Protistan Biology, HGT and Phylogenetic Evolution Debunk Intelligent Design

[RedRuth]

From this months Journal of Eukaryotic Microbiology

THE International Society of Protistologists (ISOP) organized a
pre-meeting workshop entitled ‘‘Horizontal Gene Transfer and
Phylogenetic Evolution Debunk Intelligent Design,’’ as part of the
1st North American Section meeting held June 11–13, 2009, at
Roger Williams University, Bristol, RI, USA. This workshop focused
on the acceptance of Darwinian evolution in the United States
and the role of intelligent design (ID) in the ongoing controversy
between scientific knowledge and popular belief. Intelligent design, a
doctrine born in the 1980s, proposes that a ‘‘Designer’’ is responsible
for the complexity in biological systems and that Darwinism cannot
explain holistically the origin and evolution of the natural world, nor
the intricate chemical assemblage of most organic structures (Forrest
and Gross 2007; Padian and Matzke 2009). The workshop emphasized
how to communicate evolutionary principles to student and
public audiences by using examples of protistan evolution.

And they use some examples to debunk ID, for example

ABSTRACT. Horizontal gene transfer (HGT) and common descent interact in space and time. Because events of HGT co-occur with
phylogenetic evolution, it is difficult to depict evolutionary patterns graphically. Tree-like representations of life’s diversification are
useful, but they ignore the significance of HGT in evolutionary history, particularly of unicellular organisms, ancestors of multicellular
life. Here we integrate the reticulated-tree model, ring of life, symbiogenesis whole-organism model, and eliminative pattern pluralism to
represent evolution. Using Entamoeba histolytica alcohol dehydrogenase 2 (EhADH2), a bifunctional enzyme in the glycolytic pathway of
amoeba, we illustrate how EhADH2 could be the product of both horizontally acquired features from ancestral prokaryotes (i.e. aldehyde
dehydrogenase [ALDH] and alcohol dehydrogenase [ADH]), and subsequent functional integration of these enzymes into EhADH2,
which is now inherited by amoeba via common descent. Natural selection has driven the evolution of EhADH2 active sites, which require
specific amino acids (cysteine 252 in the ALDH domain; histidine 754 in the ADH domain), iron- and NAD1 as cofactors, and the
substrates acetyl-CoA for ALDH and acetaldehyde for ADH. Alternative views invoking ‘‘common design’’ (i.e. the non-naturalistic
emergence of major taxa independent from ancestry) to explain the interaction between horizontal and vertical evolution are unfounded.
Key Words. Design creationism, Entamoeba, integrative model, lateral evolution, reticulated patterns of unicellular life.

And there's another article entitles, Using Protistan Examples to Dispel the Myths of Intelligent Design Hopefully at least some of them are open access

http://www3.interscience.wiley.com/j...118000394/home

[VoxRat]

Originally Posted by RedRuth

From this months Journal of Eukaryotic Microbiology

well, a doctrine repackaged in the 1980s.

I don't think anything Dembski, Behe, or any of the rest of them wrote had anything constructive to add to what Paley wrote in 1802, beyond restating PRATT arguments from incredulity that Hovind, Ham, Morris, et al. have been dishing up for decades.

[RedRuth]

True enough, repackaged to allow some wriggle room on the standard YEC ideology.

[Jet Black]

Is Protistan Biology different from Catholic Biology?

[Jet Black]

Originally Posted by RedRuth

From this months Journal of Eukaryotic Microbiology

And they use some examples to debunk ID, for example

And there's another article entitles, Using Protistan Examples to Dispel the Myths of Intelligent Design Hopefully at least some of them are open access

http://www3.interscience.wiley.com/j...118000394/home

is there any particualr reason they are even bothering to mention "alternative views" - I mean it's not like any of them are even seriously considered as alternatives anyway, is it?

[ericmurphy]

Originally Posted by Jet Black

Is Protistan Biology different from Catholic Biology?

Cathartic biology. Get your terms straight.

[Worldtraveller]

Originally Posted by Jet Black

Is Protistan Biology different from Catholic Biology?

I think this is worth starting a recall thread..

[Steviepinhead]

Where in southern eurasia is Protistan located, exactly?

Does it export HGT, like Afghanistan exports hashish, or Ukrania exports porn starlets...?

[Jet Black]

Originally Posted by Worldtraveller

I think this is worth starting a recall thread..

terrible puns are not mentioned on the charter anywhere

[TestyCalibrate]

Originally Posted by Steviepinhead

Where in southern eurasia is Protistan located, exactly?

Does it export HGT, like Afghanistan exports hashish, or Ukrania exports porn starlets...?

