Scripps: New Climate Risk Classification Created to Account for Potential ?Existential? Threats

If you know anything about the differences you would know they are "vast" in the sense that we can't live on the same diets. We have different nutrient needs and each species will die without some nutrients the other doesn't need.

Not sure where you get this idea. Protein is not really a nutrient, rather it is a group of nutrients, amino acids. In humans there are nine essential amino acids. Rats have different essential amino acids, in particular rats can not synthesize arginine while humans can make it from other amino acids.

That's like flying a rebel flag, Pauling already lost his battle.

I would love to give you a link, but the myth is so firmly established that I can't easily find any authoritative references that explain this properly. For example, the wikipedia article on Protein combining uses a flawed analysis that breaks down an amount of rice to show it is deficient in Lysine. But the amount of rice is selected by the total protein content rather than calorie content. If you ate nothing but 612 grams of rice they analyze you would die of calorie insufficiency from the daily 924 calories before you suffered from a protein insufficiency. Change the amount of rice to meet your calorie requirement and you obtain an adequate amount of all amino acids.

Not that wikipedia is the ultimate authority, but if a wikipedia article can't get it right, what hope is there for laymen to understand?

That question itself is curios as there is no reason to think it will provide any insight. Also, "why" questions in science are usually category errors.

Pauling did neither regarding vitamin C, that's why he was laughed at in his later years.

If we lost the ability to synthesize vitamin C it was for a reason. Evolution is not without purpose. There is a cost to every feature in an organism. If that feature is no longer needed, the cost can be shed making the animal better adapted to the environment.

--

Rick C 

Viewed the eclipse at Wintercrest Farms, 
on the centerline of totality since 1998
Reply to
rickman
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Really? You consider Watson to be an unbiased observer? Why was it that he and Crick got it *so* wrong on their first try? I believe they missed some fundamental chemistry when they proposed a triple helix with the hydrophobic bases on the outside! A third year biochemistry student should understand what was wrong with that.

Now they do, yes. Her lack of credit was partly because of her poor relationship with Wilkins who was also given credit. She left her position under him and stopped working on DNA.

Pauling did poor science when he made his fantastic claims of vitamin C. He had no real evidence to support those claims. How how was that good science? The facts are pretty clear. I have no idea what you are basing your point on.

--

Rick C 

Viewed the eclipse at Wintercrest Farms, 
on the centerline of totality since 1998
Reply to
rickman

than we do.

f it didn't confer some kind of advantage. The fact that we haven't found e xactly how and when it confers that advantage isn't proof positive that it isn't there.

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tamin C

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mical point of view, humans are just large mice (or rats). There are a few minor differences in the ways in which our biochemistries work - one of whi ch being that we don't synthesise vitamin C and they do, probably because b ack in our fruit-eating ape stage of evolution we could survive losing the capacity.

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capacity to synthesise vitamin C, but our remote ancestors ate enough orang es back then that they didn't all get scurvy and die out.

een observed to give us scurvy. Some other - much rarer - stress may only b e survivable with rat levels of circulating vitamin C.

nal

, but Pauling wouldn't have been silly enough to think that the results in a single test animal - even if it was him - would constitute any kind of "p roof".

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Wrong. It just happened.

Only if you are closet creationist. Evolution depends on imperfect reproduc tion, and weeds out the imperfections that are lethal. Anything that can su rvive is fine.

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Evolution isn't about "shedding costs". It's about making random changes, a nd any change that doesn't kill the organism gets to propagate. Some change s provide a competitive advantage, and get to dominate surviving gene-pool, but these are rare. Most of what goes on is pure noise.

--
Bill Sloman, Sydney
Reply to
bill.sloman

te:

rious

and

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ical structure for DNA was wrong, and James Watson gloats about the error i n "The Golden Helix". He made a similar kind error in calculating electron orbits, much earlier on, and his capacity to be almost - but not completely - right impressed me when I was a lot younger. I think I've posted on it h ere before.

