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  • I think that PM uses almost any topic with the intent to shock other people and that he holds pretty much no beliefs of his own. I am pretty sure that PM is the walking embodiment of schadenfreude and lacks anything resembling the conceptualization of a soul. He is not worth even trying to shock, because he is incapable of so human an emotion. But thats just my opinion.

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Messages - DaveGodfrey

51
Politics and Current Events / Re: Austin bombings
Well yes, but I was thinking more of the fact that the Unabomber was one person who wasn't a member of any particular organisation.
52
Politics and Current Events / Re: Austin bombings
If they'd said "no confirmed links to known terrorist groups" then that might be accurate as these people tend to cultivate the whole "lone wolf" thing. But it also means you can describe it as a "terrorist act" because I can't really think of a more obvious act of terrorism than sending bombs through the mail, etc. Everyone calls the Unabomber a terrorist, and that's exactly what he did.

But of course being white he can't possibly be a terrorist, but instead hangs out with "very fine people".
53
Think about this:

Quote from: Sagan
But the fact that some geniuses were laughed at does not imply that all who are laughed at are geniuses. They laughed at Columbus, they laughed at Fulton, they laughed at the Wright Brothers. But they also laughed at Bozo the Clown.
Read more at: https://www.brainyquote.com/quotes/carl_sagan_163043
They were right to laugh at Columbus based on what was known at the time. He thought the world was much smaller than everyone else and you could easily sail to Japan the other way. Most other people thought Eratosthenes' estimate of the size of the Earth was about right, even if there was some disagreement about exactly how big it was, how big Eurasia was, etc.

Columbus didn't prove anyone wrong. He went to his grave thinking he'd found a bunch of islands off Asia. Another thing they could have legitimately laughed at him for.
Well, yes. I wouldn't be surprised if the other examples turned out to be more nuanced too, or mostly wrong even.
Maybe Sagan could have picked examples that were more accurate, but if nobody has heard of these people, its not really going to work.
I don't know much about the Wright Brothers, but the fact that they were using smaller high powered motors (rather than the steam engines that Hiram Maxim tried, with a surprising amount of success), indicates that they knew something that the people who laughed at them didn't. Columbus at least, got very lucky.
54
Dave, a better version of your stupid analogy would be the difference between a pipe wrench and a crescent wrench, and a pipe wrench with a more ergonomic handle, and a crescent wrench with a more ergonomic handle. An then a whole bunch of different designs for said handles.

Even then its a stupid analogy. Why not actually learn the actual genetics, rather than trying to force things into idiotic metaphors?
I already have learned the genetics. The reason I use analogies is because you guys apparently have not and I'm trying to dumb it down for you.
Dave, I was taught genetics 101 by this guy. You're a moron.
55
Dave, a better version of your stupid analogy would be the difference between a pipe wrench and a crescent wrench, and a pipe wrench with a more ergonomic handle, and a crescent wrench with a more ergonomic handle. An then a whole bunch of different designs for said handles.

Even then its a stupid analogy. Why not actually learn the actual genetics, rather than trying to force things into idiotic metaphors?
56
DaveG ... this is exactly why I'm reviewing Basic Genetics ... there's so much confusion out there ...

Here's a very key paragraph I posted 4 years ago that will help explain my view (the correct view) ...

