The book Darwin Devolves

[shunyadragon]

So are you implying that the scientists who believe in punctuated equilibrium are deluded?

Blessings,
Lee

No it is your interpretation of punctuated equilibrium that is the problem, and ah . . . Behe's. Punctuated equilibrium occurs when you have periods of time when there is rapid diversification of species, and periods of slow or apparent stasis, equilibrium or no change. Nothing in the concept of punctuated equilibrium is there the concept of objectively verified sudden appearances of species.

Source: https://www.biology-online.org/dictionary/Punctuated_equilibrium

Punctuated equilibrium is a theory describing an evolutionary change that occurs rapidly and in brief geological events in between the long periods of stasis (or equilibrium). The theory is based on the stasis in fossil records, and when phenotypic evolution occurs, it is localized in rare, rapid events of branching speciation. Accordingly, the theory assumes that when there is a significant evolutionary change, cladogenesis occurs. Cladogenesis is the process where a species splits into two distinct species instead of one species transforming into another over time.1 The American paleontologists Niles Eldredge and Stephen Jay Gould first proposed the theory in 1972. They referred to it as punctuated equilibria.2 This theory is presented to contrast phyletic gradualism. In the latter, evolution is described to happen smoothly and continuously (anagenesis).

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Evolution is environmentally driven. Fertile environments can lead to relatively rapid diversification of species and can lead to relatively rapid evolution. For example tropical rain forests, and tropical seas around coral reefs. Static isolated environments like in some deep sea environments can lead to slow or no evolution as in the Coelacanth, even for millions of years.

Another good example is sudden extinction events like the end of the Cretaceous leads to empty fertile environments open to rapid diversification and evolution of existing species such as mammals. In the definition above this was a sudden geologic event.

[shunyadragon]

So are you implying that the scientists who believe in punctuated equilibrium are deluded?

Blessings,
Lee

It is important to realize that in the periods of relatively rapid evolution like after catastrophic events involve millions of year. Of course, not so rapid nor sudden by any means.

[rogue06]

Evolution is environmentally driven. Fertile environments can lead to relatively rapid diversification of species and can lead to relatively rapid evolution. For example tropical rain forests, and tropical seas around coral reefs. Static isolated environments like in some deep sea environments can lead to slow or no evolution as in the Coelacanth, even for millions of years.

Not a good example.

This is just a variant of the oft repeated YEC claim that the coelacanths found today are the same as the ones who lived hundreds of millions of years ago and had been thought (including by YECs) to have gone extinct.

They get all excited when they mention coelacanths not understanding that they are an order of lobe-finned fish. In their ignorance YECs seem to think that they were a species and that the ones living today are the same type that were around millions of years ago.

The modern coelacanth species, Latimeria chalumnae and Latimeria menadoensis, are not the same species or even the same genus (and IIRC, a different family as well) as any of the coelacanths in the fossil record. In fact over 120 different species have so far been identified in the fossil record – along with something like 10 families and over 20 different genera).

It should be noted that the two species of coelacanth still remaining are relatively recent, with estimates of the split between the African and Indonesian species being less than 35 million years ago. The genus Latimeria is the ONLY surviving lineage of coelacanth, and the genus Latimeria has only existed since after the dinosaurs. The Order Coelacenthiformes contains at least distinct 22 genera of lobefinned fishes, of which only one is still extant. They are simply a relict lineage of a much older group, which is common in the deep sea (crinoids, brachiopods, etc.).

Formerly coelacanths were a widespread and diverse group with fossil remains found on every continent except for Antarctica whereas today they are confined to a couple of spots in the Indian Ocean. This means that previously some made their homes in cool waters while others lived in warm tropical waters

Also, around a third of the extinct species were freshwater, living in lakes and rivers and those that dwelt in the oceans lived in shallow water with very few exceeded 55 cm (a little more than 21˝") in length while the modern ones are exclusively deep sea creatures (IIRC, they tend to die from decompression when brought up to the surface) and can reach 2 meters or slightly over 6˝'.

