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Author Topic:   The Origin of Novelty
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 646 of 871 (692646)
03-06-2013 8:27 AM
Reply to: Message 623 by bluegenes
03-02-2013 5:28 AM


Re: Novel protein coding gene in an Antarctic fish
I'm not sure if you've quite understood the paper, but that last sentence of yours is correct. It produces them randomly all the time.
It's producing useful duplications that we were discussing
Rather than me not understanding the paper, it seems you did not quite understand my comments. If in a laboratory they choose a particular organism that is lacking amplification, when the normal state of the species is known to be amplified, then they are pre-empting expected results by artificially creating amplification where nature already has it. They are just copying nature. Just the fact that they chose the place in the genome that is already known to have duplicates as their position to produce artificial duplicates, makes their conclusions about the value of coding duplicates doubtful.
You're welcome, and you're getting there! I don't know what you mean by "rare". Duplication + neofunctionalization wouldn't have to be an every day, every year, or every generation happening in order to account for the increase in number of protein coding genes in a population group from 1,000 to 20,000 (the scenario you were discussing in your debate with RAZD). The completion of such an event in one individual organism in the group every 10,000 years on average would get you there in 200 million years, and things have been evolving for far longer than that.
By rare, I mean in dispute, never convincingly observed. The e.coli example of novel genetic function is close, involves the promoter and not the gene, and mimics a close relative , the staphylococcus. Is it a new function? Or did the mutation re-activate a silent aerobic promoter that always existed in the active state of that gene in the staphyylococcus?
Shall we look for relatives to test the hypothesis that genes, like organisms, come in families with nested heirarchies?
Please! I'm happy with any proof or even schoolbook illustration of long-term nested hierarchies, I believe in short term hierarchies but everyone just seems to make sweeping statements in overconfident fashion on this site. I prefer a more scientific approach with examples of actual long-term nested hierarchies, instead of unproven philosophy.
Or do you mean high copy numbers in a created population 6,500 years ago? I'd expect there to be considerable variation 6,500 years ago in an evolutionary scenario, and before. 300 generations is not a long time to create much variation. A clue to another of the problems for your model is in the word "copy". In that paper about adaption to heat that you enjoyed, there were duplication events in 3 of the cultures that all included the same key genes. But the duplications were all different. When genes are duplicated, it's in this messy kind of way. If the AMY1 duplications look as though they are on messy randomly inserted stretches of DNA, wouldn't it be reasonable for you to ask yourself if your creator wasn't trying to make things look as though they were products of mutation? You won't find lots of neat little AMYs sitting in a row, looking pretty.
Nevertheless, if its nature copying itself badly, or nature losing genes, neither process involves new coding genes.
Let me explain it this way, not to argue from evidence, but for you to understand my view on the matter. The biblical view is a move from an exclusive vegetarian pre-flood diet (includes starch) to a protein filled diet. Thus to start off the post-flood world with many individuals with high copy numbers , and then de-selection of those with high copy numbers makes perfect sense for a vegetarian population that subsequently becomes a hunter gatherer population in certain communities. If these hunter gatherer populations undergo urbanization in modern society, and a return to a less protein filled diet (expensive meat, no hunting) those rare individuals who have retained high copy numbers will become selected into greater proportions of the population. Thus we have a change in copy numbers merely through sexual variation, and not through mutational duplication.
IF some individuals undergo a duplication mutation in the same region, this would be duplicating what nature has already produced, high copy numbers in that area. This would explain the "messy" arrangements, but this is re-establishing sequences already there, the over-producing of proteins has never been observed to add to fitness.
Deletions and duplications don't look the same. And there are far too many human CNVs to have occurred in the last 300 generations of evolution. I think you need all the deletions and duplications that you can get! You also need a very high mitochondrial DNA mutation rate for a 6,500 year old Eve. Which brings me on to the next subject.
This is what I like, to get to actual numbers. You are stating a fact here "And there are far too many human CNVs to have occurred in the last 300 generations of evolution". Could you kindly back this up with exact figures please, or alternatively refrain from making sweeping statements.
'You also need a very high mitochondrial DNA mutation rate for a 6,500 year old Eve" - this statement also needs actual figures to back it up.
If you look at the true haplogroups, rather than just at those used to illustrate population spread outside Africa, you can see that the true ones are an indicator of diversity, although they can be misleading. As the paper you linked to mentioned, older haplogroups can have arrived in an area relatively recently.
So, once again, which area of the world has the greatest diversity?
I'm happy with the information I have presented. I feel that the fact that most haplogroup maps show that the greatest diversity is in the Middle East, is satisfactorily convincing. The only evidence I have seen against this is that the DNA from Africa shows more mutations, and is therefore older. This logic is incomplete because it is a well known fact that mutation rates are higher during prolonged sun exposure, and so the higher mutations in African DNA does not necessarily reflect the older population. Without evidence presented from you, the argument favors the Middle East, although some would generalize the origin of humans from South-Western Asia.