Why doesn't that show up in the world bank reports?

[TestyCalibrate]

Originally Posted by Jet Black

terrible puns are not mentioned on the charter anywhere

they should be.

[RedRuth]

is there any particualr reason they are even bothering to mention "alternative views" - I mean it's not like any of them are even seriously considered as alternatives anyway, is it?

That's a good point, I've always been of the opinion that we should just let the science speak for it self. But then I'm a Brit and YEC isn't taken seriously here but ID sort of is, it's seen as the respectable, non bonkers, halfway house between YEC and atheist naturalism. TBH, I think alot of people here confuse it with Theistic evolution. Anyway, I thought it was a nice concise and fairly easily understood refutation of ID from the science perspective.

[borealis]

Originally Posted by Jet Black

terrible puns are not mentioned on the charter anywhere

But they should be mentioned.

(I had every intention of stealthily dropping that pun in the thread myself, dammit.)

[SteveF]

---

Staff Note Split some stuff off to here.

[SteveF]

Originally Posted by RedRuth

And there's another article entitles, Using Protistan Examples to Dispel the Myths of Intelligent Design Hopefully at least some of them are open access

This paper has some really cool stuff in it. There's an excellent smackdown of Behe:

In his book "The Edge of Evolution: The Search for the Limits of Darwinism"Behe (2007) draws heavily upon the example of drug resistance in the malarial parasite Plasmodium falciparum as one biochemical pathway that is supposedly too complex to have arisen through natural evolutionary processes. According to Behe (2007), the odds that mutations required to impart chloroquine resistance in Plasmodium could arise naturally are so impossibly long that they lie beyond what he considers "The Edge of Evolution."

To the casual observer it might appear that he has a valid point. Since its first widespread use in the 1940s, the anti-malarial compound chloroquine has proven to be remarkably effective in treating individuals infected with Plasmodium. Chloroquine's mode of action is believed to interfere with the parasite's ability to sequester heme in the biologically inert crystalline form known as hemozoin. By binding to Fe(II)-protoporphyrin IX (FP), chloroquine forms a complex that can disrupt the functioning of the food vacuole membrane of the parasite, ultimately killing it. Beginning in the late 1950s, chloroquine-resistant strains of P. falciparum, the most dangerous and therefore most often treated of the four species of Plasmodium that infect humans, were separately reported from Thailand and the Colombian–Venezuelan border (Hyde 2007). By the late 1980s, resistance had spread throughout much of Asia, South and Central America, and all of sub-Saharan Africa. Presumably, a new mutation, which conferred resistance to this anti-malarial drug, had arisen in P. falciparum, driven by the strong selection pressure of widespread chloroquine treatment.

The ability to resist chloroquine has now been tracked to mutations in a gene that codes for a 49-kDa protein that has been designated as P. falciparum chloroquine-resistance transporter (PfCRT). The gene product of pfcrt is predicted to have 10 trans-membrane domains (Fig. 2) and to function in the digestive vacuole of the parasite (Martin and Kirk 2004). To date at least 16 resistant strains of P. falciparum have been identified, and all have a lysine to threonine substitution at amino acid position 76 (K76T). In addition, most if not all of the resistant strains have a second amino acid substitution at position 220. A number of additional polymorphisms at other positions have been documented, but are not believed to be implicated in drug resistance. The existence of these two mutations in pfcrt led Behe (2007) to conclude that both mutations were required in order to confer chloroquine resistance. Based on his calculations of the likelihood of two independent mutations simultaneously occurring in order to confer a new function (Behe and Snoke 2004, 2005) and his estimates of the likelihood of anti-malarial drug resistance (White 2004), Behe (2007) went on to coin the term Chloroquine Complexity Cluster (CCC) to refer to those biochemical changes that would require two simultaneous mutations in order to show any change in protein function. Behe (2007) calculated the likelihood of a CCC event as being in the neighborhood of 1 in 1020, although some of the assumptions he relies on have been challenged (e.g. Lynch 2005). Behe (2007) concluded "On average, for humans to achieve a mutation like this by chance, we would need to wait a hundred million times ten million years. Since that is many times the age of the universe, it's reasonable to conclude the following: No mutation that is of the same complexity as chloroquine resistance in malaria arose by Darwinian evolution in the line leading to humans in the past ten million years." (Behe 2007). In reaching this conclusion he commits several errors of logic, most significantly with his initial assumption that mutations at both positions 76 and 220 are required to confer chloroquine resistance.

