 03-03-2017 7:01 AM CRR has not yet responded

Replies to this message:
 Message 63 by Pressie, posted 03-03-2017 7:26 AM AZPaul3 has acknowledged this reply
 Message 65 by caffeine, posted 03-04-2017 8:53 AM AZPaul3 has responded

  
Pressie
Member
Posts: 1685
From: Pretoria, SA
Joined: 06-18-2010
Member Rating: 2.8


Message 63 of 70 (801088)
03-03-2017 7:26 AM
Reply to: Message 62 by AZPaul3
03-03-2017 7:13 AM


Re: Step 2
So, CRR didn't tell the truth? That doesn't shock me.
This message is a reply to:
 Message 62 by AZPaul3, posted 03-03-2017 7:13 AM AZPaul3 has acknowledged this reply

    
Theodoric
Member
Posts: 5765
From: Northwest, WI, USA
Joined: 08-15-2005


Message 64 of 70 (801100)
03-03-2017 9:46 AM


Close an abandoned thread?
I think Admin should close down this thread since it has been abandoned by the creator. Micah obviously tried to do a drive by, in order to fulfill some sort of bizarre right wing fundie need to fight the evil atheists. When that failed or he felt he did his godly duty he slunked away.

There have no responses from him since the day he opened the thread.


Facts don't lie or have an agenda. Facts are just facts

"God did it" is not an argument. It is an excuse for intellectual laziness.

If your viewpoint has merits and facts to back it up why would you have to lie?


    
caffeine
Member
Posts: 1313
From: Prague, Czech Republic
Joined: 10-22-2008
Member Rating: 5.0


Message 65 of 70 (801211)
03-04-2017 8:53 AM
Reply to: Message 62 by AZPaul3
03-03-2017 7:13 AM


Re: Step 2
A different allele of the same gene. No information loss. An information difference. Different proteins resulting from the different nucleotide sequences.

CRR is not completely off on this one. The known mutations which lead to the 'red hair' alleles of MC1R are all loss of function mutations. They produce a receptor protein which is broken, in a sense, and so where the wild type would perform its role of promoting melanin production, the red hair variants don't.

However, we know that loss of function mutations are not the only ones that can happen to MC1R. In those mice that are dark on old lava flows and light elsewhere, some of the darker mice pigmentation seems to be due to MC1R mutation (but not all - different populations of melanistic mice acheived dark fur through different pathways). I don't think the functional basis is understood in the mice; but it can't simply be breaking the receptor like the mutations which contribute to lighter pigmentation in humans.


This message is a reply to:
 Message 62 by AZPaul3, posted 03-03-2017 7:13 AM AZPaul3 has responded

Replies to this message:
 Message 66 by AZPaul3, posted 03-04-2017 10:12 AM caffeine has responded

  
AZPaul3
Member
Posts: 3428
From: Phoenix
Joined: 11-06-2006


Message 66 of 70 (801218)
03-04-2017 10:12 AM
Reply to: Message 65 by caffeine
03-04-2017 8:53 AM


Re: Step 2
The known mutations which lead to the 'red hair' alleles of MC1R are all loss of function mutations. They produce a receptor protein which is broken, in a sense, and so where the wild type would perform its role of promoting melanin production, the red hair variants don't.

Is that right?

Or, do the major variants of MC1R cause the melanocortin 1 receptor to stimulate the melanocytes into eumelanin production while the minor variants of MC1R block the melanocortin 1 receptor from stimulating eumelanin production causing the melanocytes to make mostly pheomelanin instead?

Do you really consider the minor variants of MC1R to be "broken, in a sense"?

This may seem a semantic quibble, but it does get to the very heart of CRR's misunderstanding of genetics as a whole.

And, no, I do not believe you would call this a "loss" of genetic information.

So, again, no information loss. An information difference. Different proteins resulting from the different nucleotide sequences. Different proteins having different effects upon the system.

And, as often happens with evolution, some of the minor variants convey some advantage in an environment and become the major variants in a population.

CRR is not completely off on this one.

Since he wouldn't know why, I'll disagree.

Edited by AZPaul3, : No reason given.

Edited by AZPaul3, : affect/effect. I still have trouble with this.



This message is a reply to:
 Message 65 by caffeine, posted 03-04-2017 8:53 AM caffeine has responded

Replies to this message:
 Message 67 by CRR, posted 03-04-2017 6:31 PM AZPaul3 has responded
 Message 70 by caffeine, posted 03-05-2017 4:06 PM AZPaul3 has acknowledged this reply

  
CRR
Member
Posts: 437
From: Australia
Joined: 10-19-2016
Member Rating: 1.3


Message 67 of 70 (801279)
03-04-2017 6:31 PM
Reply to: Message 66 by AZPaul3
03-04-2017 10:12 AM


Re: Step 2
"A study on unrelated British and Irish individuals demonstrated that over 80% of people with red hair and/or fair skin that tan poorly have a dysfunctional variant of the MC1R gene."

"As humans migrated north, the absence of high levels of solar radiation in northern Europe and Asia relaxed the selective pressure on active MC1R, allowing the gene to mutate into dysfunctional variants without reproductive penalty, then propagate by genetic drift."

https://en.wikipedia.org/...1_receptor#Pigmentation_genetics

@caffeine also raises some interesting issues.

At this stage I'm probably getting out of my depth in genetics and particularly MC1R, so I'll make this my last comment.


