Hi TheWay,
Sorry to take so long to get back to you.
The others have given some pretty good replies to your questions on information but I'll give you my view as well.
What is it? How can it be measured? Can it be measured?
Bioportals definition is fine as far as it goes but it doesn't give us any idea how to measure genetic information. The commonly used metrics are those already mentioned, Shannon's formulation and Kolmogorov complexity. There is an extensive literature showing how these techniques have been applied to genetic sequences and none of them, other than perhaps some which have shades of ID about them, i.e.
Abel and Trevors' papers and Dembski's own work, suggest that there is any genetic barrier to genetic information change in any direction.
EO Wilson writes:
Artificial selection has always been a tradeoff between the genetic creation of traits desired by human beings and an unintended but inevitable genetic weakness in the face of natural enemies.
Far be it from me to disagree with EO Wilson but I would say here that until recently it has been outside the ability of artificial breeders to 'create' desired traits, they have only been able to select for them. And since humans can select traits entirely unconcerned, except in extreme cases, with their side effects on the populations fitness they will be more prone to breeding strains with weaknesses one would not expect to see propagated under natural selection in the wild.
All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not to increase it.
A point mutation could either increase, decrease or maintain the information depending on the specific mutation and the surrounding sequence. There is certainly nothing in what you have related of Spetner on information that would suggest otherwise and certainly nothing in the scientific literature.
believe he states that there is a switch type mechanism in the genome that activates certain things or deactivates certain things and that this system is what ultimately governs mutations. Is that right? If not I'll go back and read it more carefully.
No, that is not right. There are certain biological systems which repair DNA and correct some mutations and some organisms do show variations in their mutational rate in response to environmental stress but I can't think of anything which would fit the description you have just given.
Anyways he states that "new" information, like what the NDT requires for macroevolution, can only be added by a binary like system. Such as one bit at a time. I could have got that screwy, anyways lets move on to some examples he gives.
I don't think NDT has any such requirement for macroevolution.
Resistance of bacteria to antibiotics and of insects to pesticides. He states, "Some bacteria have built into them at the outset a resistance to some antibiotics." This resistance results from an enzyme that makes the drug inactive and this doesn't build up through mutation. He then cites J. Davies as proposing that the purpose of this particular type of enzyme had a completely unrelated primary function. Basically, a lucky side effect. He also cites a study done on antibiotics and how they are the natural products of "certain fungi and bacteria." Which we should expect to see some natural resistance to. Also non resistant bacteria can become resistant by picking up a resistant virus and the virus may have picked up the gene from a naturally resistant bacteria. Apparently, scientists can genetically modify organisms to become resistant.
OK, either Spetner has no idea what he is talking about or you have misunderstood him. Certainly there have previously been bacteria which were resistant to a variety of antibiotics well before humans started using antibiotics. Without a reference for Davies hypothesis I'm not sure what you mean, however I have seen a paper in which he suggests that horizontal gene transfer of enzymes for the transport and processing of certain antibiotics from the fungi that produce them to bacteria could confer antibiotic resistance although he himself has subsequently suggested that the evidence does not support this hypothesis.
As for 'viruses' I think either you or Spetner are getting them mixed up with plasmids. Plasmids are spread quite promiscuously through bacterial populations and can certainly confer antibacterial resistance, but the genes in the plasmids still have to originated somewhere.
None of this however controverts the fact that we can see antibiotic resistance derive
de novo in populations which previously did not show resistance and that this resistance can be traced back to genetic differences between the current population and the original population and in which the acquiring of plasmid based resistance can be ruled out.
The more specific the system or code, the more information it would contain. When it a gene's specificity is reduced by a mutation the information is lost to the subsequent generations. So based on this, how can an organism gain complexity yet lose specificity and ultimately information?
This is where you need a way to measure information exactly how Spetner intends it, because in terms of gentic information as we have discussed it previously it is nonsense. The subsequent function of the sequence is entirely irrelevant to it's genetic informational content.
As it happens the whole argument seems specious since Gartner and Orias actually say that by decreasing the rates of transcription of only mutant forms of the
amber and
ochre codons the resistant strains ribosome actually shows higher specificity (
Gartner and Orias, 1966).
Spetner claims, with help from a citation, that a change in an amino acid often affects the way a protein functions. So with resistances, the loss of specificity would result in a degradation of the organism in other ways.
A change in an amino acid certainly
can change a proteins function, but there is no reason why that change shouldn't increase specificity. Nor is there any evidence supporting the idea that a loss of specificity should degrade the organism, or that the degradation if there was any would be greater than the advantage the mutation conferred.
What about the bacterium phlagellum? Also, wouldn't it be required to have an abundant amount of information to start with, for any system to even reduce? And doesn't this seem unlikely given that the evidence is tentative for macro-evolution?
What about it? Without a clear working definition of what is IC how can we tell it is IC? For a start a flagellum will work with some components missing, IC propenents have to go to a certain core flagellar system to even demonstrate a functional form of IC, i.e. the loss of any protein component would lead to a total loss of function.
There is no reason why there couldn't have been much more information, bacteria can duplicate genes and larger genetic tracts just as easily as other organisms, not to mention the possibilities plasmids confer.
You would have to support your contention that there is only tentative evidence for 'macro-evolution' and you also probably have to tell us what you mean by macro-evolution as it certainly doesn't seem consistent with the way the term is used in evolutionary biology.
If there wasn't an introduction of the antibiotics, would the mutation have been neccessary or relevant, or would it have persisted?
That is the whole point that the beneficial nature of a mutation is highly dependent on its environmental context, the mutation probably wouldn't have been neccessary, relevant or persistant if it hadn't been for the introduction of the antibiotic to the environment but I don't see how this relates to what you said previously. The antibiotic being introduced doesn't create the mutation, it just allows it to spread and flourish, but we do know that the mutation was not present in the original population.
I believe he leans more towards point mutations, although I am unsure of what you mean by "large scale gene duplications." He talks about gene duplications, but it is rather limited. This book was pressed in 1998, if that matters.
He probably does as they are the smallest changes an consequently will probably reflect the smallest informational change by most criteria. Being published in 1998 makes no difference duplications at the gene, chromosome and whole genome level have been documented for decades.
It doesn't seem very likely that two de novo beneficial mutations could possibly occur in a population. Wouldn't natural selection have to select both of these and then would at some point these mutations have to "mate."
Or am I completely confused?
Why ever not? A large population will have large numbers of mutations between generations and a proportion of those will be beneficial. If the mutations are beneficial in their own right then they might well be maintained long enough either for the further beneficial mutation to arise or for mating to bring the two traits together.
But since I still don't know what
you mean by 'active cumulative evolution' its hard to answer.
lso, could you comment on how things like the sonar-like systems in bats and whales are similar
They are functionally similar in that they use echolocation to hunt, I don't think the genetic bases of the systems is similar.
I think the similarity is good evidence of design, now I know you disagree but without similarity we couldn't assimilate our environment which encourages me to think that that was the plan.
I'm not sure what you mean by assimilate. If you mean that without the same sort of amino acids, sugars and fats we wouldn't be able to eat and survive you are right but there is no reason that these things require similar genetic sequences and genes even if they require the same genetic framework, i.e. DNA.
Like UFO's? Some could argue using the same reasoning. It's a bit of a stretch, but hey might as well point it out.
Only if they don't understand the difference between repeated direct observation and anecdotal evidence.
I just don't understand how randomness can create such highly organized complexity.
Because randomness is not the only factor at work.
TTFN,
WK
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