Quote
HOW MANY ALLELES PER LOCUS EXIST TODAY?
According to Mani (1984, p. 282), most loci of present day animals contain between one and five alleles, although the MHC complex contains many more. �Woodmorappe ... p. 198 ...
Quote:
Quote
With the notable exception of the MHC complex, the overwhelming majority of polymorphic loci have no more than four alleles per locus (e.g., see Table 1.3.1, pp. 8-9, in Cavalli-Sforza et al. 1994). �Furthermore, when we look at the relative abundances of these alleles in a population, we see a very lopsoded distribution of frequencies (Altukhov 1990, pp. 206-9). �There is usually a single allele occurring at high frequency (at least 85%), with one to three other alleles (rarely more) found at frequencies of 1-15% (Hughes, p. 249). �In fact, of all alleles, most exist at low frequency (Fuerst and Maruyama 1986, p.174). �This is further borne out by the very definition of a polymorphic locus: one where the most common allele occurs at no more tha 95% frequency in the population (Templeton 1994, p. 60).
http://talkrational.org/archive/showthread.php?p=2396793#post2396793
Yes? And? They're talking about the locus of the whole gene, not an individual nucleotide. And in all the cases where there are more than four alleles (the 70+ in the case of the ABO gene, and the thousands in the MHC for example) you need a source for that variation. Evolution predicts that you'd find, in most populations, one very common allele (the one best suited to a particular environment), and then a bunch of rarer ones (ones that are "good enough" that they hang around and don't go extinct, with a few very bad ones that turn up from time to time persist a bit and then go away again, as their carriers don't reproduce much. When the environment changes (or the population expands into different environments) then the abundance of each allele will change depending on what the new environmental conditions are like. So a gene that was found in 80% of the population might drop to only 5%, and vice-versa.

None of this is controversial or confusing Dave. At least not to people who have read basic genetics that wasn't written by known inveterate liars. This is where you should have started this whole thing. First understand, then criticise, remember?
57
Think about this:

Quote from: Sagan
But the fact that some geniuses were laughed at does not imply that all who are laughed at are geniuses. They laughed at Columbus, they laughed at Fulton, they laughed at the Wright Brothers. But they also laughed at Bozo the Clown.
Read more at: https://www.brainyquote.com/quotes/carl_sagan_163043
They were right to laugh at Columbus based on what was known at the time. He thought the world was much smaller than everyone else and you could easily sail to Japan the other way. Most other people thought Eratosthenes' estimate of the size of the Earth was about right, even if there was some disagreement about exactly how big it was, how big Eurasia was, etc.

Columbus didn't prove anyone wrong. He went to his grave thinking he'd found a bunch of islands off Asia. Another thing they could have legitimately laughed at him for.
58
Now let's talk a little bit about the idea of genetic diversity in humans and then later we will talk about genetic diversity in bacteria.


Let's just take an example of a human gene Locus right out of the Wikipedia allele article ...

Quote
For example, at the gene locus for the ABOblood type carbohydrate antigens in humans,[7] classical genetics recognizes three alleles, IA, IB, and i, that determine compatibility of blood transfusions. Any individual has one of six possible genotypes (IAIA, IAi, IBIB, IBi, IAIB, and ii) that produce one of four possible phenotypes:

So let's take a man and a woman as founders of a population. You can call them mr. And mrs. Noah if you like or you can call them Dick and Jane. I don't care.

Now what's the maximum number of alleles that we can have in this founder pair at the Locus specified above?  The answer is four I think, right? But we are told that classical genetics only recognizes 3 so theoretically we could have four, but there are only three that are recognized so the maximum diversity we can have is three I think, right?

So if between Dick and Jane we have all three alleles represented, then I would say that  the genetic diversity of this founder pair for this Locus has been maximized. On the other hand, if only one allele were represented in both Dick and Jane, then obviously they would both be homozygous for that allele and I would say that their genetic diversity would be at the minimum for this particular Locus.

Are we on the same page so far?
Basic genetics ...
Anyway ... people have been yammering about how I don't understand genetic diversity and maybe you still think that I don't know ... but at least you now have no excuse for not knowing what I mean when I talk about HUMAN genetic diversity. 

I simply mean ... how many alleles at a particular locus are there?  In a founder pair, there would be 4 maximum, 1 minimum. 

How many loci are there in humans?  20,000?  So if a founder pair - like Mr. and Mrs. Noah has only 1 allele per locus ... that is, at each locus in both male and female, there is only 1 allele represented between both of them ... then that is LOW diversity.  The minimum possible.  If 2 alleles are represented at each locus between both of them, then the diversity is HIGHER.  If 4 at each loci ... 20,000 or whatever the number is ... then we have MAXIMUM genetic diversity.

See?  Pretty simple really.