This message is a reply to:
 Message 623 by bluegenes, posted 03-02-2013 5:28 AM bluegenes has replied

Replies to this message:
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Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


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Message 647 of 871 (692647)
03-06-2013 9:20 AM
Reply to: Message 643 by mindspawn
03-06-2013 6:19 AM


Re: Evidence again
I'm not a biologist. Who knows, maybe the eye NEEDS to be continuously fed by the retinal artery in non-marine conditions.
That doesn't explain why vertebrate fish and and vertebrate terrestrial species share the same eye while vertebrate fish and cephalopods, who share the very same environment and niches, have different eyes.
Maybe your land based cephaloid eye would make you color-blind AND shortly thereafter completely blind as your vitreous body dries up without being continuously nourished by the retinal artery.
Complete and utter speculation that just doesn't add up. Color vision is a result of having multiple types of photoreceptors that react to a narrow spectrum of light. Humans have three such receptors for blue, green, and red. There is absolutely no reason why a forward facing retina could not support color vision, or be able to support adequate perfusion of blood.

This message is a reply to:
 Message 643 by mindspawn, posted 03-06-2013 6:19 AM mindspawn has replied

Replies to this message:
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Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(2)
Message 648 of 871 (692648)
03-06-2013 9:22 AM
Reply to: Message 644 by mindspawn
03-06-2013 6:42 AM


Re: Evidence again
These are REDUCED complexity mutations, ie disabled regions. The insertion mutation of these mice caused the promotor to disable.
The promoter still functions just fine. It is a gain in function mutation as the paper discusses:
"In the laboratory mouse, loss-of-function mutations at Mc1r are recessive and result in light color, whereas gain-of-function alleles are dominant and result in dark color (16). "
Just a moment...
These mice are dark in color, so it is a mutation that confers a gain in function.

This message is a reply to:
 Message 644 by mindspawn, posted 03-06-2013 6:42 AM mindspawn has replied

Replies to this message:
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 Message 671 by mindspawn, posted 03-06-2013 4:04 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 649 of 871 (692649)
03-06-2013 9:24 AM
Reply to: Message 645 by Bolder-dash
03-06-2013 7:39 AM


Re: Evidence again
Since you are already making about stories about zero explanations about the pocket mouse, . . .
We have the mutations. We observe a gain in function. What more is there to demonstrate?

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Bolder-dash
Member (Idle past 3630 days)
Posts: 983
From: China
Joined: 11-14-2009


Message 650 of 871 (692650)
03-06-2013 9:26 AM
Reply to: Message 648 by Taq
03-06-2013 9:22 AM


where did the recess come from
Taq,
How can you have a recessive gene in a population without first having a dominant gene? I am pretty sure that is impossible.

This message is a reply to:
 Message 648 by Taq, posted 03-06-2013 9:22 AM Taq has replied

Replies to this message:
 Message 652 by Taq, posted 03-06-2013 9:51 AM Bolder-dash has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(2)
Message 651 of 871 (692652)
03-06-2013 9:46 AM
Reply to: Message 646 by mindspawn
03-06-2013 8:27 AM


Re: Novel protein coding gene in an Antarctic fish
If in a laboratory they choose a particular organism that is lacking amplification, when the normal state of the species is known to be amplified, then they are pre-empting expected results by artificially creating amplification where nature already has it. They are just copying nature.
Then all evolution needs to do is copy nature in order to produce the biodiversity we see today and to produce novel function. As we have already seen, mutations produce the copies which then result in novel function.
The e.coli example of novel genetic function is close, involves the promoter and not the gene, and mimics a close relative , the staphylococcus.
A close relative? Hardly. E. coli are Gram negative while Staph is Gram positive. They are not closely related. Secondly, we observe that changes in promoter regions produces novel function, so why is this a problem given the topic of the thread? The differences between us and other apes is probably due, in part, to changes in gene regulation, as are many of the differences between us and more distantly related species.
Please! I'm happy with any proof or even schoolbook illustration of long-term nested hierarchies, I believe in short term hierarchies but everyone just seems to make sweeping statements in overconfident fashion on this site.
We are confident because you can not show us a species with a mixture of derived mammalian and avian features. We observe the nested hierarchies just as evolution predicts while we do not observe this pattern in things that are designed.
This logic is incomplete because it is a well known fact that mutation rates are higher during prolonged sun exposure, and so the higher mutations in African DNA does not necessarily reflect the older population
This definitely needs backing up. The mitochondria that you receive as an offspring comes from your mother's egg, not from your mother's skin.