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air's breadth away from being totally right in a least two very different f ields. It's a bit odd.

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hat the stucture he proposed wouldn't work.

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. Most commentators do give her a lot of credit.

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She didn't get on with Wilkins, who showed her X-ray pictures to Crick and Watson without her permission, and moved onto another job (with a colleague - Aaron Klug - who went on to get a Nobel Prize in 1982 for the work they' d started together. Wilkins was still alive when the credit was being passe d out.

ster of proteins and didn't give his full attention to DNA.

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issue as "outside of science" and you are presenting some journalist's poin t of view when you make that claim, which really isn't impressive.

C.

The Mayo Clinic didn't duplicate his results, but they also failed to follo w his protocols, which did give him a let-out. Their claim that they had te sted Pauling regime, when they'd actually tested something rather like it, is text-book poor science - something that the medical profession was rathe r prone to at that time.

The Cochrane collaboration and evidenced-based medicine date all the way ba ck to 1993. Pauling died in August 1994.

And the medical profession tested rather different claims, which meant that nobody had any real evidence. It didn't stop the medical profession being rude about somebody they saw as an interloper.

ea what you are basing your point on.

The facts are - in fact - pretty clear. Nobody was prepared to take Pauling seriously, and what was tested was what the medical profession would have liked him to have been claiming. The medical profession hated the idea that different patients could benefit from different treatments and happily tes ted regimes intended to be used on everybody on young while males, because that made recruiting test subjects easier. The proposition that some patien ts could benefit from very high does of vitamin C wasn't something they wan ted to test.

Genome sequencing has made individual differences more respectable, but onl y recently.

--
Bill Sloman, Sydney
Reply to
bill.sloman

snipped-for-privacy@ieee.org wrote on 9/25/2017 8:30 AM:

You aren't giving this any thought. Yes, a random change that has no net impact on viability will be propagated to the offspring. That is *not* the same thing as becoming widespread in the population.

Clearly if humans had the ability to synthesize vitamin C and lost it, it wasn't random chance that it was lost from the ENTIRE POPULATION. That required selection based on some cost to having that gene.

--

Rick C 

Viewed the eclipse at Wintercrest Farms, 
on the centerline of totality since 1998
Reply to
rickman

s, and any change that doesn't kill the organism gets to propagate. Some ch anges provide a competitive advantage, and get to dominate surviving gene-p ool, but these are rare. Most of what goes on is pure noise.

I'm afraid that you are the one who isn't thinking things out.

he

Populations bottle-neck from time to time, and the genetic diversity of the surviving population plummets. This is how speciation happens. Humans - as a whole - have quite a bit less genetic diversity than bonobos, though the re are now many more humans than bonobos.

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There it is suggested that the entire pre-1492 native American population c ould have been descended from as few as 70 individuals, and that the human population in sub-Saharan Africa could have frequently dropped as low as 20

00 people during the most recent ice age.

Particular genes variants can just drop out by random drift.

Pure genetic drift will do it. As long as losing the capacity to synthesise vitamin C isn't likely to kill you before you can reproduce, the non-worki ng gene is just as likely to propagate as the working gene. It's improbably that it's incidence will drop to zero in any one generation, but there are a lot of generations involved, and once it is gone it isn't going to come back.

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--
Bill Sloman, Sydney
Reply to
bill.sloman

Waving your hands and saying "stuff happens" doesn't explain why humans would loose the ability to synthesize vitamin C if there were any advantage to having that gene rather than there being a cost to having it. You can postulate that the gene for synthesizing vitamin C dropped out of the population by accident, but that doesn't make it so. It is much more likely there was a cost to having that gene and so it was selected out.

Your link does not support your hypothesis. It defines genetic drift thus, "In each generation, some individuals may, just by chance, leave behind a few more descendents [sic]". It doesn't say this is how genes disappear from the population. It is quite a stretch to suggest that while it is possible although highly unlikely to result in the loss of a gene from the population it therefore *must* be what happened.