Also, IIRC, modern coelacanths give birth to live young where there is strong evidence that some of the extinct species laid eggs.

One type of ancient coelacanth that lived in the Early Triassic and known as Rebellatrix divaricerca (the only known member in its Family) had a large, forked as well as symmetrical tail fin and a rather slim body which is highly unusual for coelacanths. This type of tail is found on fast moving predators like tuna and barracuda which is definitely not the lifestyle of modern coelacanths nor other extinct varieties. This novel body shape demonstrates that coelacanths were not essentially morphologically static following the Early Carboniferous as was widely believed.

Further, some of the ancient coelacanths actually had well developed lungs whereas the modern species do have vestigial lungs: Allometric growth in the extant coelacanth lung during ontogenetic development

Finally, it should be kept in mind that the two modern species resemble each other superficially (though there are color differences), and it took DNA testing to reveal the significant genetic differences between the two. DNA and color differences aren't preserved in the fossil record, so only the more obvious differences are usually seen (like being a freshwater species for example).


Here is a short video that willl give you an idea as to the wide variety of coelacanths that there once was and how they evolved

Or if you prefer here is a picture showing three different types of extinct coelacanth with the top one coming from the Cretaceous and the other two coming from the Carboniferous.

[ATTACH=CONFIG]36110[/ATTACH]

[shunyadragon]

Not a good example.

I believe it is the lineage of the Coelacanths that were thought to have died out. The persistence of the primitive species found deep in the ocean is thought to have survived, but possibly evolved possibly to a limited extent, because of their adaptation to an isolated environment. The difference from the ancient species is minimal. They share all the primitive features of the ancestors. The only significant difference is size.

[tabibito]

I believe it is the lineage of the Coelacanths that were thought to have died out. The persistence of the primitive species found deep in the ocean is thought to have survived, but possibly evolved possibly to a limited extent, because of their adaptation to an isolated environment. The difference from the ancient species is minimal. They share all the primitive features of the ancestors. The only significant difference is size.

and the vestigial (instead of functional) lung.

[rogue06]

I believe it is the lineage of the Coelacanths that were thought to have died out. The persistence of the primitive species found deep in the ocean is thought to have survived, but possibly evolved possibly to a limited extent, because of their adaptation to an isolated environment. The difference from the ancient species is minimal. They share all the primitive features of the ancestors. The only significant difference is size.

Did you read my post?

Back in the past they were generally either freshwater or shallow water creatures instead of living in between the mesopelagic and bathypelagic zones some 400 to 2300 meters deep. And while modern coelacanths give birth to live young at least some of the extinct varieties laid eggs. Tabibito already brought up the lung.

The difference from the wide variety of ancient extinct species is anything but minimal.

[TheLurch]

I found the paper in question

I sincerely thank you for actually engaging in the scientific process.

Source: PLoS

The high rate at which loss-of-function mutations occur suggests that null mutations play an underappreciated role in the early stages of adaption of bacterial populations to new environments. … The combination of the rapid acquisition and broad functionality of loss-of-function mutations suggests that they play a major role in the early adaptation of bacterial populations to new challenges.

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Right, which is not at issue. Let me be perfectly explicit: There are environmental conditions where the complete loss of gene activity can be adaptive. So, if you screen using a single environmental condition, you're likely to get null mutations out of the screen.

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.

The evidence i've discussed so far is the fact that gene counts have essentially remained constant for about 100 million years of mammalian evolution, and the fact that certain pathways that are disabled in the context of single environmental conditions (like those disabled in hypermutator strains) aren't disabled among free living bacteria.

You're arguing that this paper suggests that null mutations are more generally adaptive. As evidence, you highlight the quotes, saying:

So mutations (plural) and environments (plural) indicates the principle holds in general, across all environments.

Again, you're falling back on semantics. There is nothing that indicates that any single mutation will be adaptive in more than one environment in the sentences quoted above.

I also note that you don't acknowledge the following quote from the paper:

Source: PLoS

The maladaptive properties of null mutations, including their contributions to genome decay are well known.

