What exactly is ID?

Would it be fair to include the following?Intelligent Design also claims that these signs of intelligence exist in biological species and in the fundamental properties of the universe.

If I may lend a hand here . . .You are missing out on a very important experiment, the Lederberg-Lederberg (a husband and wife team) plate replica experiment. You can read the original paper here: LinkWhat they did was start with a single bacterium. From that bacterium they created a lawn of bacteria descended from that single ancestor on an agar plate. This agar plate had the standard growth media and no antibiotics and was called the master plate. They transferred these bacteria to plates containing antibiotic using a stamp like instrument. What they found was that the antibiotic resistant colonies came from the same spot on the original plate. Even more, they could pick bacteria from this area on the master plate, grow more of them, and use these bacteria to create a new master plate. Lo and behold there were a lot more resistant colonies on the copied plates.What this showed is that they could increase the number of resistant colonies without the bacteria ever coming into contact with antibiotics. The resistant mutants existed in the absence of antibiotics. Also, they were clonal.This experiment, along with the Luria-Delbruck experiment, demonstrated that beneficial mutations occur in the absence of selection. That is, mutations are random with respect to fitness. And in fact, antibiotic resistance is due to changes in DNA. For example:"Spontaneous, streptomycin-resistant derivatives of Erwinia carotovora subspecies carotovora strain ATTn10 were isolated. Sequencing of the rpsL (encoding the ribosomal protein S12) locus showed that each mutant was missense, with a single base change, resulting in the substitution of the wild-type lysine for arginine, threonine or asparagine at codon 43. "
linkThese antibiotic mutants do not have the same genes as their ancestors. They have different genes.

How do you detect this?For example, which bases in this sequence are from the original and which have been added since then:1 atgtcttacg aagctatttg ggctaaaaat caaagactaa atgacgtaga aattataaaa
61 cttgaaaagg atggcttaga tgtaattgaa actataattg acaaatactc taaggaaggt
121 tatgattcaa taacgcctaa agatatgaat agatttaaat gggctggcgt ttacgaacaa
181 aagccaagag agggatactt tatgatgaga gttcgtatta attctggaat aatgacttca
241 gagcaagcaa aagttttagc agggattgct aaagattatg gacgtggaat tgcaaacgcc
301 tctacaagag gagctataca gtttcactgg gttcaggtag aagatttacc ttctatttat
361 gaaagattag aagcttgtgg cctaagtcct tttgaggctt gtggcgattg ccctagaacg
421 atagttggaa atcctcttgc tggaattgat aaagatgaac ttatggatac aactgaactt
481 gtagaacaag ttaataattt cttcttatta aacaaggatt tttctaattt accaagaaaa
541 tttaaaatat caatatcagc tagtatacat aatgcagctc atgcacaaat taatgatctt
601 gcctttactc cagcaacaaa aaaaattgat aatcaggacg taattggttt ccacgtatgg
661 gttggaggag gactttcagc aagccctcat ttagcacaaa aactagatat atttgttaaa
721 ccagaatatg tactaaaggt tgctgaaggt gtatgtacta tttttagaga ttatggatat
781 agggaaaaac gtactcgtgc ccgcttaaaa tttttagtag ctgactgggg agcagaaaaa
841 tttaagaata aattattaga atttactggg gatatgccaa gctcaggtga tgataaatta
901 gcttcatgga atgcatctta ttattttgga gtacattccc aaaatgaaga tggcaaaagc
961 tatattggtg ttagtttacc acttggagaa atcacttgtg atcaactttt agaacttgcc
1021 catatttcag aaaaatacgg agatagaaaa attagaacta cactatcaca aaatttaatt
1081 attacaggca taagtgatga agatatacct tctctattaa aaaaagatgt atttaaacaa
1141 ctttctccaa atccaagtat ttttacagga tacacaattt cttgtacagg taaagaattc
1201 tgtaatttag ccattgttga aacaaagaaa cgtgctaaag aagttatcga atatcttgat
1261 tctaaaatca aactagatac accgttacgt atccatttta caggttgtcc taattcttgt
1321 ggacaaaaac atatagctga tatcagcctc caaggtgcat taataaaaac cgaagatagc
1381 tgtgaggaag catttaccat atggcttggt ggtacactaa acaatggtgg gcagtttgca
1441 gaaaatctaa actaccgtgt aaaatctact gaggttcata tagttcttga gaaaataata
1501 actttctttg aaaaaagtaa gttagagaat gagactttta atgaatttat cgcaagagta
1561 ggaattagta aaatcacaga aaacatataa How do you know that DNA is not the exception to this rule? Can you please give an example using DNA sequence? What are the transmitters and receivers and how do they decide which conditions to choose?