Much more plausible is that there was a *force* motivating the change. That force would be the *cost* of having a gene that isn't needed. It's not at all hard to see that a gene working to produce a vitamin that exists in the diet would have a metabolic cost with no advantage and therefore be selected out of the population actively.

In particular it is hard to see how this gene could have had benefits (the whole reason for discussing this issue), even if small, and still be eliminated by random chance.

--

Rick C 

Viewed the eclipse at Wintercrest Farms, 
on the centerline of totality since 1998
Reply to
rickman

ges, and any change that doesn't kill the organism gets to propagate. Some changes provide a competitive advantage, and get to dominate surviving gene

-pool, but these are rare. Most of what goes on is pure noise.

  • the

the surviving population plummets. This is how speciation happens. Humans

- as a whole - have quite a bit less genetic diversity than bonobos, though there are now many more humans than bonobos.

on could have been descended from as few as 70 individuals, and that the hu man population in sub-Saharan Africa could have frequently dropped as low a s 2000 people during the most recent ice age.

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ely

You may think so, but it isn't a persuasive hypothesis.

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sise vitamin C isn't likely to kill you before you can reproduce, the non-w orking gene is just as likely to propagate as the working gene. It's improb ably that it's incidence will drop to zero in any one generation, but there are a lot of generations involved, and once it is gone it isn't going to c ome back.

s,

Sure it does. If nobody carrying that particular gene leaves a descendant, that gene is gone.

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It's a possible - if highly unlikely - result in any generation. Over enoug h generations in a small population it is quite likely to happen.

Why do you think that? What makes an unspecified and apparently totally ima ginary "force" more plausible than genetic drift?

We have loads of genes that don't do anything any more - compare the olefac tory gene sequences in humans and in rodents

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Rodents have about 1000 of these genes, most of which code for full-length proteins and presumably work. We have something between 500 and 750, about

75% of which no longer code for full length proteins and presumably don't w ork.

Your "force" seems to be not only imaginary but also non-existent.

at

efore > be selected out of the population actively.

The imaginative effort required isn't great, but inventing "just-so" storie s isn't a useful exercise.

e

You may find it hard, but if you learn a little more about the subject you may find it easier.

--
Bill Sloman, Sydney
Reply to
bill.sloman

Says you.

What are the odds that everyone has the gene and through successive generations the number of those having the gene continues to drop from statistics rather than through selection. Pretty amazingly huge. Unlikely enough to power the infinite improbability drive in the Hitchhikers Guide to the Galaxy.

Actually you have it very wrong. The population never got rid of many genes which are very bad. What are the odds that a gene would be *removed* from a population by chance alone. Not a single event, but a series of events, each one highly unlikely, which in combination would be almost infinitely unlikely. Like winning the lotto, receiving a Nobel prize and getting struck by lightning all on the same day you accidentally discover a cure for cancer.

Probability. Drift may affect gene populations, but that it would result in the removal of a gene that at one point was necessary and therefore universal, is pretty amazing. It's like the chances of everyone in the US dropping their pennies down a storm drain so we had no more pennies.

Yep, we have lots of baggage, but they aren't being expressed. A gene that was at one time essential and only became superfluous because the vitamin appeared in our diet very likely has a cost, most likely metabolic. It may be a small cost, but even small costs impact gene frequency and continue to exert pressure all the way down.

No, simply beyond your ability to understand how genes operate.

"Just so"? Not sure what you mean by that. The reality is that nearly every feature of an organism has an associated cost. You may not be able to understand that, but your lack of understanding doesn't make it any less true.

Being tall has the cost of banging your head on things, being short has the advantage of being able to fit in small spaces. Each one has an advantage and a cost.

Indeed. Good advice for yourself.