This message is a reply to:
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Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(2)
Message 652 of 871 (692653)
03-06-2013 9:51 AM
Reply to: Message 650 by Bolder-dash
03-06-2013 9:26 AM


Re: where did the recess come from
How can you have a recessive gene in a population without first having a dominant gene? I am pretty sure that is impossible.
Before the dark allele showed up there was one phenotype. The small differences in the light allele did not cause changes in fur color, so there wasn't a recessive/dominant relationship between the different genotypes because any combination produced the same phenotype. It wasn't until the dark allele showed up that you had differences in phenotype, and only then can you determine the relationship between dominant and recessive genes.
Biologically, it would appear that the mutations in mc1r allow for the continuation of melanin production. Having just one copy of the gene ensures that this increased melanin production continues causing the gain in function to dominate over the light colored genotype.

This message is a reply to:
 Message 650 by Bolder-dash, posted 03-06-2013 9:26 AM Bolder-dash has replied

Replies to this message:
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Bolder-dash
Member (Idle past 3630 days)
Posts: 983
From: China
Joined: 11-14-2009


Message 653 of 871 (692657)
03-06-2013 10:40 AM
Reply to: Message 652 by Taq
03-06-2013 9:51 AM


Re: where did the recess come from
Taq,
The function of mcr1 is to produce melanin. Mcr1 is present in all mammals, and serves this function. When it is not functioning, that is when you get light colored hair. This is why light colored hair is always recessive.
I believe you are a biology major, correct Taq? There are at least 3 or 4 things wrong with your reasoning, that take too long to explain without getting into boring details, but that you really should be aware of.
The case of the pocket mouse is a terrible example of an organism gaining function, when it was the light colored mice that originally had lost function for melanin. I can't believe you are pinning so much hope of this far-fetched example.
But the problem is, you don't have any ones better to use, so I certainly don't mind you trying to make a case for it, but frankly its a pretty easy example to debunk.

This message is a reply to:
 Message 652 by Taq, posted 03-06-2013 9:51 AM Taq has replied

Replies to this message:
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Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(1)
Message 654 of 871 (692659)
03-06-2013 10:58 AM
Reply to: Message 653 by Bolder-dash
03-06-2013 10:40 AM


Re: where did the recess come from
The function of mcr1 is to produce melanin.
Sort of. mc1r is a protein that spans the cell membrane and receives signals from outside of the cell. That then starts a signal cascade that results in the production of melanin. Think of mc1r as the trigger. Changes in that trigger produce novel expression patterns for melanin.
I believe you are a biology major, correct Taq? There are at least 3 or 4 things wrong with your reasoning, that take too long to explain without getting into boring details, but that you really should be aware of.
I have a zoology degree. Plants bored me. As to the details, bring them on.
The case of the pocket mouse is a terrible example of an organism gaining function, when it was the light colored mice that originally had lost function for melanin.
Light colored mice have melanin function as well. They had never lost the ability to produce melanin. That is why their fur is brown instead of white. What has changed is the amount of melanin that is expressed, and the timing of that expression. This is due to a gain of function mutation in mc1r. The mc1r gene in light colored mice is also operational and has function.
I can't believe you are pinning so much hope of this far-fetched example.
What is far fetched about it? We have mutations that produce a gain in function which results in a novel phenotype. That is exactly what the thread is asking for.
But the problem is, you don't have any ones better to use, so I certainly don't mind you trying to make a case for it, but frankly its a pretty easy example to debunk.
I have millions of examples just in the human and chimp genomes alone.

This message is a reply to:
 Message 653 by Bolder-dash, posted 03-06-2013 10:40 AM Bolder-dash has not replied

  
Admin
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Posts: 12998
From: EvC Forum
Joined: 06-14-2002
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Message 655 of 871 (692660)
03-06-2013 11:00 AM
Reply to: Message 653 by Bolder-dash
03-06-2013 10:40 AM


Moderator Suggestion
Bolder-dash writes:
There are at least 3 or 4 things wrong with your reasoning, that take too long to explain without getting into boring details, but that you really should be aware of.
If the things wrong are not described then it isn't possible to become aware of them.
Please, no replies in this thread.

