Evolution of complexity/information

An initial DNA sequence with ATG:atctaggtattaatccgATGactgctatgcttaacgtcgtAdd a base upstream of ATG:atctagCgtattaatccgATGactgctatgcttaacgtcgtAnd the ATG (and the rest of the sequence) downstream of the inserted base is unchanged.Perhaps you have the misconception that the DNA is "read" from start to finish to produce proteins? This is not the case - the transcription machinery reads the genes one at a time - hence the need for promotors and the ATG start codon to designate the start of each individual gene. Thus a sequence change in one gene does not effect the sequence of another - to hijack your example:we went down to the seashoretowes went down to the seashoreThe addition of a letter changes the word "we" while not effecting "seashore".Hopefully this was helpful.

Another mechanism of an "increase" in genetic information that I don't think has been mentioned in this thread: gene duplication followed by divergence.Many dismiss gene duplication as simply resulting in two copies of the same gene, as opposed to providing new information. However, the two copies can then undergo different mutation and selection, and thus result in two genes producing two proteins with different activity.We see evidence for this in "gene families", that is closely related genes that produce proteins of similar structure or function, but that are divergent and specialized to produce a net complexity of activity not present in the original gene from which the family descended. The Hox genes mentioned above are part of one such family.In many cases what we think of as "lower organisms" have only a single version of a gene, while "higher" organisms have homologs in large gene families.Another method to create new genes is duplication followed by rearrangement - this can essentially take two genes and hybridize parts or entire genes to produce a gene of new function.In any case, gene duplication followed by subsequent change is a valid mechanism to add genetic information. Since the original gene function is not necessarily lost (it is a copy that is changing), I believe this may better fit your idea of increasing information.

I'm not sure that you've quite got it from your example. (I think you meant ATG by your capital ATC). If you have already got it figured out, well, ignore this:The ATG does not tell the translation machinery when to stop, another set of codons do that (TGA, TAG, and TAA). The ATG start codon sets the reading frame, so that a change in front of the ATG leaves the gene sequence downstream of the ATG is unchanged (only gene-sequence should be thought of as codons). However, a change after the ATG will result in a change in the gene sequence.Another example, ATG = start, TAG or TAA = stop, only gene sequence (bold) is in codon form: Only the insertion into the gene sequence itself causes a frameshift, in this case making a longer transcript of different codons. It is longer because the translation will continue until a stop codon is reached.

Perhaps you've answered your own question - "natural selection" and "all that nature can throw at them" are essentially the same thing.Species must adapt to "all that nature can throw at them," that is the basis of "natural selection." Since they are the same, they are equivalently "powerful."This might seem like wordplay, but it really isn't - it is part of the simplicity of natural selection.

No problem... This seems to be a common misconception - just because detrimental mutations are more likely to occur, does not mean they are more likely to accumulate within a species' gene pool.By the definition of "detrimental", the individual organisms carrying a "detrimental" mutation are far less likely to survive and reproduce, and therefore a detrimental mutation is less likely to "accumulate."On the other hand, beneficial mutations, though rarer, give an individual organism a better chance to survive and reproduce than the rest of individuals in it species. Thus the rare beneficial mutation is more likely to accumulate.Always keep in mind that we are talking about individual organisms within the environment, usually competing with each other for resources and mates. Occasionally an individual will have a beneficial mutation, occasionally another will have a detrimental one. Beneficial and detrimental mutations do not arise in all members of a species at once, and therefore there is no reason to believe that beneficial and detrimental mutations somehow "accumulate" within a species simply based on the probability of each mutation.Hopefully that made some sort of sense....

This is precisely the problem with trying to assign a complexity value to an organism, for I could just as easily say, canines have more complex social structure and interactions, and a more acute sense of smell than cats, and are therefore more complex. Either way it's an apples-and-oranges argument.In a way I agree that it is easier to assign complexity to features. As an example, my dogs have webbed toes and an extra, clear set of eyelids as adaptations to desert hunting, so perhaps an argument could be made that their eyes are more complex than a dog without such structures.Even feature-by-feature analysis has its issues - are slitted eyes really more complex than non-slitted eyes? I don't think it is quite that simple, and I see problems with even a semi-quantitative measure of complexity in this way.When it comes to quantifying complexity, is a webbed foot equivalent to a clear eyelid as a complexity "unit"?Perhaps complexity via a genetic route is a better measure, since we could measure numbers of genes in a gene family, or number of promoters per gene, or number of gene-gene interactions. But this also has its problems - fruit flys and nematodes have one Erbb gene, mammals have four Erbb genes, minnows have sixteen Erbb genes. But all this really describes is Erbb complexity, so it is like your "features" idea, except at a genetic (quantifiable?) level.We would really need a complete understanding of every genetic interaction in the genome of two organisms to create a complexity comparison.Sorry - I've realized I've rambled quite a bit, and contributed little to a working definition. Since we can't go back and witness evolution, perhaps there will always be a bit of imagination involved (just as a theory can never be proven). However, all of the pieces are there:Scientists have witnessed/established:
- mutation
- gene duplication events
- gene rearrangements
- the creation of novel hybrid genes with novel function
- frame-shift resulting in a completely novel gene with novel function
- speciation
- genome-level analysis that follows gene-by-gene evolution within a genusAt this point, it comes down to whether or not you believe DNA-based paternity tests, since essentially the same concept is used to establish ancestry of a species as is used to determine ancestry of a child.