Pressure outweighs random chance any day. They talk about a human bottleneck of I believe 75,000 people at some point in our history. So if they all had the vitamin C gene and one person lost it through a mutation, what were the chances that the gene would be removed by random chance from the rest of the population? Pretty damn small.

You have yet to show any cases of this happening or even a reference that indicates it is even feasible.

--

Rick C 

Viewed the eclipse at Wintercrest Farms, 
on the centerline of totality since 1998
Reply to
rickman

anges, and any change that doesn't kill the organism gets to propagate. Som e changes provide a competitive advantage, and get to dominate surviving ge ne-pool, but these are rare. Most of what goes on is pure noise.

ot* the

of the surviving population plummets. This is how speciation happens. Human s - as a whole - have quite a bit less genetic diversity than bonobos, thou gh there are now many more humans than bonobos.

tion could have been descended from as few as 70 individuals, and that the human population in sub-Saharan Africa could have frequently dropped as low as 2000 people during the most recent ice age.

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hesise vitamin C isn't likely to kill you before you can reproduce, the non

-working gene is just as likely to propagate as the working gene. It's impr obably that it's incidence will drop to zero in any one generation, but the re are a lot of generations involved, and once it is gone it isn't going to come back.

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nough generations in a small population it is quite likely to happen.

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imaginary "force" more plausible than genetic drift?

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efactory gene sequences in humans and in rodents

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How? More likely that enzyme-protein involved stopped being synthesised in a form that worked - which is exactly what has happened to olefactory genes that don't work. You are trying to make a distinction that doesn't seem to exist.

ntinue to exert pressure all the way down.

So why haven't we lost the 75% of our remaining olefactory genes that don't do anything?

gth proteins and presumably work. We have something between 500 and 750, ab out 75% of which no longer code for full length proteins and presumably don 't work.

Since you don't seem to have clue about how genes operate, and want to see a magic difference between a gene that synthesises a Vitamnin-C making enzy me and one that synthesises and odour-detecting protein, you may be over-es timating your abilities in this area, and under-estimating mine.

that

herefore > be selected out of the population actively.

ories isn't a useful exercise.

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d cost. You may not be able to understand that, but your lack of understan ding doesn't make it any less true.

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This is a gene - actually a whole bunch of genes - getting expressed. The v itamin-C synthesis gene got mutated into a form where the enzyme it produce d didn't work, so it wasn't being expressed. There was no selection against it (because it didn't kill the orange-eating apes that carried it).

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you may find it easier.

If there is any. 75% of our olefactory genes don't work, but they haven't b een eliminated.

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t it > through a mutation, what were the chances that the gene would be rem oved by

The figure I dug up was 2000, not 75,000. And that bottle-neck seems to hav e lasted for an ice age - 100,000 years or 4000 generations. And we did los e it, so the chance turns out to have been 100%.

We have lost about a quarter of our olefactory genes - rodents have about 1

000 that all work, we have some 750, of which only a quarter work.

Genetic drift is perfectly feasible, and well known, even if you can't unde rstand it.

--
Bill Sloman, Sydney
Reply to
bill.sloman

And you are proposing an event with zero support. You have yet provided one reference that suggests a universal gene could be removed from the gene pool the way you suggest.

Here is support for the gene being actively eliminated.

"Some researchers have even speculated that there were additional benefits of having this gene knocked out. For instance there is less antioxidant reaction if you consume vitamin C instead of fabricating it yourself, since synthesizing it in the organism leads to the by-product hydrogen peroxide. Another researcher speculated in a 1982 paper that it might have helped to survive malaria. Another hypothesis that I like (but for no rational reason) is that it might have helped to gain weight by increasing fat storage, handy when the food supply is not stable. And that?s just skimming some references; multiple other hypotheses have been formulated."

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You may be confused over the "elimination" of a gene in the sense that it no longer produces the protein it originally coded for and the "elimination" of the gene in the sense of the DNA sequence totally disappearing from the genetic makeup.

