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See, here's the problem. You've thrown aside standard information theory, which has proven it's usefullness and applicability in many fields (as well as showing it works quite well) and replaced it with some <I>other</I> version of information theory.
It's worth noting the differences:
1) Standard Information Theory. It's been around for several decades. It's been used in several fields (rather heavily in computing), is rigorous, well-defined, peer-reviewed and has basically shown itself to be a very useful, very accurate way to define and measure information. Under Information theory, at least this sort, evolution constantly adds new information.
2) Creationist Information Theory. It's brand new. It's not being used anywhere but Creationist literature. It's not peer-reviewed. It's never been applied to any field but biology (not computer science, not telecomunications, nothing). It lacks a rigorous way to define and measure information. According to CIT, evolution does not add new information.
Now, hmm...which version is more trustworthy when it comes to evolution? The one invented for telecomunications, taught and studied in universities all over the world? Or the one created by people with an ideological opposition to evolution, used only on evolution, and claims evolution doesn't add information?
how so? explain please
how do you know that an increase in information (by your definition) is required? you don't, you're merely asserting that it is so.
One of the above articles shows that co-option of existing developmental genes may have been responsible for the evolution of the vertebrate head - simple changes in expression of existing genes
The funny thing is, by the creationist definition, God designing life couldn't qualify as "new information"...
creationist definitions always start with the assumption that evolution is false:
macroevolution - a form of evolution which is impossible (details change according to this first premise)
information - used in concert with the definition of macroevolution, the creationist definition of information is basically that which cannot arise via evolution (details change in accord with this premise)
kind - a classification of types of animals which form a distinct "kind" that are incapable of evolving into other "kinds" - if any speciation or evolution occurs to produce new types of animals , by definition, it is merely change within a kind
Wrong again. Kind def= any set of animals possessing a common ancestor. If animal x and animal y possess a common ancestor, then x and y belong to the same kind.
Simply because specifying new body plans (birds have wings, reptiles do not, addition of wings is a new body plan) requires new information.
Thanks for the definition. Now please show that there exists one more "kind" of life... I think the evidence weighs strongly against the notion that there is more than one "kind" of life, as each organism seems to have shared a common ancestor with each other organism at some point in the past.
changes in existing gene expression can change morphology, so strictly speaking this is false.
But duplication and divergence (the expansion of the hox cluster) can add information anyway.
Originally posted by Matthew
Addition of information def= if for any organism x that is a ancestor of organism y: organism y possesses body plan p in its genotype AND organism x does not possess body plan p, then organism y has new information that it has gained.
And I have yet to see any proof for this assertion.
What exactly do you mean by a "body plan"?
The problem is that you're saying "I've never seen anyone build a brick wall", and whenever people show you a few bricks mortared together, and the way in which another brick can be added, you insist that, if we can't find a single step where we went from "no wall" to "wall", that no information was added, even though we can show "before" and "after" pictures, as well as a mechanism.
Big steps, in this case, consist of lots of little steps.
duplications happen, divergence happens - this can create genes with new functions
an analogy (that i've used numerous times)
cat
(duplication)
cat + cat
(divergence)
cat + mat
duplication provides redundancy which reduces the selective constraint on the genes and allows them to diverge to have new functions
the hox cluster expansion for instance:
Hox A gene
duplication
Hox A + Hox A
divergence
HoxA1 + HoxA2
which are expressed in different regions and have different downstream targets
I fail to see how that could be anything other than new information.
(would an entire genome duplication represent new information?
1: Arch Neurol 2002 Mar;59(3):474-7
Related Articles, Links
Unequal crossing-over in unique PABP2 mutations in Japanese patients: a possible cause of oculopharyngeal muscular dystrophy.
Nakamoto M, Nakano S, Kawashima S, Ihara M, Nishimura Y, Shinde A, Kakizuka A.
