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Messages - Fenrir

Vitamin C might be rather a leap too far. The black queen could permanently wipe whatever is left of David's mind.
The pretending to have a clue stage is pretty tedious. Does it ever end?
To take one example:
in that Table 1.3.1, Cavalli-Sforza lists    1    allele for Peptidase A.

NCBI lists 2128 DNA variants of that gene.

It's probable that, in 1994 (actually, probably much earlier, as the 1994 book was reviewing published literature) the only recognized allelic differences were those detectable by a physical difference - like electrophoretic mobility - of the protein.
Yes. As In, differences that actually make a difference in the phenotype and that exceed some minimum threshold of sequence difference.

It seems that I'm going to have to back up even further and do a lesson on the difference between a brand new crescent wrench and a brand new  pipe wrench and include info about why adding an old beat-up pipe wrench and an old beat-up crescent wrench does not add diversity to the group.

At least not in the sense that matters for what I'm talking about.

You never got of the starting line so where are you proposing backing up to?

Face it, you never even made it to the track. You don't even have a picture of a race car, let alone a license to race one.
Like I've said to many people before you for the past 12 years ... If you don't like me, go away. There's plenty of "adult" science threads for you to participate in.

I took a swipe at quotas. Looks like I might have struck a nerve.

Yeah, you did. 

The nerve of any Native American person here, plus the nerve of mine you repeatedly bang whenever you tell me that I only got my job because I am a woman.

So yeah, you did.
The best way for you to prove that my insinuations are not founded on anything which even slightly resembles reality would be for you to demonstrate that here by actually doing those things that good scientists would normally do. 

Be like Barbara McClintock. 

And don't feel like Female Professors at Universities are the only persecuted, unfairly treated group. I myself am also a member of at least two unfairly persecuted groups ...

1) divorced husbands who are misunderstood and mistreated by their ex mother-in-laws, and

2) YECs

How do I demonstrate the unfairness directed at me?


Prove my detractors wrong by my actions.

And yet your every action reinforces the conclusion that you are a misogynist arsehole with ludicrous delusions regarding reality.

How could that possibly be?  :dunno:
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 ...

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?
Nope, try again.

Since the ABO gene was cloned and the molecular basis of the three major alleles delineated about 10 years ago, the gene has increasingly been examined by a variety of DNA-based genotyping methods and analysed in detail by DNA sequencing. A few coherent observations emerge from these studies. First, there is extensive sequence heterogeneity underlying the major ABO alleles that produce normal blood groups A, B, AB and O when in correct combination with other alleles. Second, there is also extensive heterogeneity underlying the molecular basis of various alleles producing ABO subgroups such as A2, Ax and B3. There are over 70 ABO alleles reported to date and these alleles highlight the extensive sequence variation in the coding region of the gene.
No matter how many alleles in the population, he's talking about two people, not the whole population.

No, he's stuck with the fantasy that two people were the whole population.

Everything after that is post hoc justification attempting to support that stupidity.

Hence the stripey sticks.
Diversity is also a word with meaning David.

Tell me, where did the animals which supposedly rode the ark come from?

Were they members of an extant population that won some sort of raffle or were their specific genomes somehow preloaded with majick divine "diversity"?

Were quantum diddling sticks involved?
Page 135 on my device and David has yet to develop any appreciation of the actual meaning of the word "random". Great start.
Tim Cooper at the Univ of Houston has studied Lenski's bugs ... his statements seem to support the creationist view that Lenski's bugs will continue to decline in fitness over time due to the inevitable buildup of VSDMs.

It was found that the beneficial mutations allowing the bacteria to increase in fitness didn't have a constant effect. The effect of their interactions depended on the presence of other mutations, which turned out to be overwhelmingly negative.

"These results point us toward expecting to see the rate of a population's fitness declining over time even with the continual addition of new beneficial mutations," he said. "As we sometimes see in sports, a group of individual stars doesn't necessarily make a great team."

They might well, being a small population.

A small static environment. The rate of increase of fitness would be expected to decline. Some smart involved people might even be able to model such a decline.

Oh wait...

Sustained fitness gains and variability in fitness trajectories in the long-term evolution experiment with Escherichia coli. Lenski et al
Dave, three points:

One : "copying errors" in the context of lay books about evolution is a shorthand for "DNA sequences that are different from the original".  The technical term however, is "mutations".

