Joined: Nov. 2011
|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.
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.
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?
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
Do we have examples of gain-of-FCT mutations in experiments similar to Lenskies?
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?
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?
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?
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???
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...
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?
Thanks for your imput on this
"Cows who know a moose when they see one will do infinitely better than a cow that pairs with a moose because they cannot see the difference either." Gary Gaulin