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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: 02-05-2002


Message 38 of 95 (28479)
01-06-2003 5:05 AM
Reply to: Message 6 by Fred Williams
12-31-2002 5:41 PM


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.

This message is a reply to:
 Message 6 by Fred Williams, posted 12-31-2002 5:41 PM Fred Williams has not replied

  
Peter
Member (Idle past 1479 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 39 of 95 (28480)
01-06-2003 5:13 AM
Reply to: Message 16 by Fred Williams
01-02-2003 12:42 PM


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 or
start 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 that
these may not even BE redundant (in PB's terms) but functionalstepping stones in the chain of events leading to protein synthesis.

This message is a reply to:
 Message 16 by Fred Williams, posted 01-02-2003 12:42 PM Fred Williams has not replied

Replies to this message:
 Message 47 by peter borger, posted 01-06-2003 9:38 PM Peter has replied

  
Peter
Member (Idle past 1479 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 52 of 95 (28627)
01-08-2003 1:59 AM
Reply to: Message 47 by peter borger
01-06-2003 9:38 PM


quote:
Originally posted by peter borger:
Dear peter,
P: P.Borger means 'unused' or 'non-functional' when he says redundant.
PB: PB stated several times that redundant genes are functional openreading frames, but can be knocked out without affecting the fitness. PB showed several times that genetic redundancies are NOT associated with gene duplications and thus are NOT merely a back up. PB also demonstrated that genetic redundacies are NOT associated with a higher rate of change.
Best wishes,
Peter

Apologies for the mis-definition ... all I was trying to do
was 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' was
a 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 you
mean 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 have
presented, 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 what
change rate we would see under the NDT model.
To be honest I feel, and I have stated this before, that without
a more detailed model of how the genotype is related to the
phenotype we cannot complete the picture in any case.

This message is a reply to:
 Message 47 by peter borger, posted 01-06-2003 9:38 PM peter borger has not replied

Replies to this message:
 Message 53 by Fred Williams, posted 01-08-2003 11:22 AM Peter has replied

  
Peter
Member (Idle past 1479 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 59 of 95 (28971)
01-13-2003 2:45 AM
Reply to: Message 53 by Fred Williams
01-08-2003 11:22 AM


quote:
Originally posted by Fred Williams:

I was not giving a definition of redundancy,

Which makes it even worse, since you were assuming a definition
by pointing to the msdata web-site.
'Redundancy as an approach to fault-tolerance'
quote:
Originally posted by Fred Williams:

I was simply pointing out that redundancy cries out design.

So we don't need genetics to proove design then since we
have two kidneys but can survive with one?
What makes you believe that redundancy cannot develop
via natural means?
quote:
Originally posted by Fred Williams:

Regardless, the redundancy I deal with is actually similar to genetic redundancies in that both are functional, and 100% operation is achieved even after knocking one out.

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:
Originally posted by Fred Williams:

If redundancies originated via an NDT process, we would not expect to see similar levels of constraint in the redundant gene as in their corresponding peer. Peter has shown that these redundant genes are equally constrained or nearly so with their corresponding peer (ie not associated with higher rate of change), which is very compelling evidence against NDT and very compelling evidence for intelligent design. As Peter pointed out, you guys need a new paradigm!

If you knock-out a gene in the lab. and the organism is still viable
that 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 the
latter is about the relationship of the idividual to the
environment.
Again, P.Borger does not mean redundant in the sense of
two sequences capable of performing the same function.

This message is a reply to:
 Message 53 by Fred Williams, posted 01-08-2003 11:22 AM Fred Williams has not replied

  
Peter
Member (Idle past 1479 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 61 of 95 (29855)
01-22-2003 5:35 AM
Reply to: Message 37 by peter borger
01-05-2003 6:37 PM


quote:
Originally posted by peter borger:
[In] Prof L. Caporale's book "Darwin in the genome" [..] She
demonstrates beyond any doubt the existence of non-random
mutations.
quote:

Having just read the paper (link posted by SLPx) by Dr. Caporale
I 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 direct
response to any stimulus'.
That is mutations occur when they occur, there is no causative
effect (beyond mutagenic effects ... and these increase
mutation rate they do not 'cause' mutation).
Mutations have not been shown, to occur in direct
response to an environmental pressure.
The relevent aspect of evolutionary theory is the bit that goes
along 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 different
proteins, 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 of
common descent.
Presumably your premise is that there are a number of created
kinds 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 from
common 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 we
need 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?