Two: mutations sometimes come about during the process of copying.  Sometimes they come about during the process of repairing damage.  Sometimes they come about during recombination (which can take place during copying, and in sexually reproducing species, does, during meiosis).  Sometimes they come about through HGT.

Three: there is very little evidence that any mutation is other than "random with respect to fitness"  at the time it appears.  But very few mutations are random in any other sense - some mutations are much more likely than others; some mutations are triggered by signals from outside the cell; some mutations are the result of cell-mechanisms that repair DNA that is not properly assembled, e.g. has broken strands. 

I don't know why you have singled out one particular source of mutations as the target of your indignation.  It's a perfectly good source.  In fact it's better than many because often the mutations are small and can have quite subtle effects.  But there are many others.  They are all mutations, and mutations are often generally described as "copying errors" not because they occur during copying (although some of them do) but because they result in a copy that differs from the original.
This is complete utter horseshit. 

"Copying errors" = "shorthand" my ass.  You know damn well that Shapiro makes a distinction.  I've posted his statements over and over again.  There is an actual fucking sophisticated mechanism - two of them actually - that are extremely proficient at preventing misincorporations.
Yet not 100% effective at "preventing misincorporations".
Right.  And because it's not 100% effective, species will soon (1000 years?) experience mutational meltdown and go extinct.

Assuming no leap years for the sake of easy calculation that's 26 280 000 generations of E. coli or 40 elephant generations.

Should I start panicking now?

Or perhaps you might realise the irrationality of the declaration?

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.

Coz diversity is created by stripey sticks.

Tremble at the power of the stripey stick you clueless heathens!
Continuing in the same article ...
Lenski and Blount concur. "We had already shown that if you put the bacteria on petri dishes where citrate was the only carbon source available and they were subject to prolonged starvation on it, we also could get . . . citrate mutants appearing on the order of a few weeks or so," Lenski told The Scientist. "It's already known [when mutants appear] depends on the ecological context."
OK so if when mutants appear depends on the ecological context, then that means that NGE is occurring, not RM + NS + MOY.

The only remaining question is HOW.  How do bacteria adapt so quickly?  What NGE processes are occurring?  What sensors to bacteria have to detect an alternate carbon source like citrate?  How is this sensory data collected?  Stored?  Processed?  Why doesn't the mutation happen immediately?  Like on Day 1?  Etc.
Here's the questions again for Fenrir. What is it with women not being able to read? Is it the spaghetti brain organization or what?

While that is phrased as a question it really isn't, it's a transparent attempt to direct discussion towards your preselected conclusion. You don't have actual honest questions, to do so would require a very basic understanding of the topic.

PS: i'd object to being tagged as female, if i thought there was any actual inferiority or intellectual distinction involved in the association. So knock youself out, i am woman hear me roar.

If you don't provide the Queen of England an instant answer to all her questions then you're bluffing because it means you really don't have any answers.


Um, David, not only do you have no answers, you don't even have actual questions.

Did you notice?
Speaking of Lenski's bugs, Entropy keeps asking why it took so many generations to generate the citrate mutation.  I guess his thought is that if it took so long, that's probably random, not "under cellular control / NGE." 

My totally wild guess as to the answer would be, based on my God paradigm, that these bacteria were "happy" with glucose for the most part for many generations, just as a person might be happy for many years eating oatmeal for breakfast and then all of a sudden they up and decide they want to start eating bacon and eggs.  What changed?  Well ... their preferences changed I guess is all we can say.

Makes the previous post look brilliant.
If goddidit wrt bacteria, i.e. created them, then we would not expect them to be simple, as in an evolutionarily less developed life form, as early scientists studying bacteria regarded them.  Also, instead of thinking of them as pests to be killed, scientists would have realized that they are "good" because God created all things good.  I think if the goddidit paradigm had been the reigning one for the last 150 years, we would have known what we know now about bacteria much earlier.  We would have been asking "how" are bacteria good for our world and we would have discovered how.  And we would have been expecting bacteria to be highly sophisticated for their size because why wouldn't God be a brilliant nano engineer along with all His other skills?  In the Lenski experiment, we should be expecting to find sensory systems and microprocessor systems within bacteria which actively control things like gene duplications for citrate uptake because, well, again, why wouldn't God be a brilliant nano engineer that can make bacteria operate in that way?