Laboratory of Functional Biology, Graduate School of Biostudies, Kyoto University, Yoshida Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
BACKGROUND: Oculopharyngeal muscular dystrophy (OPMD) is an adult-onset autosomal dominant muscle disease with a worldwide distribution. Recent findings reveal the genetic basis of this disease to be mutations in the polyA binding-protein 2 (PABP2) gene that involve short expansions of the GCG trinucleotide repeat encoding a polyalanine tract. The underlying mechanism causing the triplet-expansion mutation in PABP2 remains to be elucidated, although the DNA slippage model is thought to be a plausible explanation of that. METHODS AND RESULTS: We analyzed PABP2 using polymerase chain reaction analysis and DNA sequencing in Japanese patients with pathologically confirmed OPMD, and found mutated (GCG)(6)GCA(GCG)(3)(GCA)(3)GCG and (GCG)(6)(GCA)(3)(GCG)(2)(GCA)(3)GCG alleles instead of the normal (GCG)(6)(GCA)(3)GCG allele. These mutated alleles could be explained by the insertions or duplications of (GCG)(3)GCA and (GCG)(2)(GCA)(3), respectively, but not by the simple expansion of GCG repeats. The clinical features of our patients were compatible with those of other Japanese patients carrying PABP2 that encodes a polyalanine tract of the same length, but were not compatible with those of Italian patients. CONCLUSIONS: The mutated alleles identified in our Japanese patients with OPMD were most likely due to duplications of (GCG)(3)GCA and (GCG)(2)(GCA)(3) but not simple expansions of the GCG repeats. Therefore, unequal crossing-over of 2 PABP2 alleles, rather than DNA slippage, is probably the causative mechanism of OPMD mutations. All mutations that have been reported in patients with OPMD so far can be explained with the mechanism of unequal crossing-over. On the other hand, comparison of the clinical features of our patients with those of other patients in previous reports suggests that specific clinical features cannot be attributed to the length of the polyalanine tract per se.
1: J Hum Genet 2002;47(3):140-5
Related Articles, Links
Ethnic divergence and linkage disequilibrium of novel SNPs in the human NLI-IF gene: evidence of human origin and lack of association with tuberculosis susceptibility.
Ma X, Wright J, Dou S, Olsen P, Teeter L, Adams G, Graviss E.
Department of Pathology, Baylor College of Medicine, Houston, TX 77030, USA.
Sequence variation in the human genome has been used as a tool in studying human diseases and the evolutionary history of man. A human inherited predisposition to tuberculosis has been suggested and studied; however. genetic mechanisms are still ambiguous. In the present study, we scanned the regulatory and coding region of Nuclear LIM Interactor-Interacting Factor gene (NLI-IF), which is physically close to the tuberculosis-associated gene NRAMP1. Thirteen biallelic single-nucleotide polymorphisms (SNPs) were identified from four ethnic populations (African-American, Caucasian, Hispanic, and Asian) with population-specific distribution of alleles. The extent of linkage disequilibrium (LD) between 402T > C, and 472- 42G > A varied distinctly from complete LD in the non-African-American groups to strong but incomplete LD in African-Americans. Both SNPs were in significant LD with the polymorphism 3' UTR in NRAMP1 among these ethnic groups (P < 0.02), except 402T > C in African-Americans. In a case-control study with a Caucasian population, three cosmopolitan SNPs (204C > A, 402T > C and 472 - 42G > A) in NLI-IF showed no significant association with human susceptibility to tuberculosis. Our results support the "out-of-Africa" model of human origin, and suggest the time for the common ancestor dispersing from Africa could not have been more than approximately 385,620 years ago.
PMID: 11950066 [PubMed - indexed for MEDLINE]
This example is not analagous to your previous one as it is both complex and unintentional!
If a new function had actually arisen without the intervention of an intelligent agent, then you would have a point. But I still see no evidence of this.
Your reference assumes that:
1) Common ancestry is true AND
2) No intelligent agent ever intervened.