At the time of the publication of The Edge of Evolution, there was already evidence that this assumption was deeply flawed. Lakshmanan et al. (2005) had already demonstrated the essential contribution of the K76T substitution to chloroquine resistance by showing that wild-type levels of chloroquine susceptibility could be obtained by using allelic exchange between mutant and wildtype strains. The defects in the probability estimate by Behe (2007) became even more apparent when, less than a year later, Jiang et al. (2008) demonstrated that the single amino acid substitution at position 76 was both necessary and sufficient to confer chloroquine resistance. They conclude that "Mutations in PfCRT … particularly the substitution at amino acid position 76 (a lysine to threonine substitution) confer chloroquine (CQ) resistance in P. falciparum. Point mutations in the homolog of the mammalian multidrug resistance gene (pfmdr1) can also modulate the levels of CQ response." (Jiang et al. 2008). While the substitution at position 220 enhances resistance, it is not essential. Thus, the idea that two mutations in pfcrt had to occur simultaneously in order to confer a significant selective advantage for Plasmodium was simply not true. This was known in 2005, as noted above, yet Behe (2007) did not cite Lakshmanan et al. (2005). Indeed, this pattern of cumulative effectiveness in drug resistance mutations in Plasmodium is the rule, not the exception. For example, resistance to the anti-malarial cycloguanil is partially conferred by several independent single amino-acid substitutions (Le Bras and Durand 2003). These substitutions are often additive if present in the same organism, but each is sufficient to confer resistance in isolation as well. Because mixed infections involving more than one resistant strain would be fairly common in areas with a high incidence of malaria, it would be startling from an evolutionary standpoint if strains containing multiple protective mutations did not arise in relatively short periods of time.

What is most troubling is that the ID community continues to hold up Dr. Behe as a shining example of a credentialed scientist even as he demonstrates extraordinarily bad scholarship (Forrest and Gross 2007). While he remains a professor of biochemistry who is clearly capable of conducting rigorous research, he has largely abandoned the peer-review process that guides the scientific community. The flaws in Behe's model of simultaneous vs. two-step mutations have been pointed out by many (Carroll 2007a, 2007b; Durrett and Schmidt 2008), yet he repeatedly brushes aside such criticisms (Behe 2009) and fails to acknowledge other examples of step-wise drug resistance in Plasmodium that were published nearly a decade before his book (Sirawaraporn et al. 1997). Rather than proving to be an example of an irreducibly complex system that could not have arisen through evolutionary processes, chloroquine resistance is instead revealed to be yet another example of how a naturally occurring mutation can confer selective advantage and quickly become fixed in the genotype of a population of protists (Nagesha et al. 2003).

[eversbane]

Originally Posted by SteveF

This paper has some really cool stuff in it. There's an excellent smackdown of Behe:

In his book "The Edge of Evolution: The Search for the Limits of Darwinism"Behe (2007) draws heavily upon the example of drug resistance in the malarial parasite Plasmodium falciparum as one biochemical pathway that is supposedly too complex to have arisen through natural evolutionary processes. According to Behe (2007), the odds that mutations required to impart chloroquine resistance in Plasmodium could arise naturally are so impossibly long that they lie beyond what he considers "The Edge of Evolution."

To the casual observer it might appear that he has a valid point. Since its first widespread use in the 1940s, the anti-malarial compound chloroquine has proven to be remarkably effective in treating individuals infected with Plasmodium. Chloroquine's mode of action is believed to interfere with the parasite's ability to sequester heme in the biologically inert crystalline form known as hemozoin. By binding to Fe(II)-protoporphyrin IX (FP), chloroquine forms a complex that can disrupt the functioning of the food vacuole membrane of the parasite, ultimately killing it. Beginning in the late 1950s, chloroquine-resistant strains of P. falciparum, the most dangerous and therefore most often treated of the four species of Plasmodium that infect humans, were separately reported from Thailand and the Colombian–Venezuelan border (Hyde 2007). By the late 1980s, resistance had spread throughout much of Asia, South and Central America, and all of sub-Saharan Africa. Presumably, a new mutation, which conferred resistance to this anti-malarial drug, had arisen in P. falciparum, driven by the strong selection pressure of widespread chloroquine treatment.