This relates to Muller's Ratchet."The theory of Muller' Ratchet predicts that small asexual populations are doomed to accumulate ever-increasing deleterious mutation loads as a consequence of the magnified power of genetic drift and mutation that accompanies small population size."--sourceHowever, the evidence indicates two things. First, compensatory mutations arise which ameliorate the effects of slightly deleterious mutations:"Isolates encoding DRSeq3 also show lower ND5 deletion levels, though the difference as compared to those that encode DRSeq1 is not significant (P > 0.10, two-tailed t-test). When considered as groups, mean heteroplasmic deletion levels were higher in tropical-clade isolates (12.1%) as compared to temperate-clade isolates (7.3%), though the difference was not significant (P > 0.9, two-tailed t-test). We also analyzed fecundity variation with respect to the three sequence motifs and found that isolates encoding DRSeq2 displayed significantly elevated fecundity as compared to those encoding DRSeq1 (P < 0.001, two-tailed t-test) — see Figure 4C. Fecundities in isolates encoding DRSeq3 and DRSeq1, however, were highly similar and not significantly different (P > 0.1, two-tailed t-test). The relatively low ND5 deletion proportions and high fecundities associated with isolates encoding DRSeq2 are suggestive of compensatory mutation — in particular, the ND5-2 substitutions are expected to result in reduced interactions of directly repeated sequences in ND5-2 and ND5, thereby resulting in lower ND5 deletion incidences and higher fitness. However, we are again unable to account for the potential effects of nuclear loci."--same source as aboveSo the first mechanism to overcome genetic entropy are mutations which increase fitness. That is, beneficial mutations.The second mechanism is negative selection. That is, those with the highest deleterious mutation rate are selected against. This ongoing process stops Muller's ratchet."A decrease in nucleotide substitution rates over time suggests that selection may be limiting the effects of Muller's ratchet by removing individuals with the highest mutational loads and decreasing the rate at which new mutations become fixed."--sourceIn order for this to be an accurate analogy you need a source of selection.Edited by Taq, : No reason given.

Would a gain in specificity be a gain in specified information? Would a gain in function be an increase of specified information?

As you probably already know, this is why sexual recombination is such an important mechanism and the "cure" for Muller's Ratchet. When recombination puts several deleterious mutaitons in the same haploid genome this genome is strongly selected for resulting in selective sweeps of deleterious mutations.Using SO's CD analogy, imagine making two copies of the CD and randomly swapping bits between the copies. You then check both copies for errors and elimate the one with the most errors, or better yet eliminate the copies that fall below a specific QC level.Edited by Taq, : No reason given.

Then evolution necessarily requires a loss in information according to your definition. For example, both the chimp and human lineages lost information found in the original common ancestor. Chimps and humans are degraded, according to you. The same for all mammals (including humans) as they have degraded from the common ancestor of mammals. The same for all amniotes, all vertebrates, all eukaryotes, and ever single species since the last universal common ancestor. By extension, you are arguing that when an organism evolves from a simple state to a complex state this is a degradation event because the information for making a simple organism has been degraded.You have argued your way out of the debate. You claim that evolution requires new information, and yet observed instances of evolution do not produce this entity. Therefore, evolution does not require new information. You are out of the game. No it wouldn't, at least according to you. Any change from the original DNA sequence is a degradation.

The article claims that mammalian evolution trends towards larger body size in many lineages. Obviously, this isn't so in all lineages. Mice, for example, are quite small and they are . . . hmm, let me think . . . oh yes . . . MAMMALS. According to the paper, their population size prevents the accumulation of deleterious mutations compared to larger mammal lineages.

Our detector, in this case, is phylogenetic comparisons of DNA. This detector is capable of telling us "evolved" and "not evolved".For example, we can compare the genes of Glofish (link), jellyfish, and trout. What we should find, if evolution is true, is that the Glofish genes should more closely resemble that of trout than of jellyfish. What do we find? We find that this is false for certain genes. Why is that? Because these genes DID NOT EVOLVE. Glofish contain genes which are almost exact copies of genes found in jellyfish, but not found in trout. How did this happen? Through intelligent design. Humans moved genes from jellyfish into Glofish to make them fluoresce under UV lights.There you have it. A detector that can detect both evolution and not evolution. So what detector will tell us ID or not ID?

As the title implies, is this change in enzyme specificity an example of an increase in CSI?

quote:

---

J Biol Chem. 2009 Nov 6;284(45):30957-64. Epub 2009 Aug 26.

​

A single amino acid substitution converts benzophenone synthase into phenylpyrone synthase.
Klundt T, Bocola M, Ltge M, Beuerle T, Liu B, Beerhues L.