This message is a reply to:
 Message 37 by peter borger, posted 01-05-2003 6:37 PM peter borger has replied

Replies to this message:
 Message 62 by peter borger, posted 01-22-2003 6:14 AM Peter has replied

  
Peter
Member (Idle past 1479 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 63 of 95 (29865)
01-22-2003 7:18 AM
Reply to: Message 62 by peter borger
01-22-2003 6:14 AM


quote:
Originally posted by peter borger:
Dear Peter,
PW: Having just read the paper (link posted by SLPx) by Dr. Caporale
I 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.
PB: O I see, I have been debating for 6 months because everyone agreed on the NRM in the 1G5 genes and their impact for evolutionism. Get real, Peter. Don't fool me.

No-one (check the replies) has denied that there are mutational
hot spots. Dr.Caporale talks about mechanisms that explain
such hot-spots.
What is being contended is that there is a directing influence
on these locations, or that the mutations are non-random in the
sense of 'deterministic'.
quote:
Originally posted by peter borger:

PW: 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.
PB: Problem with you guys is that you are to blind to see what is really going on in this world. My definition of nonranom mutaions was that these mutations are random with respect to position where the are introduced and usually with respect to nucleotide. That is exactly the same as DR CAporalse's definition and if you don't believ it look at page 41: "Thus mutations are not random, at least with respect to their position in a DNA sequence". And, as Dr Caporale told me she had had a lot of dogmatic arguments from orthodox evolutionists too. So, my advise: update.

Which is what I just said ... the replied you have recieved on
this 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:
Originally posted by peter borger:

PW: 'Random' in the NDT sense is intended to mean 'not in direct
response to any stimulus'.
PB: Ever heard about the immunoglobulin genes? They mutate in response to antigen. That is a direct stimulus. The ATP6 gene mutates as a response to the climate, etcetera.

The immune system responds to 'foreign' proteins, I know, there is
even 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 previously
can equally well be explained via selection.
quote:
Originally posted by peter borger:

PW: That is mutations occur when they occur, there is no causative
effect (beyond mutagenic effects ... and these increase
mutation rate they do not 'cause' mutation).
Mutations have not been shown, to occur in direct
response to an environmental pressure.
PB: ...and the denial goes on and on and on. Why don't you just give up, like everybody els already did. In short, NRM are real and can be induced by environmental factors.

Where is the reply in this section?
quote:
Originally posted by peter borger:

PW: The relevent aspect of evolutionary theory is the bit that goes
along 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.
PB: Listen, Peter, you dont have to teach me what ToE learns as dogma. It simply cannot hold in the light of contemporary knowledge.

I wasn't attempting to teach ... merely pointing out the
relevent area (which is what the paragraph said after all)
of the theory.
quote:
Originally posted by peter borger:

PW: If there is a mechanism that can facilitate the trial of different
proteins, 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'.
PB: No of course not. Nothing can falsify your silly atheistic humbug. That's the way it was meant to be. Unfortunately, such directed NRM do falsify NDT.

The existence of a mechanism as interpreted above does not
refute NDT.
If you (or anyone) can show sufficient evidence that an environmental
factor has caused a genetic change then we can proceed.
Perhaps Lemark was right.
quote:
Originally posted by peter borger:

PW: You additionally claim that NRM's can cause an illusion of
common descent.
PB: I am glad you understand this part.

What's to understand, it's an assertion?
quote:
Originally posted by peter borger:

PW: Presumably your premise is that there are a number of created
kinds all with similiar DNA sequences, and that NRM (in your sense)
cause these to look like they were descendended from a common
ancestor.
PB: Yep.

I managed to understand something then
quote:
Originally posted by peter borger:

PW: The end result would be indistinguishable from
common descent. This is effectively the same problem that
you run into whenever you discuss common design vs. common descent.
PB: If such were true than it would be a draft for ever. However, fortunately there is the ZFY region that proofs my vision is right. You cannot have it both ways, my dear friend. It cannot be both common descent AND common design (or could it?). Since the ZFY region demonstrated clearly NRM, common design must be the right vision.

The ZFY region can be explained just as well within a common
descent framework.
The two positions start with different initial conditions and
have 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 they
are 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:
Originally posted by peter borger:

PW: If the end result would be the same for both premises then we
need something else to tip the balance ... otherwise we
can say nothing in either direction.
PB: the balance is tipped by the ZFY region and by genetic redundancies. Both clearcut evidence of design.

