The book Darwin Devolves

[lee_merrill]

Did you mean "accepting the copious morphological, fossil, and genomic evidence"?

Well, that would be another topic...

Did you actually read this? Because that's not at all what's said in the press release your link directs to.

Yes, it's the best I could find, where bacteria start mutating at a 20x rate than normal.

The point you are "granting" me is that you completely misunderstood the meaning of two fairly straightforward sentences - you interpreted them as saying what you wanted them to say, rather than what the words meant.

Well, the sentences do refer to multiple conditions, and some of the setups described in the paper show null mutations beneficial in multiple conditions.

With that out of the way, it seems like you've finally accepted the point made by the Lehigh-based reviewers of Behe's book: the null mutations that frequently arise in lab-based adaptations are not generally adaptive, because they only provide fitness in a limited range of environmental conditions (typically 1, but i'm feeling generous).

No, I'm not ceding that point, sorry for the miscommunication.

If that's the case - and again, I haven't read Behe's book - then his whole argument is a farce. He's trying to claim that evolution mostly acts by breaking things. A hypomorphic mutation is no more a broken version of the gene than your TV is broken if you turn the brightness down. It retains function, which means (unlike a null mutation) it can be subject to further selection, which can change its activity further. In fact, a simple duplication of the gene would typically be enough to double its activity. Thus, it creates no barrier to evolution at any level.

Well, it presents a hurdle, especially since we are talking about adaptive mutations, where presumably resuming its activity would be selected against.

Blessings,
Lee

[lee_merrill]

Just want to point out that your hero, William Behe himself accepts the common descent of species -- including that humans descended from other primates.

Yes, but not simply by evolutionary means!

Blessings,
Lee

[lee_merrill]

More on evolution of microbes . . .

Source: https://news.harvard.edu/gazette/story/2014/02/evolution-in-real-time/

In further testing to determine if the new bacteria were different enough to qualify as a new species, Lenski’s researchers found that beyond changes to the genes responsible for glucose and citrate consumption, other changes had occurred in the organism that had made it less fit to survive in a glucose-only environment,

“We find they are getting less fit in the ancestral niche over time,” Lenski said. “I would argue that citrate users are — or are becoming — a new species.”

© Copyright Original Source

And this fits with Behe's view.

Source: Darwin Devolves

Further computer analysis by the authors suggested that the citrate mutant would be even more efficient if two other metabolic pathways that were normally turned off were both switched on. They searched and discovered that two regulatory proteins that usually suppress those pathways had been degraded by point mutations; the traffic lights were now stuck on green.

© Copyright Original Source

Blessings,
Lee

[TheLurch]

Yes, it's the best I could find, where bacteria start mutating at a 20x rate than normal.

Read it again. I would not have said "this isn't what it says" if it was, in fact, what it says.

Well, the sentences do refer to multiple conditions, and some of the setups described in the paper show null mutations beneficial in multiple conditions.

You're defining "multiple" as 2? Or are you focusing on the single example of a hypomorph?

No, I'm not ceding that point, sorry for the miscommunication.

Given that all the evidence presented so far in this thread shows the opposite, why do you maintain that belief then?

Well, it presents a hurdle, especially since we are talking about adaptive mutations, where presumably resuming its activity would be selected against.

Only if the selective pressure is the only one acting, and remains constant indefinitely. In a natural environment, things tend to change and multiple pressures need to be balanced, so the ability to continue to evolve becomes critical. Which is why gene loss tends to be relatively rare.

[rogue06]

*Michael Behe

I believe you mixed up Dembski and Behe. lol

I mixed up their first names but not their beliefs. From Behe's Darwin's Black Box:

I find the idea of common descent (that all organisms share a common ancestor) fairly convincing, and have no particular reason to doubt it.

From his The Edge of Evolution written nine years later (2007):

For example, both humans and chimps have a broken copy of a gene that in other mammals helps make vitamin C. As a result, neither humans nor chimps can make their own vitamin C. If an ancestor of the two species originally sustained the mutation and then passed it to both descendant species, that would neatly explain the situation.