Me too - your reply reiterated what I was trying to get across... though I could see how my point might have got lost...The one part that confuses me: Your "did they?" question and DNA pattern answer seems to require using ancestry concepts ("the past") - what am I missing here?(As a clarification - my point in bringing up the ancestry tests was to state: describing relatedness of species (or comparison of genetic complexity; or description of evolution at genetic level) by DNA sequence analysis is usually considered a "leap of faith" by many anti-evos; even those that accept both the genetic changes in my bulleted list, and DNA-based paternity tests.)

Right - Hangdawg already agreed to the processes more than once, that's why I wasn't sure why you were still arguing them. Since we've established the processes, aren't we at this point?
That's why I was taken aback with the "it just doesn't matter about the past" comment.I think we're arguing but saying the same thing - no need to respond unless I'm way off...

Hangdawg - thanks for the open discussion. Perhaps you are correct when it comes to witnessing the evolution of a novel structure with interoperable features (this is very close, though, to the near impossible idea of having a mutation-by-mutation record of the entire tree of life).However, it seems you have no problem with individual features arising from genetic changes, so we already have the possibility of an individual set of parts to work from in building a interworking complex of features. So in a way it gets back to the old statement that for those that deny macroevolution, 1+1=2, and 1+1+1+1+1+1=2 also - though in your arguments we'd have to add the caveat that 1+1+1+1+1+1 arises in an interworking manner.From your statements your position seems to be: Light sensitive cells could have evolved, a lens could have evolved, but the evolution of a lens focusing light on the light sensitive cells is difficult to accept. (Please correct me if I'm wrong - I don't want to put words in your mouth.) Nosy already covered this, and I'd just reiterate that at the genetic sequence level we do often have this kind of sequence. An inability to fossilize soft-tissue may have something to with not having evidence of these at a structural level.However, there is another important point regarding the A to B transition - sometimes there are NO intermediates:- Recently a study found that a myosin point mutation unique to humans could have caused the homo skull to switch from quasiconcave to convex in a single generation - giving us room for our great big brains. Because it was such an acute transformation, no intermediate forms are expected.- Similarly, humans have a unique mutation in a gene called FOX2P that may have granted them language ability. (A few rare families exist carrying mutations in FOX2P to give an "ape-like" sequence - those with the mutation have nearly non-existent language abilities, both spoken and written.)- A recent paper using the stickleback fish and mice showed that rearrangement of promoters can result in appearance/disappearance of limb structures in a single generation.- Also, think about the hyper-muscled boy (carrying a myosin mutation) that was recently born - he likely has some pretty drastic secondary changes in his skeletal and cardiopulmonary systems that his parents do not have.- Imagine a mutation that causes overexpression of a basic growth hormone - an organism could literally double in size from one generation to the next (this experiment has been done artificially in transgenic mice).All of these examples serve to show that a single mutation can result in quite massive and complex changes from one generation to the next with no transition observed or expected. If you'd like references to the primary literature I'll try to dig them up... There is a field of study some call "regressive evolution," where organisms lose structures in the absence of selective pressure. The best example I can think of is the cavefish - cavefish have lost both their eyes and their pigment, since there was no selective pressure to keep them (this would fall under the "removal of non-essential changes"). Everytime we see an animal with a congenital defect rendering it incapable or unlikely to breed, we have evidence of removal of detrimental changes.In fact, many miscarriages in humans serve as examples of removal of detrimental changes (especially those actually tested to show the underlying genetic defect). Similarly, children born with childhood cancer syndromes are also examples.It is much, much easier to witness the culling of detrimental mutations than the establishment of a beneficial one in a population.