No, there are 20,000 or so genes. Where each gene is on the chromosome is its locus.
However, within the gene there are as many loci as there are base pairs making up the gene. Now, obviously there can only be four possible bases at each of those loci (A, C, T, and G), but are you going to seriously suggest that Mr and Mrs Noah had radically different genomes so they were heterozygous at every locus where heterozygosity has been found? Because that's just silly.
I'm not getting into that much detail.  Not getting into the nucleotide sequence differences between alleles. I'm just saying "If there are 3 common alleles at a particular locus, and if 3 - 4 common alleles per locus at all loci is fairly normal, then if Mr. and Mrs. Noah had all 3 or 4 at each locus represented between them, then that's a hell of a lot of diversity."
Dave, you need to get into that detail, because that's why people are saying there are 70+ versions of the various ABO alleles.
59
Dave, your confusing the two sorts of locus, 
60
Now let's talk a little bit about the idea of genetic diversity in humans and then later we will talk about genetic diversity in bacteria.


Let's just take an example of a human gene Locus right out of the Wikipedia allele article ...

Quote
For example, at the gene locus for the ABOblood type carbohydrate antigens in humans,[7] classical genetics recognizes three alleles, IA, IB, and i, that determine compatibility of blood transfusions. Any individual has one of six possible genotypes (IAIA, IAi, IBIB, IBi, IAIB, and ii) that produce one of four possible phenotypes:

So let's take a man and a woman as founders of a population. You can call them mr. And mrs. Noah if you like or you can call them Dick and Jane. I don't care.

Now what's the maximum number of alleles that we can have in this founder pair at the Locus specified above?  The answer is four I think, right? But we are told that classical genetics only recognizes 3 so theoretically we could have four, but there are only three that are recognized so the maximum diversity we can have is three I think, right?

So if between Dick and Jane we have all three alleles represented, then I would say that  the genetic diversity of this founder pair for this Locus has been maximized. On the other hand, if only one allele were represented in both Dick and Jane, then obviously they would both be homozygous for that allele and I would say that their genetic diversity would be at the minimum for this particular Locus.

Are we on the same page so far?
Basic genetics ...
Anyway ... people have been yammering about how I don't understand genetic diversity and maybe you still think that I don't know ... but at least you now have no excuse for not knowing what I mean when I talk about HUMAN genetic diversity. 

I simply mean ... how many alleles at a particular locus are there?  In a founder pair, there would be 4 maximum, 1 minimum. 

How many loci are there in humans?  20,000?  So if a founder pair - like Mr. and Mrs. Noah has only 1 allele per locus ... that is, at each locus in both male and female, there is only 1 allele represented between both of them ... then that is LOW diversity.  The minimum possible.  If 2 alleles are represented at each locus between both of them, then the diversity is HIGHER.  If 4 at each loci ... 20,000 or whatever the number is ... then we have MAXIMUM genetic diversity.

See?  Pretty simple really.

No, there are 20,000 or so genes. Where each gene is on the chromosome is its locus.
However, within the gene there are as many loci as there are base pairs making up the gene. Now, obviously there can only be four possible bases at each of those loci (A, C, T, and G), but are you going to seriously suggest that Mr and Mrs Noah had radically different genomes so they were heterozygous at every locus where heterozygosity has been found? Because that's just silly.
61
In b4 Dave calls Pingu the "shame of Britain", and calls Khoisan people "the children of the human race".
62
One Bristlecone pine generation. I bet many of them will still be alive.
63
It's not that hard to understand. If copying fidelity is too high, the population will be too rigid and unable to adapt, and in changing environments, will likely go extinct.

But if copying fidelity is too low, the population will not be able to keep hold of any advantages it does gain, and in a competitive but static environment, will likely go extinct (depending both on costs for error-correction and the size of the gains).

That matches what Pingu said.
Anyway, either one is complete and utter horseshit because copying errors are not needed for diversity.

But copying errors do create novel DNA sequences, and therefore can lead to increased diversity in the population.  Right?
Sure.  In exactly the same way that copying errors in the software controlling the machines at the Ford factory lead to increased diversity.