More compelling evidence for the shared ancestry of humans and other primates comes from their hemoglobin—not just their working hemoglobin, but a broken hemoglobin gene, too.^[10] In one region of our genomes humans have five genes for proteins that act at various stages of development (from embryo through adult) as the second (betalike) chain of hemoglobin. This includes the gene for the beta chain itself, two almost identical copies of a gamma chain (which occurs in fetal hemoglobin), and several others. Chimpanzees have the very same genes in the very same order. In that region between the two gamma genes and a gene that works after birth, human DNA contains a broken gene (called a "pseudogene") that closely resembles a working gene for a beta chain, but has features in its sequence that preclude it from coding successfully for a protein.

Chimp DNA has a very similar pseudogene at the same position. The beginning of the human pseudogene has two particular changes in two nucleotide letters that seem to deactivate the gene. The chimp pseudogene has the exact same changes. A bit further down in the human pseudogene is a deletion mutation, where one particular letter is missing. For technical reasons, the deletion irrevocably messes up the gene's coding. The very same letter is missing in the chimp gene. Toward the end of the human pseudogene another letter is missing. The chimp pseudogene is missing it, too.

The same mistakes in the same gene in the same positions of both human and chimp DNA. If a common ancestor first sustained the mutational mistakes and subsequently gave rise to those two modern species, that would very readily account for why both species have them now. It's hard to imagine how there could be stronger evidence for the common ancestry of chimps and humans.

That strong evidence from the pseudogene points well beyond the ancestry of humans. Despite the remaining puzzles, there's no reason to doubt that Darwin had this point right, that all creatures on earth are biological relatives.

Laurence ("Larry") Moran, Professor Emeritus in the Department of Biochemistry at the University of Toronto, has said that this "clear statement [the second quote] by Micheal Behe is a way of separating the kooks from the serious ID proponents."

[shunyadragon]

Yes, but not simply by evolutionary means!

Blessings,
Lee

There is no other hypothesis that may be falsified by scientific methods other than the science of evolution.

[shunyadragon]

And this fits with Behe's view.

Source: Darwin Devolves

Further computer analysis by the authors suggested that the citrate mutant would be even more efficient if two other metabolic pathways that were normally turned off were both switched on. They searched and discovered that two regulatory proteins that usually suppress those pathways had been degraded by point mutations; the traffic lights were now stuck on green.

© Copyright Original Source

Blessings,
Lee

No it does not fit Behe's view.

[lee_merrill]

Only if the selective pressure is the only one acting, and remains constant indefinitely. In a natural environment, things tend to change and multiple pressures need to be balanced, so the ability to continue to evolve becomes critical.

Well, now the goalposts have shifted. But getting out of a null mutation hole is difficult, the gene duplication that you mentioned is about the only way to improve back to a previous level, for a damaged gene. And one duplication might not be enough, a number of duplications might be required.

Which is why gene loss tends to be relatively rare.

I'm not sure why gene loss is rare if adaptive null mutations must face continued, different evolutionary pressures.

Blessings,
Lee

[lee_merrill]

No it does not fit Behe's view.

Well, yes, it does fit, Behe has a whole section on Lenski's experiment in his book, part of which I quoted.

Blessings,
Lee

[shunyadragon]

Well, yes, it does fit, Behe has a whole section on Lenski's experiment in his book, part of which I quoted.

Blessings,
Lee

. . . attempting to make it fit in Behe's bad science is not a fit.

[TheLurch]

Well, now the goalposts have shifted.

No, that's the argument i've been making the whole time. Have you just not been paying attention?

Here, let me help you with it.

The issue we're discussing (or at least i think we're discussing) is whether these mutations are likely to be generally adaptive to a variety of environmental conditions, and therefore end up fixed in the population. Behe (and you) are arguing yes; i'd suggest the evidence indicates otherwise.

Remember that? All the way back from... 2 days ago? You responded to the post, so i'd assumed you'd read it. Maybe i was mistaken.

In fact, my argument here for weeks has been consistent: null mutations aren't generally adaptive, because they eliminate genes that can be adaptive under other environmental conditions.

Why are you so consistently dishonest?

But getting out of a null mutation hole is difficult, the gene duplication that you mentioned is about the only way to improve back to a previous level, for a damaged gene. And one duplication might not be enough, a number of duplications might be required.

Ugh, so, so much stupid in so few words.

