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Author | Topic: Are mutations enough to explain natural selection? | |||||||||||||||||||||||
Peter Member (Idle past 1479 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
Surely if 'bird 10' can catch more fish, it can support
more young than a 'bird 9' individual, and so make a greater contribution to the gene pool by virtue of larger numbers of offspring.
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Peter Member (Idle past 1479 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
It depends what you mean by redundancy ...
I think you are referring to redundancy in the'triple redundancy' sense in which you have a number of working alternatives so that if one goes wrong there is a back-up. P.Borger means 'unused' or 'non-functional' when he says redundant. This only requires a modification/mutation that adds a stop orstart without creating a dead critter ... some might contend that that is impossible and that's another debate. There is a New Scientist article recently that suggests thatthese may not even BE redundant (in PB's terms) but functionalstepping stones in the chain of events leading to protein synthesis.
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Peter Member (Idle past 1479 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
quote: Apologies for the mis-definition ... all I was trying to dowas point out to Fred that his use of redundant was not the same as yours ... which still stands. I was not suggesting that you felt that such 'redundancy' wasa back-up mechanism, but that the meaning Fred ascribes to that word is suggestive of a common engineering approach to fault tolerance. To be a little pedantic, I don't think 'fitness' is what youmean above. To assess the 'fitness' of a phenotype one needs detailed knowledge of the environment with which that phenotyped organism interacts. I think 'viability' would have been a better choice of word. The problem with the 'rate of change' reasoning that you havepresented, for me, is that if the so-called 'junk' regions (a usage which I know is falling from favour) are actually some kind of place-holder (for example) for a wider mechanism then without knowing exactly which chain of events they are used in we can make no comment on whether the change rates observed are expected/unexpected. We need to know the function of these regions to predict whatchange rate we would see under the NDT model. To be honest I feel, and I have stated this before, that withouta more detailed model of how the genotype is related to the phenotype we cannot complete the picture in any case.
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Peter Member (Idle past 1479 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
quote: Which makes it even worse, since you were assuming a definitionby pointing to the msdata web-site. 'Redundancy as an approach to fault-tolerance'
quote: So we don't need genetics to proove design then since wehave two kidneys but can survive with one? What makes you believe that redundancy cannot developvia natural means? quote: But once one is 'knocked out' you loose 'safety function',meaning that the 'system'is no longer 100% operational. P.Borger is suggesting that there is NO impact on fitness(well in a lab. environment anyhow ... hmmm wait a minute doesn't changing the environment change the 'fitness'?) quote: If you knock-out a gene in the lab. and the organism is still viablethat does not mean it is equally fit for it's natural environment as it was. There is a difference between 'viability' and 'fitness'. The former is soley about the individual, while thelatter is about the relationship of the idividual to the environment. Again, P.Borger does not mean redundant in the sense oftwo sequences capable of performing the same function.
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Peter Member (Idle past 1479 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
quote: Having just read the paper (link posted by SLPx) by Dr. CaporaleI would agree that she has provided detailed explanation of features of DNA sequences that can lead to a higher or lower rate of mutation at any particular location. I have not disagreed with this, and niether has anyone else I have seen taking a counter-view to your NRM posts. What I have contended is that your choice of defintion of'random' is not that used in NDT, nor indeed that used by Dr.Caporale. 'Random' in the NDT sense is intended to mean 'not in directresponse to any stimulus'. That is mutations occur when they occur, there is no causativeeffect (beyond mutagenic effects ... and these increase mutation rate they do not 'cause' mutation). Mutations have not been shown, to occur in directresponse to an environmental pressure. The relevent aspect of evolutionary theory is the bit that goesalong the lines that heritable variation within the population is either selected for or against, causing a shift in trait frequencies over time. Random (as in 'unprovoked') changes to these heritable characteristics is the origin of that variation. If there is a mechanism that can facilitate the trial of differentproteins, mitigate mutations (leading to lower fatal mutations?), or other biochemical processes that govern mutations this does not 'falsify NDT'. The mutations still cause variation, and are still 'unprovoked'. You additionally claim that NRM's can cause an illusion ofcommon descent. Presumably your premise is that there are a number of createdkinds all with similiar DNA sequences, and that NRM (in your sense) cause these to look like they were descendended from a common ancestor. The end result would be indistinguishable fromcommon descent. This is effectively the same problem that you run into whenever you discuss common design vs. common descent. If the end result would be the same for both premises then weneed something else to tip the balance ... otherwise we can say nothing in either direction. For the common descent argument we have comparative anatomy,fossil data, observed speciation, and observed natural selection (there may be more, but this will do for now). What do we have for NRM as a cause of apparent common descent?