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So, even the semantics you are trying to rely on are a problem for your argument. But there's more significant problems than that: many of the mutations here aren't really loss of functions.

This other thing you quote:

Source: PLoS

similar to the mechanism of action of a recently characterized rho hypomorph that proved beneficial in more than ten different conditions.

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does not support your argument. A hypomorphic mutation retains function, and is therefore not a null. So the fact that you seem to need to retain function in order to be adaptive in multiple environments runs counter to Behe's argument.

Finally, there's simply some weird stuff in the paper itself. In its section on "beneficial null mutations", we find this:

Source: PLoS

The RNA case in particular is dominated by two conditions under which transposon insertions in ribosomal RNAs were beneficial, and thus must be viewed with some caution.

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Now, functional ribosomal RNA its required to make any proteins; null mutations in these genes would invariably be fatal - except for the fact that most organisms carry multiple copies of these genes precisely because it's advantageous to prevent that (E. coli, for example, has 7 copies). Essentially, these genes come pre-duplicated; as a result, even a null mutation in one would allow continued function of ribosomal RNA thanks to the other copies of the gene.

(I'm leaving aside for a moment the question of whether inserts into an rRNA that suppressed a phenotype would be a null - my suspicion is not, but it's somewhat a tangent. If anyone cares, i'll discuss it in more detail.)

All of this indicates that not everything these authors discuss as being adaptive are actually null mutations, and thus aren't even relevant to Behe's argument.

What you or Behe would need to do to support your argument from this paper is find out how many of these mutations are actually complete losses of a function (nulls of the only copy of a gene), and whether those are adaptive to multiple environmental conditions.

The paper comes has some relevant information on this in figure five, which tests growth rates under 3 different selective conditions using gene deletions, which we know are nulls. These aren't really independent conditions, because they're testing for amino acid utilization. Many of the amino acid biochemical pathways overlap, so you'd expect some overlap in the genetics underlying them; you can think of this as a non-stringent test.

Even under these non-stringent conditions, of the 24 tested, 22 were only adaptive under 1 of the 3 conditions. The remaining two were only adaptive in 2 conditions; no mutations were adaptive for all 3.


The conclusion I reach from this is that most null mutations are only adaptive to a limited number of environmental conditions, often only 1. This severely undercuts Behe's argument, which had already been undercut by the gene counts in mammals mentioned above.

[lee_merrill]

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.

Yet a mutation need only be adaptive in one condition to be fixed in that population.

The evidence i've discussed so far is the fact that gene counts have essentially remained constant for about 100 million years of mammalian evolution...

Assuming common descent via evolution!

… and the fact that certain pathways that are disabled in the context of single environmental conditions (like those disabled in hypermutator strains) aren't disabled among free living bacteria.

Yet bacteria in the wild can go into a hyper-mutation mode when subjected to high stress.

Source: PLoS

The high rate at which loss-of-function mutations occur suggests that null mutations play an underappreciated role in the early stages of adaption of bacterial populations to new environments. … The combination of the rapid acquisition and broad functionality of loss-of-function mutations suggests that they play a major role in the early adaptation of bacterial populations to new challenges.

© Copyright Original Source

There is nothing that indicates that any single mutation will be adaptive in more than one environment in the sentences quoted above.

Okay, I'll grant you that point.

I also note that you don't acknowledge the following quote from the paper:

Source: PLoS

The maladaptive properties of null mutations, including their contributions to genome decay are well known.

© Copyright Original Source

Well, yes, null mutations are often harmful, everyone agrees.

This other thing you quote:

Source: PLoS

similar to the mechanism of action of a recently characterized rho hypomorph that proved beneficial in more than ten different conditions.

© Copyright Original Source

does not support your argument. A hypomorphic mutation retains function, and is therefore not a null. So the fact that you seem to need to retain function in order to be adaptive in multiple environments runs counter to Behe's argument.

