I mean, they talk for about 10-15 pages about the happening of life in ancient-earth oceans, then about how bacterias evolved into fish, to ampibians, etc. from dinosaurs to birds, from australopithecus to humans, etc.
Let's just take a step back and look at the big picture. Let's take a look at humans and chimps.
Are the differences between humans and chimps due to a difference in DNA? Yep, they sure are. Already we can show that changing DNA does not result in a non-functional organism, and can result in well adapted species too boot.
When looking at the chimp and human genome, how much of a difference is there? Depends on the comparison. Of the DNA stretches that humans and chimps share the sequence is about 98% identical. That is, out of every 50 bases there is one point mutation. But what about the whole genome? Overtime genomes can gain and lose DNA also known as insertions and deletions (indels for short). When these are part of the comparison there is an overall similarity of 95%.
So the question that must be posed to those critical of evolution is this. Of the differences between humans and chimps, which CAN NOT be produced by the observed mechanisms of mutation? I know of none. For me, these simple premises lead to an unavoidable conclusion. There is nothing stopping evolution from evolving humans and chimps from a common ancestor.
I like this explanation, can I quote it for future reference? It will avoid creationists muddling the issue with their "information theory".
Quite right. The "muddling" occurs when their model runs into reality. As Dr. Adequate says above:
quote:A look through the reviews of it suggests that he has a theoretical argument that what we observe can't happen and what we never observe must. It reminds me of the (apocryphal) story of the scientists who claimed to have proved that bees can't fly.
When a model claims that something is impossible, and that impossible thing is observed to happen, then we should chuck the model.
When creationists claim that no new information can be produced through mutation then there are only two options:
1. All life contains the same amount of information.
2. The creationist model is wrong.
This is made plain by the fact that different morphologies are produced through changes in DNA. The question is how those changes got there, as it pertains to the Evo v. Creo debate. The problem with the creationist model is quite obvious. It lacks a pragmatic explanation of the facts.
However, genetics and the genome of a replicating population is not a matter of sending messages between two parties. You see, some additional information has been added to the theory to use it in discussing genetics.
A good example of that is Tom Schneider's program EV which treats a DNA binding protein and a DNA binding site as the reciever and transmitter.
How do genetic systems gain information by evolutionary processes? Answering this question precisely requires a robust, quantitative measure of information. Fortunately, 50 years ago Claude Shannon defined information as a decrease in the uncertainty of a receiver. For molecular systems, uncertainty is closely related to entropy and hence has clear connections to the Second Law of Thermodynamics. These aspects of information theory have allowed the development of a straightforward and practical method of measuring information in genetic control systems. Here this method is used to observe information gain in the binding sites for an artificial ‘protein’ in a computer simulation of evolution. The simulation begins with zero information and, as in naturally occurring genetic systems, the information measured in the fully evolved binding sites is close to that needed to locate the sites in the genome. The transition is rapid, demonstrating that information gain can occur by punctuated equilibrium.
Man and chimp differ by at least 150 million nucleotides, representing at least 40 million hypothetical mutations. So if man evolved from a chimp-like creature, then during that process there were at least 20 million mutations fixed within the human lineage (the other 20 million being in the chimp lineage). This means you have to fix over 3 mutations per year in the population (considering the divergence 6 millions years ago). Even considering generations of 1 year, this is, at best, unrealistic. (human generations are currently 20 years)
Haldane had calculated in 1957, that it takes, on average, 300 generations to select a single mutation to fixation in a population. Although I agree there has been revisions of his calculations in the past fifty years, there are no actual numbers that come even close to the fixation rates needed. All the fixations not done by selection have to be done by genetic drift, which is way slower then selection.
Not all mutations are point mutations. You must also factor in indels. If a 100 base indel becomes fixed you are fixing 100 bases all at the same time.
So to answer your question, even if we assume that mutations can create the different information between chimps and humans, even the evolutionnary time scale is not long enough to allow for such massive changes, unless you assume impossible fixation rates.