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Peter Member (Idle past 1479 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
quote: No-one (check the replies) has denied that there are mutationalhot spots. Dr.Caporale talks about mechanisms that explain such hot-spots. What is being contended is that there is a directing influenceon these locations, or that the mutations are non-random in the sense of 'deterministic'. quote: Which is what I just said ... the replied you have recieved onthis subject accept hot-spots ... i.e. that there are areas with a higher mutation rate than others, and that there is a mechanism involved in this. 'not random with respect to position' is the phrase. When they occur and why is still considered 'random'.
quote: The immune system responds to 'foreign' proteins, I know, there iseven suggestion that the DNA sequences within the brain change and may be how memory is stored, so perhaps there is a precedent for change as a response to direct encounters with unusual proteins .... this is very far removed from a change in DNA being provoked by a change in climate. The differences in the ATP6 that you mentioned previouslycan equally well be explained via selection. quote: Where is the reply in this section?
quote: I wasn't attempting to teach ... merely pointing out therelevent area (which is what the paragraph said after all) of the theory. quote: The existence of a mechanism as interpreted above does notrefute NDT. If you (or anyone) can show sufficient evidence that an environmentalfactor has caused a genetic change then we can proceed. Perhaps Lemark was right.
quote: What's to understand, it's an assertion?
quote: I managed to understand something then
quote: The ZFY region can be explained just as well within a commondescent framework. The two positions start with different initial conditions andhave a slightly different set of processes, but then end point is the data as we see it now. Both explanations can work, but the assumptions upon which theyare based are radically different. Your assumptions are harder to justify. It comes down to evidence of design ... and for you that NRM's,which are founded upon the presumption of design ... which makes them no evidence at all. You cannot proove something objectively if you start with an assumption which makes the conclusion correct. quote: The ZFY region would look as it does if common descent iscorrect .... or are all other genetic researchers mistaken? We can come back to the redundancies again if you want.
quote: What about the discovery that some supposed 'redundant' regionsare essential links in the chain of actions leading to protein synthesis? Knock-outs leaving viable organisms isn't the same as havingno impact of a creatures fitness for some natural environment or another. quote: But this is the problem ... all of your evidence is the data thatcan be equally well explained in the common descent framework. You need to find something that common descent cannot explainfor your suggestions to carry weight. You might want to start trying to identify and justifyyour starting assumptions while your at it.
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Peter Member (Idle past 1479 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
If you check back I think SLPx did quote Dr.Caporale
in a previous post ... can't seem to find it to reference for you but I'm sure it's there. Dr.Caporale's work seems to indicate a mechanism behind theexistence of differing mutational rates in different parts o genomes. There is nothing in the work which suggests that the mutations are 'non-random with respect to environmental conditions or time'. Re: NRM's:: Yes you mailed your 'examples' a while ago,but you have also just stated that you view is just another interpretation of the data. The problem you seem to be missing with you assertion that youare right and everyone else is wrong can be summed up like this:: You say:: 10 + 5 = 15 therefore 3 X 5 cannot possibly be 15. i.e. you are looking at a data set and proposing an explanation whichfor you fits the data. The mainstream view also fits the data. The departure from my above analogy in this case is that youhave no support for your starting assumptions (the one's that I can identify anyhow) nor have you fully stated what those assumptions are. Perhaps now would be the time for that.
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Peter Member (Idle past 1479 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
quote: Check post 56.
quote: So you are entering into the 'No new information can beintroduced into the genome by random mutation' argument? But you don't believe in random mutations, or do you? If there were a naturalistic mechanism which gives direction toevolution how is that creation? quote: Jumping in before an actual point has been made ...
quote: The following i.e. was an elaboration ...
quote: Your jumping in without reading properly again. I wasn't suggesting taking the mainstream view because it isthe mainstream view ... I was pointing out that in the context of this discussion the mainstream view explains the data equally as well as your view. The flat-earth view did not fit the data very well, even less soonce we could confirm it wrong by simple observation. Your view is based upon an alternate interpretation of the sameobservation. The problems, for me, with your view come under the next segmentwhich you chose to ignore. quote: What are your initial assumptions, and why? As I understand it:: Observation:: i) We have a number of genome segments which code forsimilar genes. ii) There are differences between these genes in differentorganisms. iii) There tend to be more differences between these genes in organisms which would tend to be considred less related on morphological grounds. iv) There tend to be more similarities between these genes in organsims that would tend to be considered more closely related onmorphological grounds. Conclusion:: The current organisms represent leaves of a 'tree of life', wherethe greater the differences between any two organisms is an indication of the distance between the branch point that separated them. Assumptions:: i) Organisms pass their genome on to their offspringii) The genome passed to offspring may carry unanticipated differences from that of the parent(s). iii) Differences in the genome will build up over generations. iv) If some combination of events occur that separate a population then the unanticipated differences in the offpsring can be different in different groups. v) A tree structure is an acceptable representation of the generations of any particular organism, so this is true of species. Perhaps you could critique my list of observations and then providea conclusion and assumption list for your view point. Hopefully you will see (though you may claim sub-conscious bias) thatI have not assumed evolution in the first place, I have concluded evolution.
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Peter Member (Idle past 1479 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
quote: The above is completely incorrect. Everything in the universe exists in one particular way,and follows its natural 'laws' of behaviour. An interpretation of data which says that something operatesin a manner other than the manner in which it actually operates is a mis-interpretation of the data. Determining whether something is a mis-interpretation or not,in the above context, is a laborious process, often requiring experimentation and supporting observations. An interpretation of another person's work, which is itselfinterpretative, which does not match the original intent of the author is definitely mis-interpretation.
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Peter Member (Idle past 1479 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
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