Just because Ford don't use machine learning to design the software in their factories doesn't mean they couldn't. There's no reason why they couldn't use it to design parts of the car either. Google uses it to do all sorts of things. So do many other companies.

Watch and learn Dave, watch and learn.

https://youtu.be/R9OHn5ZF4Uo
64
Dave, no protection at all wouldn't work very well for obvious reasons. Perfect protection 100% of the time would mean we never got beyond LUCA, and nobody would be around to think about it. Protection that works pretty well lots of the time, but doesn't always work, and which is under a degree of control by the cell so it can respond to changes in the environment are going to work even better for a population. There will be an optimum rate of "copying errors" for the population to survive long term.

It's another example of the Weak Anthropic Principle. If things were significantly different then we wouldn't be here.
65
I have a waffle brain, not a blockhead brain. Come on, get it right!

And yes it has its own set of disadvantages. Different disadvantages than spaghetti brain people.

There aren't two kinds of brain, Dave.  We all have spaghetti.
Some are just more congealed than others.
66
Dave, the growing media Lenski used has almost no glucose at all. It's not a case of the bacteria "being happy with oatmeal", but them being happy with regularly starving to death.
67
Now the interesting question will be what kind of sensory and control circuitry triggered the gene duplication? Or did it just happen randomly with no sensory and control circuitry involved at all?
Notice how dave uses his 'switch' analogy for everything BUT the gene duplication itself. He just calls it a gene duplication.

Quite telling.

What would that be in your BS analogy, dave, if not NEW CIRCUITRY?
The switch is analogous to the repressor protein, not the duplicated gene. 
Then it's not analogous to aquiring the Cit+ ability. The duplicated gene did that, dave. What is THAT in your 'analogy"?



Quote
In the electronic circuit analogy, the citT gene would be a bit like an electronic black box like say one of my Basic Stamps that I use to control things.  They are cheap so I have quite a few on hand for various widgets I want to control.  On one of my control boards which has a Basic Stamp on it controlling things, I could of course install a switch to turn the thing off and on.  And if I wanted to, I could add a second Basic Stamp that is "always on" for some other purpose and that would have the advantage of retaining the "on / off" functionality of the first Basic Stamp.
Exactly.

That is NEW CIRCUITRY.

Quote
I'm obviously just guessing as to the reason the cell did the gene duplication as opposed to just turning the switch on, but it's a possibility I think.
Yup. The possibility is that your analogy is BS, and can only get you that far.

The "unseen mind" would have some kind of "turn on/off" system for the same configuration, using it as needed. They would not rewire the whole thing with new circuitry to bypass it.

What does THAT tell you?
It's only new circuitry in the same sense that making a copy of the poem Mary Had a Little Lamb on a xerox machine is a new poem.
Once again, you drop your (already poor) analogy when you realize it doesn't help you, and youswitch to an even dumber one.

No dave, it's not "in the same sense". Those genes DO something. And a gene duplication with no repressor performs a NEW function.
Incorrect.

But thanks for playing... You'll get another opportunity to do better. And here's a participation trophy. Good job!

The duplicated Gene does not perform a new function. It performs the same function as the parent Gene.
Under different conditions though. What with the repressor not working any more. If the repressor stops the gene working in the presence of oxygen, and the duplicated gene doesn't have that repressor then it has gained function. The gene now works in an environment it didn't work in before.
68
I have an idea. 

Just shut up for a day.

Let me and Entropy go back and forth uninterrupted for one day.  He has a burning question that he wants answered and I want to answer it but I can't yet.
I'd rather talk with Pingu to be honest.  You're a bit of a twat, and you don't listen.  For the questions I want answered you would be the last fucking person alive that I would ask.
Ahead of Socrates and Pahu? Good god Dave, you really don't have a clue about this stuff.
69
Lurkers ...
Aha!
So you are performing fro YEC audience.