The gene mutation that deactivated the GULO gene may well be beneficial to a species that has adequate vitamin C in its diet. That gene change would spread through the population by virtue of selection pressure resulting in a species without the gene to synthesize vitamin C. Once that gene mutation is spread deactivating vitamin C production in humans, *then* genetic drift can do much to it since there is no longer pressure to keep the gene. The gene can mutate much more extensively because there is no cost to those mutations. Or the gene can be completely removed. Those changes would be genetic drift because there is no evolutionary pressure to either keep or lose a gene that is not expressed.

I don't know. Do you? Why not deal with the issue at hand rather than changing the subject?

That's a funny comment coming from you. You have offered zero evidence to support your idea. You sound a bit like Trump actually. Don't offer evidence, just undermine the opponent through weak barbs.

Ok, more ad hominem.

That's the part you don't get. The apes that still carried the vitamin C producing gene may well have had a cost as postulated above. So there was a small pressure to remove that gene from expression. Once there was a mutation to it, that mutation propagated through the population due to the selection pressure. Evolution doesn't require a gene be fatal to exert selection pressure. It simply has to make some tiny difference in the viability of organisms to gradually dominate the population.

So? We haven't lost the genes for vitamin C either. It's there. It just doesn't work like the olfactory genes.

We were both wrong. It was 70,000 years ago, resulting in maybe as few as

10,000?30,000 according to wikipedia. But that is just a theory.

Regardless you don't seem to understand cause and effect. You suggested that such a small population would be more likely to have genetic drift result in a non-viable gene replacing a viable gene in the genome of the species. The trouble is the genetic change didn't happen to humans. It took place many species back, about 61 million years ago affecting anthropoid primates, not just man. So the human genetic bottleneck is of no relevant to this issue and certainly can't be said "to have been 100%".

It's not a question of understanding the concept, but proper application of the principles. Of course you do need to understand the concept before you can apply the principles, but I assume you are not that ill informed.

While genetic drift can produce changes in the genome of a population, it's very unlikely to result in the removal of an active gene. An active gene has selective pressures to either keep or to remove it.

--

Rick C 

Viewed the eclipse at Wintercrest Farms, 
on the centerline of totality since 1998
Reply to
rickman

The cost of having a useless gene is very small, thus genes that are no longer used are often left hanging around.

But I don't imaging that is the "force" or "cost" Rick is considering here. If there was a gene for the synthesis of Vitamin C, and that gene is lost, then it /could/ have happened by accident - a mutation causing it to be lost, and where the person with that mutation simply suffered no ill effects due to Vitamin C in their diet.

However, it is certainly plausible - arguably more likely - that there was a direct advantage in the removal of the gene that selected for the mutation. There are many perfectly reasonable possibilities here - I have no idea which ones might fit best, because I don't know anything about this particular gene (if our ancestors ever had it). It could be that the gene required significant energy to use. It could be that we were getting too much Vitamin C. It could be that it had side-effects on other useful genes or biological processes. It could be that it caused men to have orange hair, and our female ancestors didn't like men with orange hair. When humans had enough Vitamin C from their diet, there is no longer a positive need to keep that gene - if it had a negative effect, rather than just being a now-unused extra, then selection would go against it.

Reply to
David Brown

e.

ly imaginary "force" more plausible than genetic drift?

olefactory gene sequences in humans and in rodents.

that

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in a form that worked - which is exactly what has happened to olefactory g enes that don't work. You are trying to make a distinction that doesn't see m to exist.

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Genetic drift is widely accepted. If you can't get your head around it. it' s you that has the problem, not me.

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Sure. Endless speculation and no proof. Genetic drift happens, ans it is a sufficient explanation even if you don't like it.

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It doesn't much matter. I'd have expected - correctly as it turns out - tha t we still had the gene but one that coded for an enzyme that didn't work.

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continue to exert pressure all the way down.

on't do anything?