Source: biology-online

A type of mutation wherein the change in gene leads to the partial loss of the normal (wild-type) gene function, such as by reduced expression (of protein or RNA)

Source

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So such mutations do fit Behe's paradigm, his book is about reduced or eliminated function in genes.

All of this indicates that not everything these authors discuss as being adaptive are actually null mutations, and thus aren't even relevant to Behe's argument.

Though they do discuss adaptive null mutations in detail.

The conclusion I reach from this is that most null mutations are only adaptive to a limited number of environmental conditions, often only 1.

Though sometimes two! But in any case, in each environment, null mutations were fixed.

Blessings,
Lee

[shunyadragon]

Yet a mutation need only be adaptive in one condition to be fixed in that population.

A mutation that is adaptive is never necessarily fixed in the population. As long as it is adaptive in remains. An example is the gene for activating the gene for teeth in the ancestors of birds was adaptive, but in birds the gene was no longer adaptive. The gene for teeth remains in birds, but the gene or genes for activating teeth gene are gone. The teeth gene can be activated artificially in birds, but the birds die.

Assuming common descent via evolution!

Not based on assumptions, unfortunately Discovery Institute's Intelligent Design is based on Theistic assumptions

The rest has been responded to by The Lurch <snip. . . snip>

[TheLurch]

Let's get a couple of things out of the way quickly, shall we?

Assuming common descent via evolution!

Did you mean "accepting the copious morphological, fossil, and genomic evidence"? Because what you're saying is the equivalent of saying "assuming the earth is round".

Yet bacteria in the wild can go into a hyper-mutation mode when subjected to high stress.

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

Okay, I'll grant you that point.

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. And here you're doing it again.

This is incredibly sloppy, and shows a lack of respect for yourself and everyone else on this board. And you've not apologized once that i can remember for your frequently misleading statements.


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).

The consequence of this, which you don't seem to have accepted yet, is that this means they're probably not a major factor in wild populations, which have to balance a range of selective pressures caused by multiple environmental factors. But if you do accept the former now - and the very paper you and Behe cite argues strongly for it - then you have to explain the reasons why the latter isn't an obvious consequence of it.


With that, we can move on to the issue of hypomorphs, which you don't have to define for me since i have done genetics for a living.

So such mutations do fit Behe's paradigm, his book is about reduced or eliminated function in genes.

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.

Put differently, Behe's argument is that damage to genes is cumulative, and ultimately presents a barrier to further speciation. But a hypomorphic mutation presents no barrier at all, and therefore is irrelevant to Behe's argument.

If he says otherwise, then, well, he's not even trying to make a decent argument anymore.


EDITS: typos, so many typos...

[rogue06]

Assuming common descent via evolution!

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

[Seeker]

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

*Michael Behe

I believe you mixed up Dembski and Behe. lol

[Roy]

Yet bacteria in the wild can go into a hyper-mutation mode when subjected to high stress.

Sigh. That article says nothing about hyper-mutation.

[shunyadragon]

Yet bacteria in the wild can go into a hyper-mutation mode when subjected to high stress.

The reality of the evolution of microbes:

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2937522/

Origins and Evolution of Antibiotic Resistance

INTRODUCTION
The successful use of any therapeutic agent is compromised by the potential development of tolerance or resistance to that compound from the time it is first employed. This is true for agents used in the treatment of bacterial, fungal, parasitic, and viral infections and for treatment of chronic diseases such as cancer and diabetes; it applies to ailments caused or suffered by any living organisms, including humans, animals, fish, plants, insects, etc. A wide range of biochemical and physiological mechanisms may be responsible for resistance. In the specific case of antimicrobial agents, the complexity of the processes that contribute to emergence and dissemination of resistance cannot be overemphasized, and the lack of basic knowledge on these topics is one of the primary reasons that there has been so little significant achievement in the effective prevention and control of resistance development. Most international, national, and local agencies recognize this serious problem. Many resolutions and recommendations have been propounded, and numerous reports have been written, but to no avail: the development of antibiotic resistance is relentless.

