Joined: Feb. 2006
|Quote (Southstar @ Nov. 27 2011,10:18)|
|Quote (OgreMkV @ Nov. 26 2011,08:44)|
Some help needed to fight behe's silly work.
Okay I have made the following case against this paper presented by the Tards. but before I write it down I want to check with you guys if I'm on track. I don't want to mess this part up.
here is the link to the paper:
Ioseb is using the paper in the following way:
He is arguing that, the paper proves beyond doubt that there are hardly any gain of FCT mutations. So evolution can't occur. So it's all wrong.
Here are my accusations:
1) The paper is limited in that it only analises bacteria and viruses. No eukyrots are analised. So how the hell can you say that it applies to life in general.
I don't think this is a compelling argument on your part. First, the paper does include eukaryotes. All the mutations discussed in Table 1 are in human genes. Second, even if the paper does focus mostly on prokaryotes, they still comprise the longest extant lineage, dating back some 2 billion years, and a huge range of distinct functions first arose in prokaryotes. So if Behe's analysis really presented a fundamental problem for evolution, even just in prokaryotes, that would be a significant issue. Fortunately, his analysis does no such thing.
|2) The paper is limited to artificial experiments in which the process of natural selection has been removed. The only natural case examined was malaria.|
I don't think this is a good criticism either. Even if most of the experiments involved selection in a lab environment, it's still a matter of some organism adapting to a new environment. The only real issue with lab-based studies, IMO, is that they're only able to assess evolution over periods of years to (at most) decades. They're not capable of directly observing the slow accretion of mutations and new functions that take place over thousands to billions of years. Naturally, the kinds of changes we see over ~ 10 years will look trivial compared to what can happen in 10 million years.
|3) Concerning the case Gain of FCT function i found a comment on a critic site: http://whyevolutionistrue.wordpress.com/2010.......w-paper |
stating that: "The construction by mutation of a new promoter, intron/exon splice site, or protein processing site are gain-of-FCT mutations. Also included in this category is the divergence by mutation of the activity of a previously duplicated coded element.” In other words, mutations in this category produce new genes, parts of genes, or confer drastic new capabilities on genes by adding new splicing sites.
Also note that because almost no bacteria or viruses have introns in their cellular genes, it’s impossible to even see one class of this mutation in lab experiments on these groups.
a) What does this last paragraph mean?
b) How does this relate to FCT gains?
c) Is there evidence to support this?
Eukaryotes often have their protein coding sequences broken into separate bits called exons, with non-coding sequences called introns in between each exon. Bacteria don't usually do this - their protein coding sequences are typically uninterrupted. Some types of FCT gains involve rearrangement of introns and exons. Since bacteria don't usually have those, they can't generate that type of FCT gain.
All that said, I don't think this is a good criticism either. As noted above, bacteria have unquestionably developed new functions over evolutionary time. Really complicated structures like ribosomes, flagella, replication complexes, transporter proteins, etc., etc., all arose in prokaryotes first. So one way or another, bacteria must have developed novel functions over time.
|4) Behe states regarding Lenskies experiments: |
If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.
Do we have examples of gain-of-FCT mutations in experiments similar to Lenskies?
Behe's paper already lists some mutations that he classifyies as gain-of-FCTs. See Tables 2 & 4.
|5) Is there a specific reason that has arisen in other papers as to why most of the experiments lead to loss of FCT? I would answer that it is only due to the experimenters removing natural selection from the equation. Would I be right?|
No, it's almost certainly because loss-of-FCT mutations are much more common than gain-of-FCT mutations. I can't readily offer a citation, but it's widely accepted that the vast majority of mutions in a protein coding sequence, for example, will either be neutral or deleterious to protein function. Only a few will enhance function or generate new functions (assuming we can agree on what a 'new function' really means). I don't think it's surprising that there will often be cases where a loss of FCT provides a selective advantage.
|6) The work is based on three organisms, prokaryotes, viruses and hemoglobin? |
Eukyrotes are not included in the study. Or does table 1 automatically include eukyrotes?