Because it's a relevant question. All genes that drive the synthesis of pro teins that don't do anything useful represent some kind of cost, but - tak ing the olefactory genes as an example - it isn't a big cost.

Genes that aren't doing anything useful can accumulate additional errors, a s our vitamin-C synthesis gene seems to have done, and it's not all that su rprising that the version that worked became a low enough incidence gene to fall out of existence.

ength proteins and presumably work. We have something between 500 and 750, about 75% of which no longer code for full length proteins and presumably d on't work.

see a magic difference between a gene that synthesises a Vitamnin-C making enzyme and one that synthesises and odour-detecting protein, you may be ove r-estimating your abilities in this area, and under-estimating mine.

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I've offered several links to well-informed opinion, but you don't seem to able to process the message,

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e and > >>>> therefore be selected out of the population actively.

stories isn't a useful exercise.

You aren't performing at an impressive level.

ated cost. You may not be able to understand that, but your lack of unders tanding doesn't make it any less true.

s the

tage

he vitamin-C synthesis gene got mutated into a form where the enzyme it pro duced didn't work, so it wasn't being expressed. There was no selection aga inst it (because it didn't kill the orange-eating apes that carried it).

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e

The proposition that the cost of synthesising vitamin-C that we didn't actu ally need was the driving force. We've still got the enzyme, which is presu mably still depleting our stock of the vitamin-C precursor, even if it does n't carry the process through to giving us vitamin-C. That "force" would le ad us to reduce the expression of the gene, but that would happen even if t he gene was producing vitamin C which we could use but didn't need, so it's not relevant to what is being said here.

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t you may find it easier.

't been eliminated.

t

It just doesn't work - in the sens of doing anything useful - and the olefa ctoruy genes don't work, in the same sense. They both tie up resources maki ng enzymes that don't do anything useful. Neither of them has been eliminat ed, in the sense that they are both taking up space in the genome. Regulati ng how much work the genes do - how much protein they actually churn out - depends on the separate system that controls gene activity - gene expressio n.

We aren't talking about that because there isn't that much published on the subject - at least about genes coding for ineffective enzymes.

point in our history. So if they all had the vitamin C gene and one perso n lost it through a mutation, what were the chances that the gene would be removed by random chance from the rest of the population? Pretty damn smal l.

have lasted for an ice age - 100,000 years or 4000 generations. And we did lose it, so the chance turns out to have been 100%.

s

It's one of number of theories. We do know that the human species did go th rough some kind of bottleneck, but there's still a lot of evidence to be co llected, and quite a few different theories waiting to be shot down.

The theory depends on looking at the genome. Chromosome segments including useful genes - ones under selective pressure - end up over-represented in t he genome, so there's less variability between people in these segments, an d this is theory fodder too.

There's still a lot of looking going on. The duff vitamin C gene could have been physically close to a gene that was under high selective pressure, an d got itself over-represented through mere propinquity

no

It is 100% certain that we - and all the anthropoid primates - can't synthe sis vitamin C. There was quite a lot of speciation (each with it's own gene tic bottleneck) on the way back to our 61 million years ago ancestors, and the working version of the gene clearly did get junked somewhere along that route.

It only had to drift out of existence once along that path to be permanentl y absent, so genetic drift does look like a sufficient explanation.

hat

ut 1000 that all work, we have some 750, of which only a quarter work.

understand it.

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Sure. And if your ancestors were eating enough oranges, there was no select ive pressure to get rid of duff versions of the gene. The gene doesn't know that it is duff - it keeps on going through the motions even if it doesn't synthesise a useful compound.

--
Bill Sloman, Sydney
Reply to
bill.sloman

It wouldn't give men orange hair. Vitamin C - ascorbic acid - is a rather simple compound, and doesn't absorb in the visible. Pigments are lot more complicated. Vitamin C is also remarkably non-toxic.