But historical evidence could never prove (2), and (1) I find quite doubtful.
Natural examples of changes of the sorts equivalent to adding a brick have been shown all over the place.
duplications happen -
divergence happens
duplication + divergence is the most parsimonious explanation for the intragenomic homology that we see. Especially considering we have living examples of pre and post duplication organisms and we know that the additional genes in the post duplication organisms affect morphology
exactly, NDT
duplication and divergence can both occur independently of intelligence as witnessed in the above references (there are dozens of articles on duplications, and probably thousands on divergence) - the most parsimonious explanation for the data is therefore NDT. You can insert intelligence in the gaps if you want, but theres no evidence that it was required
historical evidence could never disprove (2) either.
Evidence we have today suggests that complexity can arise via the NDT algorithm independent of intelligence. The question is whether intelligence was "needed" for the diversity of life. I believe the answer is no, NDT is capable of what the IDists attribute to intelligence
If you doubt (1) then theres a thread way back that provides compelling evidence for common ancestry in the form of the "urate oxidase pseudogene" theres also a link in there to the chromosome challenge
Originally posted by Matthew
I see no reason to believe that duplication and divergence can produce information.
Well, I would certainly be interested in this evidence.
From 1972 through 1996 I worked on the experimental evolution of a new enzyme in E. colias a model for understanding how organisms evolve new functions. Strong selection applied to large populations allowed that new enzyme function to evolve as the result of spontaneous mutations in a previously unknown gene.
Originally posted by Late_Cretaceous
"I am still waiting for their evidence that they can produce a grape from a fig tree. Or was it a olive from a grape vine?"
That would be cool. However, I don't see what impact it would have on evolution one way or the other.
This is something we have to deal with in our Bible.
Romans 11:17 And if some of the branches were broken off, and you, being a wild olive tree, were grafted in among them, and with them became a partaker of the root and fatness of the olive tree,
The Hebrews were the origional tree. But as branches they were cut off of their own tree so that the gentiles could be grafted in. But the roots do not change the branches and the branches do not change the roots. Even though they can grow together.
Originally posted by JohnR7
[BThe UCSD team, which included Matthew Ronshaugen and Nadine McGinnis, showed in its experiments that this could be accomplished with relatively simple mutations in a class of regulatory genes, known as<I> Hox"</I>[/font]
I think they got there spelling wrong on that. It is spelled Hoax.
"the scientists showed how modifications in the<I> </I>gene Ubxwhich suppresses 100 percent of the limb development in the thoracic region of fruit flies
You guys are just to funny. Thanks for the laugh. [/B]
Matthew, look at the first phrase._ Doesn't that sound familiar? It is the same phrase atheists use to dismiss deity "I see no reason to believe a deity exists."_ What you are expressing here is your personal opinion or stubborness, not whether the data actually shows the phenomenon.
Matthew, follow what I'm saying: increasing information in biological organisms is a TWO-step process._ 1. Mutations to provide the possibilities. Particularly duplicating genes and chromosomes to give you more DNA._ 2. Selection among the possiblities.
Enlighten me._ Show me how you separate the information in biological organisms from the DNA that it is stored on._ How can you have information in biological organisms without molecules?
Thank you for showing the shell game._ Natural selection can't increase information and then increasing DNA isn't increasing information.
Since you say increased DNA is not "necessarily" increased information, when is it? And when isn't it? And why for both?
I provided the "proof"._ The information equation. You haven't shown me that this is an erroneous equation._ Mutation increases the variation. But, according to the equations, it's selection that actually increases information.
If that is the case, then their argument is refuted because data shows it can happen. However, to preserve the "it can't happen" they then move on to systems that haven't been studied. For instance, Behe's orginal definition of IC was any system where removal of any component made it nonfunctional._ Examples included flagella._ When Miller showed that different species had flagella missing pieces of Behe's IC flagella, Behe has attempted to change the definition of removal of the right components.
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