​

Institute of Pharmaceutical Biology, Technical University of Braunschweig, Mendelssohnstrasse 1, D-38106 Braunschweig, Germany.

​

Benzophenone metabolism provides a number of plant natural products with fascinating chemical structures and intriguing pharmacological activities. Formation of the carbon skeleton of benzophenone derivatives from benzoyl-CoA and three molecules of malonyl-CoA is catalyzed by benzophenone synthase (BPS), a member of the superfamily of type III polyketide synthases. A point mutation in the active site cavity (T135L) transformed BPS into a functional phenylpyrone synthase (PPS). The dramatic change in both substrate and product specificities of BPS was rationalized by homology modeling. The mutation may open a new pocket that accommodates the phenyl moiety of the triketide intermediate but limits polyketide elongation to two reactions, resulting in phenylpyrone formation. 3-Hydroxybenzoyl-CoA is the second best starter molecule for BPS but a poor substrate for PPS. The aryl moiety of the triketide intermediate may be trapped in the new pocket by hydrogen bond formation with the backbone, thereby acting as an inhibitor. PPS is a promising biotechnological tool for manipulating benzoate-primed biosynthetic pathways to produce novel compounds.

---

Adding to this, when sequences are treated in this arbitrary manner you also commit the Sharpshooter Fallacy. ATP synthase was not the target or goal. Rather, increased fitness was the goal. It is entirely possible that an enzyme catalyzing a different chemical reaction could have been found. Calcuating the odds of a specific enzyme arising through evolution misses the boat. You also need to add in every single amino acid sequence that would have increased fitness through a new metabolic pathway.The same applies to the flagellum. You need to find every single possible motility system in order to calculate the probabilities. Using an analogy, using the ID version of CSI the probability of anyone winning the lottery is 1 in 150 million or so. According to ID logic it should take 150 million lottery drawings before anyone wins.

So let me get this straight. Simple unicellular organisms are the acme of evolution while multicellular metazoans are just a degraded version of these unicellular organisms. Is that correct? But we observe evolution occuring and we do not observe what you define as new information. Obviously, evolution does not require this "new information" in order for it to proceed. You have argued your way out of the debate. I am assuming nothing. I make a prediction. I predict that if a gene descended from a common ancestor that a phylogenetic comparison should produce a nested hierarchy consistent with the morphological trees. As I have already shown the GFP gene in Glofish causes them to fail this test. We are testing FOR common ancestry, not assuming it.

Flawed? Your claims lead to a very serious problem. You claim that an accumulation of mutations, filtered through selection, which lead to a more complex organism constitute a loss of information. What about mutations that result in a different function?Edited by Taq, : No reason given.

The nucleotides in DNA are no more arranged for a specific effect than lottery numbers are drawn to get a specific winner. You are specifying after the fact.What we see with DNA is a continuous record of winners. The environment doesn't know which sequence of DNA to pick. The organism doesn't pick which mutations will be occur in it's germ line cells. The offspring doesn't choose which of these mutations it will inherit. The whole process of evolution is completely blind to DNA sequence, and it works just fine.Better yet, look at my avatar. Can you point to the bits of information in that picture? If you saw the same arrangement of string on the floor would you call it information? Better yet, if you saw my avatar represented with string next to the word "SOS" written in string which would you say contains information? Meet the Nylon Bug:http://www.nmsr.org/nylon.htmThis bacteria evolved a new enzyme capable of breaking down nylon oligomers. This new enzyme arose by the insertion of a single base resulting in a new reading frame.Can you explain why an insertion of a new base resulting in a new enzyme with novel function constitutes a loss in information?

It's not in the paper. If you notice the dates of publication these papers were written before DNA was fully understood. Nonetheless, their observations (i.e. the Lederbergs, Luria, and Delbruck) were spot on. They observed the emergence of a new, beneficial mutation in the absence of selection for that mutation. It is an unavoidable conclusion from the data.Since then the mutations are well understood. For bacteriophage resistance, the mutations which confer this phenotype occur in the tonB gene (ton refers to T-1 phage, the phage type used in the original Luria-Delbruck experiment). For antibiotic resistance there are a host of different mutations which confer resistance, and these occur at the same rate whether or not the antibiotic is present. It's not as if the bacteria have an antibiotic sensor protein that automatically mutates a specific region of DNA when it senses antibiotic. Then evolution does not need a gain in information in order for it to occur. All evolution needs is a change in variation due to mutation, and that is exactly what is observed. If we were to observe every mutation occuring from the first life to current humans you would conclude that every single DNA change is a loss in information. You might as well claim that you need to see magical gravity pixies in order to accept that planes can fly. Evolution works just fine without needing an increase in what you call "information" just as a plane flies just fine without magical gravity pixies.Edited by Taq, : No reason given.