The enzyme - which we can still synthesise - that doesn't quite make vitamin C might - with advantage - have been down-regulated, but control of gene-expression depends on different bits of the genome, and we don't have any data on that.

But nobody has detected any negative effect.

--
Bill Sloman, Sydney
Reply to
bill.sloman

No one disputes that genetic drift happens. I'm disputing your flawed application of the process.

That's funny coming from you. You provide no support what so ever that genetic drift is responsible and then claim I provide no proof. The math alone makes your theory unreasonable. Genetic drift is *very* unlikely to eliminate a gene from a population. It's like saying random chance is responsible for the total elimination of the color Harvest Gold from the population of kitchen appliances. Much more likely is that tastes changed and exerted a selection pressure against the color.

It matters in that the active gene would be expressed and therefore use resources and incurring *cost*. Even though that cost is small it is a pressure which would explain how the mutated gene spread through the population. Genetic drift would be a poor explanation for the removal of a gene from a large population. Why can't you provide any evidence that this idea is supported by anyone other than YOU?

I see you decided not to respond to logic.

None of which address the issue of genetic drift removing a gene from a large population.

The trend continues. lol

I don't think you understand how enzymes work. They are like a catalysts that mediates a reaction, essentially providing a site where the reaction can take place with more favorable kinetics. If the enzyme is defective it doesn't provide that site and the reaction doesn't take place. So no consumption of precursors.

I think you are trying to suggest that in multiple, separate branches of evolution the same gene was eliminated by genetic drift, at about the same time! Now you are compounding the odds even further against the idea. MUCH more likely is that the gene was selected out whether at one point in the evolutionary tree or at several.

Above you just talked about multiple bottlenecks affecting many species. Make up your mind. Was it once some 61 million years ago in a single species which we have no evidence for a bottleneck or was it in multiple species at many bottlenecks at about the same time?

But it produces that superfluous vitamin at a cost. That cost creates selection pressure and the gene is eliminated over some long period of time. Sounds like a very simple explanation to me. Or we can invoke "deus ex machina" and say the working gene disappeared in a large population by random chance.

Feel free to continue without me. We have gone back and forth enough that there are no mysteries, no new facts being pointed out. You have nothing to support your idea that genetic drift eliminated a gene in a large population and your attempt to reduce the population size was shown to be a red herring. Believe what you wish, there is no information to support your idea that a selective pressure was not at work when it is very clear there was a selective pressure present.

--

Rick C 

Viewed the eclipse at Wintercrest Farms, 
on the centerline of totality since 1998
Reply to
rickman

nge.

ally imaginary "force" more plausible than genetic drift?

.

e olefactory gene sequences in humans and in rodents.

ne

he

ed in a form that worked - which is exactly what has happened to olefactory genes that don't work. You are trying to make a distinction that doesn't s eem to exist.

ed

gene

it's you that has the problem, not me.

I'm not "applying" anything. I'm just pointing out that genetic drift is a adequate explanation of how we lost the version of the gene that built a ve rsion of the Vitamin-C synthesis enzyme that worked. You want to invoke a f orce above and beyond random shuffling.

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since

ide..

d to

just skimming

oof-for-evolution/

s a sufficient explanation even if you don't like it.

It's a sufficient explanation. None of us have got a version of the gene th at creates a version of the Vitamin-C synthesis enzyme that works, though w e have a variety of versions of the gene which create various proteins that looks a bit like the enzyme but not enough like the effective enzyme to wo rk.

That's clearly genetic drift.

You invoke an imaginary "force" to explain something that doesn't need expl anation.

You haven't posted a line of mathematics anywhere in this thread.

It has given us several versions of the ineffective gene - the gene is stil l present in the genome, but none of the versions that survive generate a p rotein that will act as an enzyme that can synthesise Vitamin C.

of the color Harvest Gold from the population of kitchen appliances.

Why? The colours provided for household appliances aren't selected by rando m chance, or evolved by imperfect replication.

against the color.