This message is a reply to:
 Message 66 by AZPaul3, posted 03-04-2017 10:12 AM AZPaul3 has responded

Replies to this message:
 Message 68 by Coyote, posted 03-04-2017 6:41 PM CRR has not yet responded
 Message 69 by AZPaul3, posted 03-04-2017 10:04 PM CRR has not yet responded

  
Coyote
Member
Posts: 5901
Joined: 01-12-2008
Member Rating: 4.3


(1)
Message 68 of 70 (801281)
03-04-2017 6:41 PM
Reply to: Message 67 by CRR
03-04-2017 6:31 PM


Re: Step 2
...dysfunctional variants

Since when is lighter skin color in a region with lower UV intensity dysfunctional?

I would suggest it was entirely functional, and both a beneficial and a necessary mutation.

The body does not work well without Vitamin D and other photochemicals.

African Americans are at greater risk of vitamin D deficiency, because if you have dark skin, you may need as much as 10 times more sun exposure to produce the same amount of vitamin D as a person with pale skin!

http://articles.mercola.com/...eficiency-signs-symptoms.aspx

So, as people migrated away from the equator, different mutations that allowed for increased Vitamin D and other photochemical production were beneficial!


Religious belief does not constitute scientific evidence, nor does it convey scientific knowledge.

Belief gets in the way of learning--Robert A. Heinlein

In the name of diversity, college student demands to be kept in ignorance of the culture that made diversity a value--StultisTheFool

It's not what we don't know that hurts, it's what we know that ain't so--Will Rogers

If I am entitled to something, someone else is obliged to pay--Jerry Pournelle

If a religion's teachings are true, then it should have nothing to fear from science...--dwise1

"Multiculturalism" demands that the US be tolerant of everything except its own past, culture, traditions, and identity.


This message is a reply to:
 Message 67 by CRR, posted 03-04-2017 6:31 PM CRR has not yet responded

  
AZPaul3
Member
Posts: 3428
From: Phoenix
Joined: 11-06-2006


(4)
Message 69 of 70 (801293)
03-04-2017 10:04 PM
Reply to: Message 67 by CRR
03-04-2017 6:31 PM


Re: Step 2
As humans migrated north, the absence of high levels of solar radiation in northern Europe and Asia relaxed the selective pressure on active MC1R, allowing the gene to mutate into dysfunctional variants without reproductive penalty, then propagate by genetic drift.

Poor presentation and word choice on the part of the Wiki author.

The variants of MC1R are fully functional, they just function in a different way. Where the MC1R gene in the, shall I say, standard form produced proteins that stimulate the melanocytes into eumelanin production (the darker brown/black melanin) several variants produce proteins that disrupt and lessen that production allowing more production of pheomelanin (the yellow/red melanin).

As Coyote points out in his message such variants proved beneficial for migrants into northern climes (increases in vital photo chemical production). And by beneficial we mean fitter for the environment they had moved into and fitness is measured in differential reproductive success. Nothing dysfunctional about a gene that lets a population make more successful babies.

Still no loss of information. Different information doing different stuff.

Edited by AZPaul3, : No reason given.



This message is a reply to:
 Message 67 by CRR, posted 03-04-2017 6:31 PM CRR has not yet responded

  
caffeine
Member
Posts: 1313
From: Prague, Czech Republic
Joined: 10-22-2008
Member Rating: 5.0


Message 70 of 70 (801371)
03-05-2017 4:06 PM
Reply to: Message 66 by AZPaul3
03-04-2017 10:12 AM


Re: Step 2
Or, do the major variants of MC1R cause the melanocortin 1 receptor to stimulate the melanocytes into eumelanin production while the minor variants of MC1R block the melanocortin 1 receptor from stimulating eumelanin production causing the melanocytes to make mostly pheomelanin instead?

Do you really consider the minor variants of MC1R to be "broken, in a sense"?

Yes, I would. The loss of function alleles of the MC1R gene produce a protein that functions less effectively or, in a few cases, does not function at all. The phenotypic effect is an individual with higher proportion of pheomelanin than eumelanin; but the point is the way that this is acheived - it's acheiving by 'breaking' the protein. This, I believe, is what the wiki author was trying to say. The variant MC1R alleles are not dysfunctional in the sense of the individual's overall phenotype - they are dysfunctional in the sense of coding for a dysfunctional MC1R protein.

And, no, I do not believe you would call this a "loss" of genetic information. So, again, no information loss. An information difference. Different proteins resulting from the different nucleotide sequences. Different proteins having different effects upon the system.

And, as often happens with evolution, some of the minor variants convey some advantage in an environment and become the major variants in a population.

Information theory is not something I ever got my head around, so I would steer clear of such things. However, I can understand (in a non-formal sense) how a mutation that led to a protein which doesn't 'work' can be described as information loss. There are many different ways you can stop a protein from functioning effectively, which is why there are so many different loss-of-function variants of MC1R known.

I'm not claiming that CRR is right in general, of course. There are other ways to acheive lighter pigmentation. ASIP is the gene which makes agouti protein; which inhibits the MC1R protein from stimuating the production of eumelanin, and there are known variants of this gene in populations with lighter skin. This seems to me like two different mechanisms to acheive lighter pigmentation - one by making a protein which more effectively inhibits eumelanin production; and one by breaking the protein which should stimulate that production.

I am probably just adding to confusion here though, so maybe I will stop typing.


This message is a reply to:
 Message 66 by AZPaul3, posted 03-04-2017 10:12 AM AZPaul3 has acknowledged this reply

  
Prev1234
5
Newer Topic | Older Topic
Jump to:


Copyright 2001-2015 by EvC Forum, All Rights Reserved

™ Version 4.0 Beta
Innovative software from Qwixotic © 2017