To begin with, the "null mutation hole" is exactly my point. Evolution doesn't tend to select for null mutations in freely evolving populations, because they're not adaptive to anything more than a limited number of selective pressures. That's why we don't see many null mutations occurring in naturally evolving populations, since they limit the possibility of adapting when conditions change.

That has been the whole point of pages of discussion now.

The second bit is your claim that "the gene duplication that you mentioned is about the only way to improve back to a previous level." That's laughably, comically wrong. Off the top of my head:
Reversion of the original mutation.
Compensatory mutations in the same gene.
Compensatory mutations in some other gene.
Mutations in regulatory DNA.
Mutations in the proteins that control gene expression.

Again, you don't know enough about biology to say anything on this topic, yet you make definitive claims regardless. Why? These sorts of falsehoods are a recurring pattern with you, they keep getting pointed out, and yet you keep repeating the pattern. I'm beginning to reach the conclusion that you enjoy trafficking in falsehoods.

I'm not sure why gene loss is rare if adaptive null mutations must face continued, different evolutionary pressures.

Because, as the paper you cited shows, the majority of null mutations are not adaptive to more than a single environmental condition? Remember that? That was Monday, too.

[lee_merrill]

In fact, my argument here for weeks has been consistent: null mutations aren't generally adaptive, because they eliminate genes that can be adaptive under other environmental conditions.

Well, we've been missing each other, Behe is discussing mutations that either degrade or disable genes. And no one is saying that null mutations are generally adaptive, rather hypomorphic / null mutations can be adaptive. And such mutations are the usual ones selected.

Evolution doesn't tend to select for null mutations in freely evolving populations, because they're not adaptive to anything more than a limited number of selective pressures.

Well, all that has to happen is for the environment to stay consistent long enough for a null mutation to become fixed.

The second bit is your claim that "the gene duplication that you mentioned is about the only way to improve back to a previous level." That's laughably, comically wrong. Off the top of my head:
Reversion of the original mutation.
Compensatory mutations in the same gene.
Compensatory mutations in some other gene.
Mutations in regulatory DNA.
Mutations in the proteins that control gene expression.

And all of these are unlikely, is the point, once a null mutation has become fixed, it's difficult for it to be undone.

Source: Darwin Devolves

Even in limited cases where damaged genes are confined to just a segment of the population, the baleful effects stick around for a very long time, as malaria researchers have noted. If they become fixed in a species, however, the affected gene or control region is (barring very improbable reverse mutations) gone for good.

© Copyright Original Source

Blessings,
Lee

[TheLurch]

Well, we've been missing each other, Behe is discussing mutations that either degrade or disable genes. And no one is saying that null mutations are generally adaptive, rather hypomorphic / null mutations can be adaptive. And such mutations are the usual ones selected.

But the nulls aren't the ones usually selected, as we've been going over in detail. And, as I described above, hypomorphs don't help his argument, because they don't create a barrier to further evolution.

Well, all that has to happen is for the environment to stay consistent long enough for a null mutation to become fixed.

Not true. The environment has to be constant, and there have to be no other selective pressures on the gene.

I'm not saying this never happens. Null mutations clearly can become fixed, or vitamin C wouldn't be a vitamin (1). Just that there is no evidence that they play a major role in speciation or the gene content of organisms.

And all of these are unlikely, is the point, once a null mutation has become fixed, it's difficult for it to be undone.

WHICH IS WHY I SUGGESTED THE WERE RELEVANT TO HYPOMORPHS. Today. Just a few posts above.

I see why Roy calls you Dory. You seemingly have no memory of the discussion that you're supposedly taking part in.


And i would like to note that, rather than acknowledging that you made a false statement and apologizing for it, you're avoiding the subject entirely. It speaks to your character.



1: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145266/

[lee_merrill]

But the nulls aren't the ones usually selected, as we've been going over in detail. And, as I described above, hypomorphs don't help his argument, because they don't create a barrier to further evolution.

They are usually selected, says Behe, because it's a lot easier to degrade or break something, and evolution can often use desperate measures.

Source: Darwin Devolves

if an unneeded gene were active, breaking it would turn it off, saving energy. If a gene that would help make a useful product to outcompete other bugs were normally turned off, breaking the controls so the product would be made continuously would be beneficial. There are many circumstances in which getting rid of something can be helpful. And the more complicated and sophisticated a system, the more ways it can be broken in more situations to yield an advantage.