Of course, but the manufacturers know what they are doing, and evolution do esn't.

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that we still had the gene but one that coded for an enzyme that didn't wo rk.

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The fact that we have several different version of the ineffective gene. Ge netic drift has clearly been going on for long enough to mess up the amino- acid sequence in several different ways.

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Genes mutate at the same rate whether or not the protein produced is doing anything helpful. The difference is that if what the gene is doing is helpf ul enough that it not being done kills the carrier, the gene (and it's asso ciate genome) get eliminated from the gene pool.

If the protein being synthesised by the gene doesn't have to work, then the genome can can incorporate any kind of rubbish it likes, and that sequence can keep on mutating. Gene duplication is common in evolution, and the sec ond copy can keep on mutating and one of the end results can sometimes end up being useful in some very different job.

You can't produce the kind of logic that generates the response you want to read.

to able to process the message,

Genetic drift doesn't remove the gene. It just means that the versions of t he gene that survive don't have to work. There's no particular reason why t he version of the gene that did work should get eliminated, but if you wait long enough it's pretty much bound to happen.

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I don't think that you have processed the fact that I have Ph.D. in Physica l Chemistry, which meant that I went through an undergraduate course that m ade sure that I knew exactly what enzymes (and other catalysts) did, in so far as anybody did at the time. All the X-ray crystallography that has been done on enzymes since then has made the picture a bit clearer - and becaus e I was a computer user as a graduate student I did get to know our crystal lographers. One of them ended up as a post-doc with Max Perutz for a few years - she's a professor now, back in Melbourne.

Even a defective enzyme can couple to its intended substrate - unless the f olding goes a completely different way. It won't catalyse the desired react ion (otherwise it wouldn't be defective) but there's nothing to stop it cat alysing some undesired reaction, producing something that isn't quite Vitam in C, but close.

nthesis vitamin C. There was quite a lot of speciation (each with it's own genetic bottleneck) on the way back to our 61 million years ago ancestors, and the working version of the gene clearly did get junked somewhere along that route.

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No. It only had to get eliminated once, and there were several potential bo ttlenecks where it would have been relatively easy to lose it.

But the gene wasn't selected out. We've still got it, or rather one of the several versions that generate a protein that doesn't quite catalyse the sy nthesis of vitamin C.

ently absent, so genetic drift does look like a sufficient explanation.

Drift out of effectiveness.

I don't have to. Any one bottleneck would have been enough to deplete the g ene pool of the version of the gene which could synthesise vitamin C. Grant ing that the gene pool has had 61 million years to accumulate mutations on a gene that we haven't relied on since we took to eating oranges, we may no t even need to invoke a bottleneck.

lective pressure to get rid of duff versions of the gene. The gene doesn't know that it is duff - it keeps on going through the motions even if it doe sn't synthesise a useful compound.

me.

That's your hypothesis. You can't quantify the cost - nor even say what it is - but you are convinced that an ape synthesising more vitamin C than it needed would have been more likely to die than one that didn't.

This gets back to Pauling's original argument. We need about 10 milligrams a day of vitamin C to avoid scurvy

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and rats synthesise far more than that, while apes tend to have circulating blood levels that are much higher than we'd get on 10 milligrams a day.

It looks very much as if vitamin C is cheap to synthesise.

Genetic drift happens. If you don't need a working version of a gene, the v ersion you have is likely to be non-working, as exemplified by the olefact ory genes.

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But quite a few facts that you don't want to take on board.

ne in > a large population and your attempt to reduce the population size w as shown to > be a red herring.

Genetic drift has lumbered us with some 500 hundred non-working olefactory genes. That's not nothing, but you refuse to understand what it ought to be telling you.

That you are willing to appreciate.

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If you don't understand how genetic drift works. Because you can't get your head around genetic drift, you feel obliged to invoke some kind of improba ble selective pressure, which isn't - in fact - necessary.

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Bill Sloman, Sydney
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bill.sloman

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