Michael Behe in Peer-Reviewed Journal!

grass, What I find interesting about that is that Dr Behe's paper deals with scientific evidence and that other paper deals with a straw man and is devoid of content. Joseph

does anyone else find it interesting that the following paper is also going to be published in the same volume? "Irreducible Incoherence and Intelligent Design: A Look into the Conceptual Toolbox of a Pseudoscience" grass

Thanks BA77 for the Abel citing! scordova

Here is Luskin's second installment on Behe's paper: Michael Behe's "First Rule of Adaptive Evolution" Could Undermine the Evolution of Functional Coding Elements http://www.evolutionnews.org/2010/12/michael_behes_first_rule_of_ad041461.html bornagain77

This is a quote from Casey's article about the paper:

Behe argues that we do not generally observe the evolution of new adaptive FCTs in the laboratory. Rather, when we observe adaptive evolutionary changes in the laboratory, they typically involve loss of function or modification of FCTs. This leads to the question, How do new adaptive FCTs arise?

Wouldn't a Darwinist argue that the modification of FCTs is exactly what leads to new adaptive FCTs? I can't access the paper yet, so I don't know exactly what Behe argues. uoflcard

here is a better link to the Genetic Selection principle: http://www.scitopics.com/The_GS_Principle_The_Genetic_Selection_Principle.html bornagain77

Dr. Anderson pointed out that even antibiotic resistance is mostly achieved via loss of function: Is Bacterial Resistance to Antibiotics an Appropriate Example of Evolutionary Change?

Evolutionists frequently point to the development of antibiotic resistance by bacteria as a demonstration of evolutionary change. However, molecular analysis of the genetic events that lead to antibiotic resistance do not support this common assumption. Many bacteria become resistant by acquiring genes from plasmids or transposons via horizontal gene transfer. Horizontal transfer, though, does not account for the origin of resistance genes, only their spread among bacteria. Mutations, on the other hand, can potentially account for the origin of antibiotic resistance within the bacterial world, but involve mutational processes that are contrary to the predictions of evolution. Instead, such mutations consistently reduce or eliminate the function of transport proteins or porins, protein binding affinities, enzyme activities, the proton motive force, or regulatory control systems. While such mutations can be regarded as “beneficial,” in that they increase the survival rate of bacteria in the presence of the antibiotic, they involve mutational processes that do not provide a genetic mechanism for common “descent with modification.” Also, some “relative fitness” cost is often associated with such mutations, although reversion mutations may eventually recover most, if not all, of this cost for some bacteria. A true biological cost does occur, however, in the loss of pre-existing cellular systems or functions. Such loss of cellular activity cannot legitimately be offered as a genetic means of demonstrating evolution.

scordova

scordova, do FCTs (Functional Coded ElemenTs) directly, or indirectly relate to Prescriptive information? If so how? and how does this relate to Dembski and Marks's COI and Sanford's Genetic Entropy? i.e. What is the coherent 'progressive' thread amongst them. notes: The GS (genetic selection) Principle – David L. Abel – 2009 Excerpt: Stunningly, information has been shown not to increase in the coding regions of DNA with evolution. Mutations do not produce increased information. Mira et al (65) showed that the amount of coding in DNA actually decreases with evolution of bacterial genomes, not increases. This paper parallels Petrov’s papers starting with (66) showing a net DNA loss with Drosophila evolution (67). Konopka (68) found strong evidence against the contention of Subba Rao et al (69, 70) that information increases with mutations. The information content of the coding regions in DNA does not tend to increase with evolution as hypothesized. Konopka also found Shannon complexity not to be a suitable indicator of evolutionary progress over a wide range of evolving genes. Konopka’s work applies Shannon theory to known functional text. Kok et al. (71) also found that information does not increase in DNA with evolution. As with Konopka, this finding is in the context of the change in mere Shannon uncertainty. The latter is a far more forgiving definition of information than that required for prescriptive information (PI) (21, 22, 33, 72). It is all the more significant that mutations do not program increased PI. Prescriptive information either instructs or directly produces formal function. No increase in Shannon or Prescriptive information occurs in duplication. What the above papers show is that not even variation of the duplication produces new information, not even Shannon “information.” http://bioscience.bio-mirror.cn/2009/v14/af/3426/3426.pdf http://www.us.net/life/index.htm Dr. Don Johnson explains the difference between Shannon Information and Prescriptive Information, as well as explaining 'the cybernetic cut', in this following Podcast: Programming of Life - Dr. Donald Johnson interviewed by Casey Luskin - audio podcast http://www.idthefuture.com/2010/11/programming_of_life.html bornagain77