The ability to resist chloroquine has now been tracked to mutations in a gene that codes for a 49-kDa protein that has been designated as P. falciparum chloroquine-resistance transporter (PfCRT). The gene product of pfcrt is predicted to have 10 trans-membrane domains (Fig. 2) and to function in the digestive vacuole of the parasite (Martin and Kirk 2004). To date at least 16 resistant strains of P. falciparum have been identified, and all have a lysine to threonine substitution at amino acid position 76 (K76T). In addition, most if not all of the resistant strains have a second amino acid substitution at position 220. A number of additional polymorphisms at other positions have been documented, but are not believed to be implicated in drug resistance. The existence of these two mutations in pfcrt led Behe (2007) to conclude that both mutations were required in order to confer chloroquine resistance. Based on his calculations of the likelihood of two independent mutations simultaneously occurring in order to confer a new function (Behe and Snoke 2004, 2005) and his estimates of the likelihood of anti-malarial drug resistance (White 2004), Behe (2007) went on to coin the term Chloroquine Complexity Cluster (CCC) to refer to those biochemical changes that would require two simultaneous mutations in order to show any change in protein function. Behe (2007) calculated the likelihood of a CCC event as being in the neighborhood of 1 in 1020, although some of the assumptions he relies on have been challenged (e.g. Lynch 2005). Behe (2007) concluded "On average, for humans to achieve a mutation like this by chance, we would need to wait a hundred million times ten million years. Since that is many times the age of the universe, it's reasonable to conclude the following: No mutation that is of the same complexity as chloroquine resistance in malaria arose by Darwinian evolution in the line leading to humans in the past ten million years." (Behe 2007). In reaching this conclusion he commits several errors of logic, most significantly with his initial assumption that mutations at both positions 76 and 220 are required to confer chloroquine resistance.

At the time of the publication of The Edge of Evolution, there was already evidence that this assumption was deeply flawed. Lakshmanan et al. (2005) had already demonstrated the essential contribution of the K76T substitution to chloroquine resistance by showing that wild-type levels of chloroquine susceptibility could be obtained by using allelic exchange between mutant and wildtype strains. The defects in the probability estimate by Behe (2007) became even more apparent when, less than a year later, Jiang et al. (2008) demonstrated that the single amino acid substitution at position 76 was both necessary and sufficient to confer chloroquine resistance. They conclude that "Mutations in PfCRT … particularly the substitution at amino acid position 76 (a lysine to threonine substitution) confer chloroquine (CQ) resistance in P. falciparum. Point mutations in the homolog of the mammalian multidrug resistance gene (pfmdr1) can also modulate the levels of CQ response." (Jiang et al. 2008). While the substitution at position 220 enhances resistance, it is not essential. Thus, the idea that two mutations in pfcrt had to occur simultaneously in order to confer a significant selective advantage for Plasmodium was simply not true. This was known in 2005, as noted above, yet Behe (2007) did not cite Lakshmanan et al. (2005). Indeed, this pattern of cumulative effectiveness in drug resistance mutations in Plasmodium is the rule, not the exception. For example, resistance to the anti-malarial cycloguanil is partially conferred by several independent single amino-acid substitutions (Le Bras and Durand 2003). These substitutions are often additive if present in the same organism, but each is sufficient to confer resistance in isolation as well. Because mixed infections involving more than one resistant strain would be fairly common in areas with a high incidence of malaria, it would be startling from an evolutionary standpoint if strains containing multiple protective mutations did not arise in relatively short periods of time.

What is most troubling is that the ID community continues to hold up Dr. Behe as a shining example of a credentialed scientist even as he demonstrates extraordinarily bad scholarship (Forrest and Gross 2007). While he remains a professor of biochemistry who is clearly capable of conducting rigorous research, he has largely abandoned the peer-review process that guides the scientific community. The flaws in Behe's model of simultaneous vs. two-step mutations have been pointed out by many (Carroll 2007a, 2007b; Durrett and Schmidt 2008), yet he repeatedly brushes aside such criticisms (Behe 2009) and fails to acknowledge other examples of step-wise drug resistance in Plasmodium that were published nearly a decade before his book (Sirawaraporn et al. 1997). Rather than proving to be an example of an irreducibly complex system that could not have arisen through evolutionary processes, chloroquine resistance is instead revealed to be yet another example of how a naturally occurring mutation can confer selective advantage and quickly become fixed in the genotype of a population of protists (Nagesha et al. 2003).

Damn. I thought that was going to be a video showing an actual smack down.

[supersport]

nice quote mines in your sig, stevef

[supersport]

Originally Posted by RedRuth

From this months Journal of Eukaryotic Microbiology

And they use some examples to debunk ID, for example

And there's another article entitles, Using Protistan Examples to Dispel the Myths of Intelligent Design Hopefully at least some of them are open access

http://www3.interscience.wiley.com/j...118000394/home

this is a joke, right? darwinists spent decades ignoring/downplaying HGT....and now that it's coming out that HGT contradicts neo-darwinism, they're not only trying rewrite history, but lying about reality. The fact is, HGT is a direct assault on ToE, a theory that says only populations evolve genetically, which gets debunked by HGT, not to mention the fact that organisms genomes are individually adaptive, responsive, and changeable.