As others have shown, the mutation rate needed to produce the differences seen between humans and chimps is pretty close to the mutation rate observed in humans as others have pointed out.
1. Muller's ratchet can be overcome through recombination. While bacteria are considered asexual they do exchange DNA on occasion.
2. Beneficial mutations can compensate for deleterious mutations. This is exactly what was found in this study:
quote:However, we also observed the accumulation of putative compensatory mutations (DRSeq2) in temperate-clade C. briggsae lineages (Figure 4) that likely reduce ND5 deletion levels. The DRSeq2 mutations can only be considered beneficial, however, in the context of the preexisting deleterious øND5-2 insertion mutation – in fact, virtually any mutation in øND5-2 that reduces its homology to ND5 is likely to be beneficial to some extent.
In other words, mutations that compensate for the deleterious mutations will be selected for.
3. A genome can only handle a certain amount of deleterious mutations. At some point new deleterious mutations will be face strong selective pressures. This appears to be the case in the primary endosymbiots of lice (this study).
quote: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. This countering effect of selection could slow the overall rate of endosymbiont extinction.
So it would seem that there are at least 3 mechanisms by which asexual genomes can avoid the effects of Muller's Ratchet.
Information theory is concerned solely with the problem of transmitting sequences of bits from one point to another.
So what is this problem? From my understanding, the problem is how to get a message between the sender and receiver and have the sender's message understood.
So for DNA, what is the sender and who is the receiver? You need these parameters in order to apply information theory, if my understanding is correct.
Cavediver, being a physicst, and you Percy, a software engineer, we've all done these things, we know given another hour or so we will be able to reduce the amount symbols on the sheet. What you are telling me is that no intelligence is required.
If you are using software to compare with DNA then you are missing an important mechanism, descent with modification passed through selection. If the software language is as malleable as DNA sequence then it is enitrely possible to remove unnecessary code from the program without an intelligence. Just allow for random changes, including deletion of code (just as DNA deletions occur), and then select on the basis of function.
Going even further, we can also look at a comparison between computer hardware and biological hardware. I've only done a tiny bit of programming, but I have done enough to know one thing, the computer will blindly follow instructions no matter what the consequences of those instructions are. The genetic systems of life are EXACTLY like this. The ribosome does not come up to a specific codon and proclaim, "I can't attach this amino acid because it will cause disease". The ribosome is an automaton just like the computer. It will carry out it's tasks blindly, without knowing or caring about the consequences. The same goes for each of the processes within genetics, from replication to transcription to translation.
So what really imparts information into DNA? The usefullness of it's function just as it is with computer programs. If a computer program does not work we throw it out. The same for organisms. If the organism does not function in a given environment it is chucked.
So it is the environment that inputs information into the genome through selection. Variation in information is created by mutation. No intelligence required.
There are additional ways of answering the question, but I think these are the most obvious. Hopefully there's no reason why creationists wouldn't look at it the same way.
I would add a 3rd option as the most important. Since DNA is always spoken of as a code with four letters, 3 codons, and so forth it is important to relate these to the actual chemical reactions.
For making a cell work the sender is DNA, the reciever is ribosomes. The intermediate communication transfer system is the transcription of RNA template from DNA.
So I guess you can break it down into cell function (my 3rd option), fitness (your first option), and change in populations (your 2nd option). In order for anyone to discuss information as it relates to DNA and evolution they need to be specific on these issues. Sadly, such specification (pun intended) is lacking most of the time.
The amount of information in the dna and mdna, I suspect, is related to the number of base pairs.
That causes serious problems then. According to this measure a random, non-functional 2,000 base pair stretch of DNA carries more information than a functional gene with 1,000 base pairs.
The entire TOE is hypothetical...please.
The entire TOE is a collection of hypotheses that have passed testing.
Tiktaalik is a fish and archaeopteryx is a bird. There is not one single shred of evidence that they had a baby that was an amphibian or that their parent was a dinosaur, respectively. Any suggestion is pure speculation.