Table 1 exclusively lists human mutations that provide malaria resistance, so yes, it's about eukaryotes.
|7) Plasmodium falciparum (malaria) is a eukyrote but the genetic mutation that is being studied is of Hemoglobin not of the malaria. Is this correct?|
Hemoglobin and other genes in humans, yes.
|8) Isoeb makes the following case: The adaptation to Malaria is the sickle cell. Which is obviously due to FCT loss and leads to premature death. Only on extremely rare occasions do we get gain of FCT by Chloroquine Complexity Cluster or C Harlem. How rare is this gain let me tell you with C Harlem where the are two conections sites in the plasmid: it required 10^40 organisms to get this mutation. Seeing as there is only one known case.|
Want to know how many organisims are estimated to have been around since start of life on the planet? 10^40.
Do you know how may conection sites ther are in a cell 10.000.
Okay point one: I would say that he's making the stupid probability error again so I just fight this with the "evil killer dust bunny".
Point two: What has this got to do with anything???
I have to guess with this one, because Ioseb is talking gibberish. I have no idea what "connection sites" are supposed to be, and plasmids have nothing to do with either chloroquine or malaria resistance.
A quick google of "C harlem" reveals that it's a particular hemoglobin variant where the B chain has two different amino acid substitutions. Most likely, Ioseb is trying to make the argument that it's nearly impossible for both of those mutations to have arisen simultaneously in one person, given the known mutation rate and the likely number of humans that have ever existed.
If so, there are two huge flaws in his argument. The first is his assumption that no other single or double mutations would have afforded malaria resistance. But in fact we know that's wrong, as Behe's own Table 1 shows. Thus, it's not a question of the probability of getting exactly those two mutations at some time during human evolution. It's a question of how many possible combinations of mutations would confer resistance, and whether it's reasonable that at least some of them could have arisen by chance during human evolution.
The other huge flaw is that Ioseb seems to be assuming that both mutations would have to arise at the same time in the same person. But that's obviously wrong. Nothing prevents one mutations from occurring and spreading through the population, before the second mutation occurs. And here's the kicker: it turns out that one of the two mutations in hemoglobin C harlem is the same mutation seen in conventional sickle cell disease. And we already know that lots of people have only that one mutation, and that that mutation alone confers malaria resistance. So it's easy to imagine that the sickle mutation happened first and spread to many individuals due to conferring resistance. The second mutation could have happened at some later date. Maybe the second mutation adds some additional selective advantage. (I didn't see anything about that either way in my brief search.) If so, that would be a perfect example of how evolution often works - incremental advantages adding on to previous ones.
|8) Ioseb calls my attenton to this site: www.ncbi.nlm.nih.gov/books/NBK7574/|
Saying that you see another study say exactly the same thing.
I looked at it and could find nothing of the sort...
Well, the first sentence of section 16.5.1 reads: "Making random changes in a gene is quite likely to stop it working, but very unlikely to give it a novel function." So Ioseb's point is probably again that gain-of-FCT mutations are uncommon. I already addressed this in my previous post: yes, but so what? Just because gain of function mutations are less common doesn't mean they don't happen (as even Behe acknowledges), and it doesn't mean they're too rare to support evolution. If Ioseb thinks they are too rare, he's going to need a lot more evidence than Behe's paper to make his case.
|9) My main argument is that okay so he saw loss of FCT functions in controlled environments in a few species of bacteria and virus (except the malaria) sooo what?|
Exactly. Evolution clearly requires gain-of-FCT mutations, so if we never saw such mutations in lab studies, that might raise some questions. But we do see such mutations, so that's all fine. The fact that we see more loss-of-FCT mutations isn't a problem for evolution.
|Thanks for your imput on this|
You're welcome. I hope that's helpful.