In regards to intelligent design, HGT only passes genes along, it is not an originator of genes, much less a random generator. Why must so many darwinists lie?

[ericmurphy]

Originally Posted by supersport

this is a joke, right? darwinists spent decades ignoring/downplaying HGT

"Darwinists" discovered HGT, you fucking half-wit.

....and now that it's coming out that HGT contradicts neo-darwinism, they're not only trying rewrite history, but lying about reality.

Oh, really? How does HGT "contradict" evolutionary theory? You have no fucking idea. It just sounds good to your retarded ears.

The fact is, HGT is a direct assault on ToE, a theory that says only populations evolve genetically, which gets debunked by HGT.

How does HGT "contradict" the notion that populations evolve? You have no fucking idea. It just sounds good to your retarded ears.

In regards to intelligent design, HGT only passes genes along, it is not originator of genes. Why must so many darwinists lie?

Intelligent design has nothing intelligent to say about HGT. Or anything else, for that matter. It just appeals to retards like you.

[VoxRat]

Originally Posted by supersport

...
this is a joke, right? darwinists spent decades ignoring/downplaying HGT...

I have an hypothesis that (1) you're lying, and (2) you know full well you're lying.
Let's test my hypothesis, shall we?
If I'm wrong, you will produce a citation that backs up your assertion.
If I'm right, you won't.

<----- (The smiley I use when I'm pretty sure no response is forthcoming)

[Entropy]

Originally Posted by supersport

this is a joke, right? darwinists spent decades ignoring/downplaying HGT....and now that it's coming out that HGT contradicts neo-darwinism, they're not only trying rewrite history, but lying about reality. The fact is, HGT is a direct assault on ToE, a theory that says only populations evolve genetically, which gets debunked by HGT, not to mention the fact that organisms genomes are individually adaptive, responsive, and changeable.

In regards to intelligent design, HGT only passes genes along, it is not an originator of genes, much less a random generator. Why must so many darwinists lie?

Why should HGT and Evolution be mutually exclusive? Could organisms not have evolved the capacity to incorporate genes from their environment? Seems like a pretty fricking good way to increase the information in your genome.

Here are 1800 papers with the search "horizontal gene transfer" AND evolution Yeah, we're totally ignoring it...

[RedRuth]

This is how much sporty doesn't understand HGT and endosymbiosis. From another forum

supersport
Forum Member


Join Date: May 2006
Location: Ft. Worth Texas
Posts: 23,774
supersport has disabled reputation

Quote:
Originally Posted by RedRuth View Post
Can you actually read sporty? The OP is about Common Descent, the ToE is the best explanation for the mechanism of Common Descent. Do keep up sporty it's not that difficult.
she swings she misses! funny how you avoid every one of my points.

but I'll humor you -- What is your evidence that this mechanism is a mechanism of common descent....in otherwords...what is your evidence that this mechanism could turn a bacteria into a human over time?

And ruth, you need to learn something, and this is very important so listen up: Your ONLY adaptive mechanism, the ONLY mechanism of materialism is RMNS. The rest of them are mine....the rest of them point away from materialism and directly towards saltationism, lamarckism and intelligence. This is the cruel, cruel reality for you. So don't go stealing my mechanisms -- endosymbiosis is my mechanism, not yours. Your side has been fighting HGT and endosymbiosis, non-selectionist mechanisms (lateral exchanges of genes and genomes) for decades, and I'm not about to let you start using them now as some sort of evidence that a monkey can turn into a human. You get RMNS and that's it: that's the mechanism of gradual cumulative selection, of which Richard Dawkins promotes, it's the mindless "watchmaker" mechanism of neo-darwinism, it's the only materialistic mechanism on the planet. I'm sorry you don't have any instances of it happening -- that's your problem, not mine....but keep your grubby hands off my intelligent, cooperative, saltationalist mechanisms and stop playing like they validate your revolting selectionist hypothesis of adaptive gradualistic, accidental, mindless genetic change, of which no one has ever validated even once.

[VoxRat]

Originally Posted by RedRuth

This is how much sporty doesn't understand HGT and endosymbiosis. From another forum

That sort of says it all, doesn't it?

[SteveF]

sporty sounds a bit like Gollum when he's talking about HGT.

[ck1]

Olivia Judson had an interesting piece yesterday about protists and their reproduction:

http://opinionator.blogs.nytimes.com...olivia-judson/

She stopped short of discussing the very odd mechanics of how the macronucleus is reconstructed after sexual reproduction.