The hypothesis is that if a lineage of lobed finned fish evolved into amphibians that there had to exist species that had a combination of lobed finned fish features and amphibian features. This is exactly what we observe in Tiktaalik. The same for Archaeoptyrex with it's combination of avian and non-avian dinosaur features. Another example of a hypothesis that passed the test.
So the hypothesis should also explain the bizarre appearance of this egg-laying, venomous, duck-billed, beaver-tailed, otter-footed cute little mammal;
Sure. I bet you that the platypus jaw is completely mammalian and completely unlike an actual duck's bill. I bet you that the lower jaw is made up of a single dentary bone. I bet you that the jaw is even home to specialized mammalian cheek teeth. I even bet that the platypus has a multiple bone middle ear that is derived from reptilian jaw bones. Want to find out who is right?
As for egg-laying, the platypus lays reptile-like leathery eggs, kind of what one would expect due to the fact that mammals evolved from basal reptiles.
As for the tail, beavers are hardly the only species with a flat tail and such a small change in morphology is not that hard to evolve in separate lineages.
As for webbed toes, there are humans with webbed toes. It's a very common variation in a ton of mammalian species.
Test with the bar set really low.
Since when is a fish with legs a low bar? Are you saying that we should not see a fish with legs if tetrapods evolved from lobed finned fish?
You might lose that one --- platypods have lost most of their teeth (some people will tell you that they're completely edentate, but as far as I can make out they're wrong).
quote:Scanning microscopy of platypus teeth Anatomy and Embryology, Volume 174, Number 1 / April, 1986
Keith S. Lester1, 2 and Alan Boyde1, 2
(1) Westmead Hospital Dental Clinical School, Westmead, N.S.W., Australia (2) Department of Anatomy and Embryology, University College London, London, United Kingdom
Accepted: 15 November 1985
Summary Anorganic unerupted developing teeth and airdired erupted teeth of the platypus (Ornithorhynchus anatinus) were examined in a scanning electron microscope and in a tandem scanning reflected light microscope. Typically mammalian developing fronts of enamel and dentine were identified in the anorganic unerupted specimens. The developing teeth were particularly small and fragile and the enamel elusive and difficult to examine in the normal way for morphological detail. Prepared fractured surfaces of unerupted specimens revealed preferentially oriented crystallite groups in the enamel generally perpendicular to the developing front and a highly globular, mineralized pattern in the dentine with fine diameter, sparsely distributed dentinal tubules. Although optically homogeneous, the enamel of both developing and mature teeth displayed well-defined incremental lines, radial clefts, crystallite domains of variable size and outline, and fine tubules when examined by high contrast, back-scattered electron imaging. The enamel is prismatic only in part; well-formed, regular prisms not being a primary feature of platypus enamel. This can be related to the variability inherent in the developing surface and the thinness of the enamel layer. No surface was found which could be confidently identified as cementum; those developing surfaces not covered by enamel displaying small calcospherites which elsewhere marked the outer aspect of the dentine.
I had read about ERV's but didn't realize fully how directly involved they are in turning switches on and off, moving genes around that function without killing the host.
You must also remember that this is exactly what the viral genes evolved for. Bookending the viral genomes are the long tandem repeats which serve as strong promoters for the viral genes that sit between them. This is how the virus hijacks the host transcription machinery to produce more virus. Then you also have the viral reverse trascriptase gene which makes DNA copies from the viral RNA. You also have viral integrase genes that are involved in inserting the viral genome into the host DNA. There are also viral envelope genes that are involved in making viral particles that are capable of binding to other cells (which may explain why these genes are important in placental development).
So we can see that the roles these genes evolve into within the host genome are very similar to their original roles as part of viral replication and infection.
The life that lives around the deep sea vents live at a pressure level that would make eukaryotes explode. How is it that there are creatures living down there? They apparently are not eukaryotic life forms so what are they?
All of the multicellular animals you see around deep sea vents are eukaryotes.
What really gets a person is the difference in pressure. This is a big problem for us because we need air spaces within our bodies. No such problem for aquatic life. The pressure between the outside of their bodies and the inside is the same, so no pressure differences. This prevents the body from being crushed.