I DO think Shapiro and Co. are moving us closer to a "God view" but not because they advocate any kind of woo.  Rather, it's because they are helping biologists recognize the "chicken / egg' nature of all biological systems.  They are forcing biologists into head scratching mode.  Which is where creationists have been forever.  We look at biology and scratch our heads and say "WTF ... we cannot figure out how this stuff could come to be except via some Highly Sophisticated ET that we know very little about."  In human technology, stuff like we see in biology comes about only via Intelligence.  So why should it be any different in Biology?  Until we know better, that's the best explanation, although admittedly it's not an "explanation" at all in the normal sense ... it's just "all we've got."

Argument from incredulity.


Same as it ever was.
More armchair enginerding.

Seems failure may have occured during post-tensioning.

With piccies of proposed smoking gun.

Obs an Obama deep-state black-flag operation to take all our guns.
Too many ninjas.  :whyyou:
So here is the real challenge in biology today and Shapiro articulates this. We haven't the foggiest clue how the cell really operates from a hardware software computer analogy perspective.

That's because it doesn't.

We've been operating under this lousy paradigm of coding and non-coding parts of the genome and nobody's paid any attention to the intelligence of the cell itself. But that's all changing. It's a new game.

WaPo illustration:

Looks like it should have had temporary supports until they built the suspension structure.  Looks like they forgot that part.

Youtube vijeo by some random bystander saying the same thing in somewhat more detail:
PD - can we read anything into the fact that the documents are being subpoenaed, as opposed to just requested?

I reckon we can. I reckon we can read in that Mueller knows that specific relevant documents exist and where, and possibly what font and formatting they were prepared in.

It isn't a trip to see if fish are there, it's a trip targetted at specific tagged fish.
I guess.  But it is sorta ironic.

And at some level he DOES get it.  He does get that culling cows who don't calve well is bad for the cow but good for the herd.

And that if you only breed from the best specimens, you will get an increasingly better herd.

But he can't seem to make the leap to seeing that a system that produces varying offspring will allow a population of bacterial cells to adapt to changing conditions, at the trivial cost of losing a few hopeless monsters.

Yebut the population of a kind was only two so not a lot different from one, and look at all the diversity that came from those two of each kind in such a short time, that took some serious directed cell-brain intelligence. Natural Genetic Engineering baby!  :cheer:
Today's genome, the post-genomic genome, looks more like an exquisitely sensitive reaction (or response) mechanism - a device for regulating the production of specific proteins in response to the constantly changing signals it receives from its environment - than it does the pre-genomic picture of the genome as a collection of genes initiating causal chains leading to the formation of traits. The first job of the new genome is to detect the signals that impinge, and its second, to respond (e.g. by change in its conformation) in ways that alter the patterns of gene expression.

I thought your beef was with molecular genetics. What does a snippet about physiology have to do with that?

Still no support for the proposition that mutations are not random wrt fitness.
Research dating back to the 1930s has shown that genetic change is the result of cell-mediated processes, not simply accidents or damage to the DNA.

--James Shapiro
Yep, mainstream.

Yep, coz that snippet totally means the changes themselves aren't random wrt fitness.  :facepalm:

Works for David.
Now you are saying "Bah all those 3,000 differences couldn't possibly be due to NGE. If so, in GE is pretty stupid."

Which carries with it an enormous, arrogant assumption...

Namely that you are informed enough to really understand how bacteria operate.
No, as usual, that was not what was being said. What I took it to mean, and perhaps I am wrong, is that the author was asking you if all those 3000 differences were due to NGE, and given they were not used (useless) your NGE (not necessarily Shapiro's) doesn't seem all that amazing. Think about it, 1 success out of 3000 failures. Not real effective. It worked, but it looks a lot more like simple trial and error than some deliberate intentional process.
1 one out of 100,000,000 cells

If your mechanic only had a 1:100,000,000 chance of fixing your car, but would also give 3000 random pieces a whack with a ball peen hammer then I think you'd probably take your car somewhere else...
Your problem is that you don't appreciate how far beyond human technology biology really is. The technology literally blows our minds. It's like sci-fi. And you're stuck in the mud comparing it to human automotive technology. Sad.

Aaand back to the argument from incredulity.

It's where you always start and where you always end up, almost like you never left.