--Percy
EvC Forum Director

This message is a reply to:
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Bolder-dash
Member (Idle past 3630 days)
Posts: 983
From: China
Joined: 11-14-2009


Message 656 of 871 (692664)
03-06-2013 11:13 AM


Percy,
The Chinese football team needs you when you have time. How much do you charge to throw a game?
I am still waiting for the evolutionists to give some more examples of beneficial mutations that lead to novel functions, since THAT is the topic of this thread. (Though I can certainly understand why you don't mind letting it continue way off topic-its a lot better to keep the fence sitters from seeing how clearly you have nothing).
Is the bulk of the theory resting on the fact that some mice have dark fur? I am happy to explain all the reasons this is so lame, as soon as we can first acknowledge that this is all the evidence you have. I just don't want you changing the goalposts after I go through all the trouble of refuting it, again!

Replies to this message:
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Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(2)
Message 657 of 871 (692665)
03-06-2013 11:15 AM


How MC1R Works
Just so that we are on the same page, here is the signaling cascade for melanin production. As you can see, the MC1R protein starts the cascade when it binds alpha-MSH:
Caption: -MSH and MC1R receptor. -melanocyte stimulating hormone (-MSH) binds to its cognate receptor, melanocortin-1 receptor (MC1R). Ligand binding activates adenylate cyclase via coupled G-protein, which subsequently increases cytoplasmic cyclic AMP (cAMP). cAMP directly activates protein kinase A (PKA), which can transcriptionally activate MITF via activation of CREB. In parallel, cAMP can activate the Ras-Raf-MAPK-RSK cascade, which results in activation of MITF. MITF then modulates transcription of downstream pigmentation and proliferation genes. In melanoma, upregulated branches of this signaling pathway are indicated in black. The dashed arrow indicates modulation of transcriptional programming by MITF to favor tumorigenesis.
http://www.springerimages.com/....1007_978-3-7091-0371-5_7-0
As you can see, there are several steps that control melanin production, and mutations in any of those genes can result in a change in melanin production.

  
Taq
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Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


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Message 658 of 871 (692666)
03-06-2013 11:18 AM
Reply to: Message 656 by Bolder-dash
03-06-2013 11:13 AM


I am still waiting for the evolutionists to give some more examples of beneficial mutations that lead to novel functions,
Why should we give you more when you are ignoring the ones we have already given you?
If you want to work ahead you can do a comparison of the human and chimp genomes. The differences between those genomes contain the beneficial mutations that were responsible for the novel functions found in humans and chimps.

This message is a reply to:
 Message 656 by Bolder-dash, posted 03-06-2013 11:13 AM Bolder-dash has replied

Replies to this message:
 Message 659 by Bolder-dash, posted 03-06-2013 11:38 AM Taq has replied
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Bolder-dash
Member (Idle past 3630 days)
Posts: 983
From: China
Joined: 11-14-2009


(1)
Message 659 of 871 (692668)
03-06-2013 11:38 AM
Reply to: Message 658 by Taq
03-06-2013 11:18 AM


Did you just ignore my posts or what? The ONE (not ones!) you have given is dark fur in pocket mice. Clearly I have addressed that on many many occasions.
Now the article that you just cut and pasted reiterates my point that the production of melanin is much more complicated that claiming a simple mutation can suddenly cause an animal to produce melanin when it never had the system requirements in place to do so. As the article shows, the system is contingent upon so many factors, that you could pretty much call it both specified complexity, AND irreducibly complex to be selected for piece by piece.
How is a comparison of the human and chimp genomes going to explain how novel functions arrive and get selected for?
I know you side likes diversion, but come on, you are already paying the referee, he has already said in the media which team he hopes wins, plus he is waving around a towel with your team logo on it while he is calling penalties, isn't that enough?

This message is a reply to:
 Message 658 by Taq, posted 03-06-2013 11:18 AM Taq has replied

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New Cat's Eye
Inactive Member


(4)
Message 660 of 871 (692671)
03-06-2013 12:03 PM
Reply to: Message 659 by Bolder-dash
03-06-2013 11:38 AM


I knew it
From my Message 6:
quote:
Is this going to be one of those threads where a creationist has the evolutionists try to prove evolution to them while they do everything they can to avoid accepting it? One where no amount of evidence is ever going to matter and its just a game for you by having a bunch of people taking shots that you get to waste our time defending yourself against? Because if it is, then I don't want to play. But lets see.

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