A male YEC audience, it would appear.
I'm not sure Sucky's actually a YEC, but he certainly is even more confused about biology than Dave is. Pahu on the other hand never leaves his thread, but Dave will be pleased to know he's utterly convinced that the Avis Delk print is genuine. Although he doesn't think that Per, Teeth, or SteveF are scientists.
70
Except when the environment changes and cells don't try and protect themselves as much. ...also Shapiro.

Dave, if the organism is well adapted to its environment and the environment is stable then changes are generally going to be detrimental. So it makes sense to ensure that as few of them as possible happen. If the environment changes and the organism is no longer well adapted then all bets are off. Some changes will be advantageous. (Some will obviously still be detrimental), but if the organism doesn't change it will go extinct. So organisms that have some degree of control over how many changes to their genome can happen will be at an advantage. And a really fucking obvious way of doing that is via not repairing copying errors that are going to happen anyway and are more common than waiting around for stray gamma rays to transmute pyramidines into purines. If that's even possible.
No.  That's NOT a really fucking obvious way of doing.  It's a fucking stupid way of doing it and cells are not that stupid.  https://www.ncbi.nlm.nih.gov/pubmed/18053935 The really fucking obvious way of doing it is "natural genetic engineering" you dolt.  Now Pingu and Entropy are correct when they say that I don't fully understand NGE yet.  For example, I don't know if the cell is sensing the environment and saying "Gee, I need a 5/16" Allen wrench and then building it" ... or saying something more like "Gee, looks like we need some wrenches ... let's make a bunch of different kinds and see what works."  I tend to think that the latter is closer to the truth.
What DaveGodfrey is suggesting fits with Shapiro's definition of NGE.    That's not the way that YOU would do it, but it is the way a CELL does it because there is no finely tuned machine to swap specific bits of the genome around to give the cell a function it needs at the time.
Yes there IS a finely  tuned machine.  You're wrong.  But no I'm not sure exactly HOW this finely tuned machine works.  But I'm fairly certain that the misicorporations that escape the cell's fantastically accurate copying and error correction system that
Shapiro raves about ARE NOT the sorts of things that Shapiro groups under the heading of NGE.  Especially since Shapiro states this explicitly in several places where I've read him.
3000 mutations per cell in a population of 100,000,000 before one of them acquires the ability to utilize citrate.  I'm sorry you are too ignorant to see what this does to your theory of a "finely tuned machine".

Shapiro discribing exactly what happened in Minnish's experiment: https://www.huffingtonpost.com/james-a-shapiro/experimental-evolution-ho_b_1619171.html

Quote
Longer incubation of the selection plates often produces a large increase in the number of colonies. This indicates that mutations continue to occur under selection conditions. By counting these colonies and analyzing the population dynamics of the selected bacteria, we can determine whether selection affects the process of genome change.

When selection significantly stimulates mutations above prior levels, the process is called "adaptive mutation." Molecular geneticists agree that adaptive mutation (observed in different microorganisms) occurs when selective stress triggers natural genetic engineering activities that carry out DNA changes allowing mutated cells to form colonies.

In some cases, we know the consensus interpretation is correct. Together with my colleague Genevieve Maenhaut-Michel, I confirmed this. We studied an experimental situation where the required DNA change (a special type of coding sequence fusion) was never detected during normal growth but increased at least 100,000-fold after selection.

Other groups confirmed selection stress triggering natural genetic engineering by detecting evidence of "induced hypermutation" at various locations throughout the genome and by direct measurement of mutator function.
I don't get all the details as of yet ... but what I do know is that Shapiro says this ...
Quote
Discoveries in cytogenetics, molecular biology, and genomics have revealed that genome change is an active cell-mediated physiological process. This is distinctly at variance with the pre-DNA assumption that genetic changes arise accidentally and sporadically. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048091/
And that seems like kind of a big deal.

