Theism, Intelligent Design, and Science

Remove all ads!

Ah, Climbing Mount Improbable. They talked about this. Dawkin may know his evolutionary biology, but he doesn't know his cellular biology (not that I think he ever claimed to). This was specifically an attack on evolution from the cellular biology side. The issue is that, on the macroscopic scale, it's a lot easier to have minor modifications to a system still be functional, because minor modifications can be, well, minor. The issue in cellular biology is that any modification must come at a certain level or higher (protien). The claim is that anything short of a complex, organized mass-mutation would fail to produce a viable system, thus harming the creature and reducing it's odds of reproduction dramatically.

 

Wrongg!

Not dramatically. There are several mutations in hemoglobin, as we know, a complex protein. One of these mutations produce sickle-cell anemia, which does reduce the fitness of the organism, but not nearly dramatically enough to make carriers of the harmful mutation to become extinct.

But oh yeah, this just a prime example of a macroscopic mutation being harmless...it's not that anyone'd die from anemia.

 

AND it provides an advantage in malaria infested areas.

 

Hm, I wonder if this abstraction from Michael J. Behe's research would interest anyone:

Of course this is only an abstraction. It is interesting however, how in this discussion (and in this abstraction, if not the research as well), or in discussions like these epigenetics is overlooked as if non-existent. Basically, one thing what epigenetics make possible is a dramatical increase of mutations. Especially in single-celled organisms.

 

It's been a while since I've studied this, but I do not find such a suggestion implausible. The cilia obviously needs some mechanism that allows it to remain attached to the organism.

But that simply isn't true. A mutation does not have to confer a benefit for it to be preserved in a species genome, it just cannot do something that decreases the organism's chances of passing its genes on. Heck, even severely deleterious mutations can (and if fact are) preserved in species genomes due to heterozygote viability (an example of which Iku stated).

Every person - and for that matter every organism - on the planet has mutations that don't do anything positive for them, but also don't harm the organism's chances of passing these mutated genes to future generations. In fact, that gene expression is so consistent throughout all forms of life, from DNA replication, to protein formation, to even cellular division is a strong arguement in favor of evolution, as it suggests a common thread of life.

 

That sounds like something my father told me once ... oh yes, he also called me a bum (American version of the word meaning "vagrant or loafer" -- he could have meant the English version as well...).

 

Do you mean the British version? I mean, you're an American, but you speak English...

 

My, aren't we getting picky; but yes, British version.

 

Hey, here's a wikiarticle on Behe

 

1.) That's an example of a mutation on the protein level. It changes one hemaglobin protein into another, thus replacing one protein with another.
2.) As Faye pointed out, it's a functional system under some environmental pressures.
3.) It isn't extinct in humanity because it's managable with extreme care and medications. In most wild animals, this isn't likely to happen and individuals with sicle cell anemia typically don't fair well.

It is highly debatable whether epigenetics can play any feature in overall evolution at all. Even those features that can be passed on from one generation to another typically die out over successive generations. In essense, it's a temporary change only, not a permanent one. By pure coincidence it may help a creature survive through non-profitable genetic mutations, but that's relying on even more chance and isn't likely to be a consistent mechanism.

If that's the case, then the 'simpler' cillia aren't actually simpler at all. They still rely on the same number of different types of proteins, it's just which proteins it needs that are different.

To expect that to preserve a non-functional mutation until it becomes functional, then activate it, then spread that activated, homozygous mutation to a species seems a bit of a stretch. Still, it does add a level of complexity to the issue.

It's highly suggestive of a common thread of life, but so is DNA by itself. That doesn't necessitate evolution, though.

Yeah, I don't really trust Wikipedia, and this issue has only reinforced that distrust. You see, the Wikipedia page for the book only mentions the experts interviewed as things like 'ID advocate' and 'Theologian' and ignores all their professional credentials. To break it down (bolded is Wiki, italicized is added):