The most striking examples, and probably the most costly in terms of morbidity and mortality, concern bacteria. The discovery of these infectious agents in the late 19th century stimulated the search for appropriate preventative and therapeutic regimens; however, successful treatment came only with the discovery and introduction of antibiotics half a century later. Antibiotics have revolutionized medicine in many respects, and countless lives have been saved; their discovery was a turning point in human history. Regrettably, the use of these wonder drugs has been accompanied by the rapid appearance of resistant strains. Medical pundits are now warning of a return to the preantibiotic era; a recent database lists the existence of more than 20,000 potential resistance genes (r genes) of nearly 400 different types, predicted in the main from available bacterial genome sequences (85). Fortunately, the number existing as functional resistance determinants in pathogens is much smaller.

Many excellent reviews describing the genetics and biochemistry of the origins, evolution, and mechanisms of antibiotic resistance have appeared over the last 60 years. Two of note in recent times are those of Levy and Marshall (82) and White et al. (149). The goal of this short article is not to summarize such a wealth of information but to review the situation as we see it now (most particularly with respect to the origins and evolution of resistance genes) and to provide some personal views on the future of antibiotic therapy of infectious diseases.

Antibiotic discovery, modes of action, and mechanisms of resistance have been productive research topics in academia (27) and, until recently, in the pharmaceutical industry. As natural products, they provide challenging intellectual exercises and surprises with respect to their chemical nature, biosynthetic pathways, evolution, and biochemical mode of action (26, 134). The total synthesis of such natural products in the laboratory is difficult, since these small molecules are often extremely complex in functionality and chirality (98). The antibiotic penicillin was discovered in 1928, but the complete structure of this relatively simple molecule was not revealed until 1949, by the X-ray crystallographic studies of Dorothy Crowfoot Hodgkin (73), and was confirmed by total synthesis in 1959 (125). Studies of modes of action have provided biochemical information on ligands and targets throughout antibiotic history (59, 147), and the use of antibiotics as “phenotypic mutants” has been a valuable approach in cell physiology studies (142). The field of chemical biology/genetics grew from studies of those interactions. We have a meager understanding of how antibiotics work, and in only a few instances can the intimate interactions of the small molecule and its macromolecular receptor be interpreted in terms of defined phenotypes. More surprisingly, there is a paucity of knowledge of the natural biological functions of antibiotics, and the evolutionary and ecological aspects of their chemical and biological reactions remain topics of considerable interest and value (3, 8).

© Copyright Original Source

more to follow . . .

[shunyadragon]

More on evolution of microbes . . .

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

59,000 generations of bacteria, plus freezer, yield startling results

Though the bacteria were originally genetically identical, they have evolved. Today’s populations grow roughly 80 percent faster than the original lines, a development that Lenski called “a beautiful example of adaptation by natural selection.”

An analysis of the 12 lines after 20,000 generations showed 45 mutations from the ancestral population among the bacteria’s roughly 4,000 genes. Many of the same genes were mutated in all lines, but it was rarely exactly the same mutation within the genes, Lenski said. He equated the bacteria’s evolutionary feats in the glucose-limited “flask world” with those of mountain climbers finding other routes to the peak.

“Populations are climbing Mount Glucose in similar, though not identical, ways,” Lenski said.

After 30,000 generations, researchers noticed something strange. One population had evolved the ability to use a different carbon-based molecule in the solution, called citrate, as a power source.

Researchers wondered whether it was the result of a rare, single mutation, or a more complex change involving a series of mutations over generations. To find out, one of Lenski’s postdocs, Zachary Blount, took some of the frozen cells and grew them in a culture lacking glucose, with citrate as the only potential food source.

After testing 10 trillion ancestral cells from early generations, he got no growth. But when he tested cells from the 20,000th generation on, he began to get results, eventually finding 19 mutants that could use citrate as a power source. The results showed that the citrate-eating mutation was most likely not the result of a single mutation, but one enabled by multiple changes over 20,000 generations.

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.”

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