© Copyright Original Source

Not true. The environment has to be constant, and there have to be no other selective pressures on the gene.

Agreed, long enough for the change to become fixed.

I'm not saying this never happens. Null mutations clearly can become fixed, or vitamin C wouldn't be a vitamin (1). Just that there is no evidence that they play a major role in speciation or the gene content of organisms.

Alrighty...

WHICH IS WHY I SUGGESTED THE WERE RELEVANT TO HYPOMORPHS. Today. Just a few posts above.

Well, yes, I should have added hypomorphs, they also are difficult to undo.

Source: Darwin Devolves

Remarkably, [Lenski] discovered fifty-nine genes that had changed their activity levels, either increased or (mostly) decreased them, all in the same direction in eight of the twelve mutant strains. … The eight affected replicate strains all had point mutations in the spoT gene that caused single amino-acid changes in the encoded regulatory protein. Interestingly, all the mutations were different—that is, they had all changed the same gene, but at different places in it. Although the workers didn’t explicitly test for it, that’s the hallmark of a mutation that degrades or eliminates the activity of the protein it alters. It’s difficult for a mutation to improve the activity of a protein, because most work very well already. Any improvements, if any are possible, tend to be limited to one or a very few potential positions.

© Copyright Original Source

So more than half of 59 genes decreased their activity, and these changes were due to changes in the spoT regulatory gene, and were fixed, and not undone.

Blessings,
Lee

[TheLurch]

They are usually selected, says Behe, because it's a lot easier to degrade or break something, and evolution can often use desperate measures.

That is indeed what Behe says. But it's been demonstrated multiple times over in this discussion that Behe gets things wrong. So the question is what the evidence says. And so far in this discussion, the evidence has been one sided in favor of null mutations not being a major factor in speciation. Most of what you've presented have been your own evidence-free claims about biology, which have served to demonstrate little more than that you don't know anything other than biology. The one paper you cited ended up supporting a position contrary to the one you brought it in to support.

Until that changes, you don't have an argument here.

Nevertheless, i got a laugh out of this:

Source: Darwin Devolves

if an unneeded gene were active, breaking it would turn it off, saving energy. If a gene that would help make a useful product to outcompete other bugs were normally turned off, breaking the controls so the product would be made continuously would be beneficial. There are many circumstances in which getting rid of something can be helpful. And the more complicated and sophisticated a system, the more ways it can be broken in more situations to yield an advantage.

© Copyright Original Source

For years it's been "oh, complexity, obviously needs a designer, clear evidence evolution won't work!" Now, when it's convenient, that becomes "oh, complexity, so easy for evolution to break, therefore must have a designer".

Well, yes, I should have added hypomorphs, they also are difficult to undo.

No, they're not. That was the whole point off that extensive list of ways you can increase the activity of a hypomorph.

How about, instead of making unsubstantiated claims on a topic you know nothing about, you bring some evidence?

Speaking of making up stuff...

Source: Darwin Devolves

Remarkably, [Lenski] discovered fifty-nine genes that had changed their activity levels, either increased or (mostly) decreased them, all in the same direction in eight of the twelve mutant strains. … The eight affected replicate strains all had point mutations in the spoT gene that caused single amino-acid changes in the encoded regulatory protein. Interestingly, all the mutations were different—that is, they had all changed the same gene, but at different places in it. Although the workers didn’t explicitly test for it, that’s the hallmark of a mutation that degrades or eliminates the activity of the protein it alters. It’s difficult for a mutation to improve the activity of a protein, because most work very well already. Any improvements, if any are possible, tend to be limited to one or a very few potential positions.

© Copyright Original Source

So more than half of 59 genes decreased their activity, and these changes were due to changes in the spoT regulatory gene, and were fixed, and not undone.

There are absolutely no numbers there from which you can derive "more than half". You also don't know anything about whether the mutations were reverted, suppressed elsewhere, or what - it literally says "the workers didn't explicitly test for it."

You're making stuff up. Again.


This is a question for the other posters here - is there any moderation recourse if pretty much every post by a user contains a fabrication? Is that sort of thing policed here?