Intelligent design advocate, Discovery Institute Center for Science and Culture (CSC) fellow and Unification Church theologian Jonathan Wells presents a case against evolution; Double Bachelor's from University of California in geology and physics, with a minor in biology, Doctorate from Yale in religious studies, Doctorate from Berkeley in molecular and cell biology
Intelligent design advocate, CSC fellow and philosopher of science Stephen C. Meyer discusses the relationship between science and religion, as well as the origin of life, arguing against the likelihood of abiogenesis without the assistance of a creator; Degrees from Cambridge University in physics, geology, history, and philosophy, Doctorate Degree from Cambridge in history of molecular biology, history of physics, and evolutionary theory
CSC fellow and philosopher of religion William Lane Craig discusses the Big Bang and argues for a creator as first cause, invoking the Kalam cosmological argument; Doctorate from University of Birmingham in philosophy, Doctorate from University of Munich in theology Only consulted on philosophical issues
International Society for Complexity, Information and Design fellow and philosopher Robin Collins discusses the anthropic principle and argues that the universe must be designed by a creator; Triple major from Washington State University in physics, mathematics, and philosophy, Doctorate from University of Texas in physics
Intelligent design advocates and CSC fellows Guillermo Gonzalez (an astronomer); Double major from University of Arizona in astronomy and physics, Master's and Doctorate from University of Washington at Seattle in astronomy, professor at Iowa State University
and Jay Richards (a theologian) present a case that the Rare Earth hypothesis supports intelligent design; Honorary Doctorate from Princeton in philosophy and theology
Intelligent design advocate, CSC fellow and biochemist Michael Behe discusses irreducible complexity in biology as an argument for a creator;Bachelor's from Drexel University in chemistry, Doctorate from University of Pennsylvania in biochemistry, postdoctorate research at University of Pennsylvania and National Institutes of Health, professor at Lehigh University
CSC fellow, philosopher and theologian J.P. Moreland examines the supposed existence of consciousness separate from the brain, including near-death experiences, as an argument for a creator; Bachelor's from University of Missouri in chemistry, Master's from Dallas Theological Seminary in theology, Doctorate from University of Southern California in philosophy

All have published numerous articles in various professional and scientific journals, and all have either pubblished or co-published numerous books, yet the Wiki review would make you think these were hacks off the street. This is a perfect example of why and how I don't trust Wikipedia.

 

nevermind....

 

My thoughts exactly.

 

NOG, it's not the same proteins that drive the motor mechanism of cillia as attach the cillia to the membrane - they are different proteins. Therefore, the non-motile cillia have the attachement proteins, while the motorized one have the attachment proteins and other ones, thus the non-motile cilia are less complex. Proteins are coded for in the DNA, and so the ones with non-motile cilia lack the gene that generates that protein.

There is no need for a mutation to become homozygous to be spread. That is the entire concept behind heterozygous viability. It's also reasons why certain severely deleterious mutations (like hemophilia) haven't been eliminated from the population - because the heterozygotes are fine.

And you don't have to "activate" genes. Either you got them, or you don't.

 

Sorry, I meant 'activate' by having two of them. If you've only got one, and it's recessive, it's 'inactive'. If you have two of the same, it's 'active'.

As for the cillia, I thought there were only three pieces. Are you saying the motive ones have four?

 

OK, this was just a terminology issue. In Genetics, you don't refer to genes as being active, but expressed. The reason for the difference is that activation refers to the point on a chromosome that is like a start marker for where transcription RNA attaches to the chromosome and begins the copying process. Sorry for the confusion - you have to remember that I'm a biochemistry geek.

There's actually even more than four, as with the exception of the cillia itself, none of the other proteins are monomers. But in short, yes, the attachment piece has a different shape that allows the cillia to move. In fact, it's shaped similar to a cork screw, allowing it to spin.

 

Then this should be an interesting read:

http://linkinghub.elsevier.com/retrieve/pii/S0092867407001213

or this:

http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000530

I'll dig up some more articles if you want, but later. I'm in a bit of a hurry at the moment...

 

The first one refused to show up, but the second was interesting. It still doesn't show that epigenetics can influence DNA mutation in a reliable form, but it does suggest that we may need to expand the model of evolution from one of DNA to one of DNA+Epigenetics if such traits are found to often be stable. This may even help to explain the sudden jumps that modern evolutionary theory has had so much trouble with, if these Epigenetic factors can be more drastic in impact.

 

These miaght be interesting as well:

The problem with a self-adaptative mutation rate in some environments: a case study using the shaky ladder hyperplane-defined functions

Does Mutation Rate Depend on Itself? Especially the reference to the study of Cairns and Foster should be quite interesting, similar findings have been noted in single-celled organisms in other studies. Which is, to put it shortly, that microbial mutation rates increase during stress conditions.

This article at least seemed to be very good and through cross examination of the subject The Evolution of Mutation Rate in Finite Asexual Populations

So, to summarize this a little:

Yes, there are some interesting bits that need to be straightened out when one starts to consider evolution.

It still is a general misconception that evolution affects species. This is not the case, as Dawkins at least has pointed out in The Selfish Gene.

Mutations are and are not random, at least not in single-celled organisms. Epigenetics should be definitely be considered crucial to evolution, since they not only control the rate of mutations, but possibly also in which parts of the genome those mutations might occur.

Transposable genetic elements should be taken into account, especially in single-celled organisms, but also in multicellular organisms. What's more, transposable genetic elements that travel between the boundaries of species (which is rather hazy already as it is).