The "active cell mediated process" he's talking about is that cells use mutagenic DNA repair in times of stress in order to generate innovations that might allow them to survive.  Which is exactly what Minnish's cells did.  3000 mutations before one in 100,000,000 cells was able to use citrate.
Hold on a minute. You are telling me tha a simple change in the environment like adding citrate or changing  from glucose to citrate or some such thing causes DNA damage which has to be repaired? I thought DNA damage was only caused by something more drastic like an antibiotic attack or radiation.
Dave, the change to the environment put the cell under stress. The cell responds by not repairing so many copying errors and not being so fussy about how accurate its repairs are to changes to the DNA that are always happening, but get picked up and fixed before they can spread.
71
Except when the environment changes and cells don't try and protect themselves as much. ...also Shapiro.

Dave, if the organism is well adapted to its environment and the environment is stable then changes are generally going to be detrimental. So it makes sense to ensure that as few of them as possible happen. If the environment changes and the organism is no longer well adapted then all bets are off. Some changes will be advantageous. (Some will obviously still be detrimental), but if the organism doesn't change it will go extinct. So organisms that have some degree of control over how many changes to their genome can happen will be at an advantage. And a really fucking obvious way of doing that is via not repairing copying errors that are going to happen anyway and are more common than waiting around for stray gamma rays to transmute pyramidines into purines. If that's even possible.
72
Dave, I've asked you this before, how common do you think it is that stray gamma rays transmute pyramidines into purines?  And how common do you think that might be compared to DNA replication that isn't perfect and makes errors that aren't corrected every time a cell reproduces?

Furthermore do you think that cells somehow *know* what effect a substitution will have before the mutation arises, and can ensure that mutations like that are more likely than others?
73
Dave, think.about it, bacterial cell division can happen lots of times an hour. Being smacked by a stray gamma ray not so much. (And that would trigger the DNA repair mechanisms that might make a mistake, it won't substitute one base pair for another). The mechanism that allows the bacteria to reproduce first replicates its genome, and then the cell splits in two. Making a copy of the genome is not perfect. Mistakes get made, instead of grabbing a C, the cell sticks a G in the sequences, base pairs get left out, etc, etc. They aren't always picked up by the error correcting mechanisms the cell has.

Cell division, and the associated DNA replication, and the fact that replication isn't perfect, is therefore one of the most common ways to introduce new variation into a genome. Shapiro's ideas are that cell "directs" mutations by turning down how good the error-correction mechanisms are.

How else do you think changes to the genome occur other than if the cell makes a mistake when copying the DNA, or repairing a break? Pyramidines don't spontaneously change into purines. You do know that, don't you?
74
Yes, the latter phrasing is preferable.  Here's phrasing that's better still ...

"Damaged sequences happen as a result of DNA copying errors during cell division."

Define "damaged"? If you have a "damaged" sequence to the gene for Beta-Lactamase that means it can bind to expanded-specturm cephalosporins and hydrolyse them, as well as penicillins would you describe that as "damage"? It might be more susceptible to inhibitors, but its's able to deal with a wider range of antibiotics.
75
Dave do you understand that when a bacteria (and indeed every cell that goes through mitiosis) undergoes cell division it makes a copy of its entire genome?

Do you understand that the mechanisms that do this copying do not have 100% fidelity?
How is it possible for an adult human being who presumably made it past the eight grade could ask me this question with a straight face?  After I have been posting for WEEKS on this very topic?  I understand that not everyone reads all my posts.  But surely you read 1 of the hundreds I've made on this topic?  Sheesh.

I can answer this question, Dave.  It is possible, because your posts are so confused, ignorant and self-contradictory that it is very hard to figure out how much you do understand. 

And as you greet any requests for clarification with this kind of tantrum, it makes discussion with you virtually impossible.
This is a cop out answer.  And it shows your "Darwin Club" bias.  If it were ME asking this dumb of a question, you'd be all over me.  But card carrying Darwin Club members can ask the most asinine questions and almost never get "jumped" (once in awhile they do by people like Heinz and Uncool, but it's quite rare)


Well, do you or do you not understand that  "when a bacteria (and indeed every cell that goes through mitiosis) undergoes cell division it makes a copy of its entire genome?"

Yes or no?
Well yes, I think it does.
And do you understand that the mechanism by which it does this does not do so with 100% fidelity?