The ZFY region would look as it does if common descent is
correct .... or are all other genetic researchers mistaken?
We can come back to the redundancies again if you want.
quote:
Originally posted by peter borger:

PW: 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).
PB: The comparative anatomy is utterly subjective. It doesn't mean anything to me. It could as well be common design. Observed speciation is nothing but the GUToB, and natural selection is included in the GUToB. However, natural selection can not explain the existence of genetic redundancies. And I am not going into that again. (Okay, only if you really don't get it).

What about the discovery that some supposed 'redundant' regions
are essential links in the chain of actions leading to protein
synthesis?
Knock-outs leaving viable organisms isn't the same as having
no impact of a creatures fitness for some natural environment
or another.
quote:
Originally posted by peter borger:

PW: What do we have for NRM as a cause of apparent common descent?
PB: The mtDNA for one, the ZFY for two, the rest of the alignments that you take as evidence for common descent.

But this is the problem ... all of your evidence is the data that
can be equally well explained in the common descent framework.
You need to find something that common descent cannot explain
for your suggestions to carry weight.
You might want to start trying to identify and justify
your starting assumptions while your at it.

This message is a reply to:
 Message 62 by peter borger, posted 01-22-2003 6:14 AM peter borger has not replied

Replies to this message:
 Message 64 by derwood, posted 01-22-2003 9:28 AM Peter has not replied
 Message 66 by derwood, posted 01-22-2003 10:01 AM Peter has not replied

  
Peter
Member (Idle past 1479 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 70 of 95 (29992)
01-23-2003 5:31 AM
Reply to: Message 69 by peter borger
01-22-2003 10:39 PM


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 the
existence 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 you
are 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 which
for you fits the data. The mainstream view also fits the data.
The departure from my above analogy in this case is that you
have 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.

This message is a reply to:
 Message 69 by peter borger, posted 01-22-2003 10:39 PM peter borger has replied

Replies to this message:
 Message 71 by peter borger, posted 01-23-2003 6:05 AM Peter has replied

  
Peter
Member (Idle past 1479 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 72 of 95 (30017)
01-23-2003 8:38 AM
Reply to: Message 71 by peter borger
01-23-2003 6:05 AM


quote:

PW: 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.
PB: You're too eager. It was me who contacted Dr Caporale and I quoted her, not Page. It was about orthodox evolutionists and not understanding NRM (like Page and you).

Check post 56.
quote:

PW: Dr.Caporale's work seems to indicate a mechanism behind the
existence 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'.
PB: The point that is pretty clear here is that the observed change that Darwin[..] observed is already present in the genome, and therefore [..] cannot be extrapolated to microbe to man, because it implicated that evolution is mechanistically dericted and that is creation. Listen, Peter, you evo-guys have a problem. I don't, I have the GUToB.

So you are entering into the 'No new information can be
introduced 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 to
evolution how is that creation?
quote:

PW: 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.
PB: Yes, and as it stands now, my interepretations discribe equally well, and often better what we see.
PW: The problem you seem to be missing with you assertion that you
are right and everyone else is wrong can be summed up like this::
PB: It took Darwin almost a lifetime to produce his Origin of Species. He first had to convince himself.
It is no argument.

Jumping in before an actual point has been made ...
quote:

PW: You say:: 10 + 5 = 15 therefore 3 X 5 cannot possibly be 15.
PB: I fail to see the connenction. I mentioned several times that evolutionism superficially seems a
nice theory, but not any longer.

The following i.e. was an elaboration ...
quote:

PW: i.e. you are looking at a data set and proposing an explanation which for you fits the data. The
mainstream view also fits the data.
PB: No, the mainstream view is held up by so many tricks I don't accept it anymore. And mainstream
view has been demonstrated to be always wrong. The mainstream view used to be a flat earth,
remember, or generatio spontanea (still present in the atheist community, though). So, that can hardly be an argument, too.
And now we have NRM. And now we have genetic redundancies. They also cannot be explained by evolutionary theory as I have mentioned several times before. I illustrated it with examples like alpha
actinin genes, for which you have to introduce neutral purifying selection and the src-family of phosphatases (their existence cannot even be explained by duplication). It is not only one little
incongruence, it is the one after the other after the other after the other. So, evo = false, GUTob =
less false. I know what to choose.

Your jumping in without reading properly again.
I wasn't suggesting taking the mainstream view because it is
the 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 so
once we could confirm it wrong by simple observation.
Your view is based upon an alternate interpretation of the same
observation.
The problems, for me, with your view come under the next segment
which you chose to ignore.
quote:

PW: The departure from my above analogy in this case is that you
have 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.
PB: If you CHOOSE to be blind, than that is NOT my responsiblity.

What are your initial assumptions, and why?
As I understand it::
Observation::
i) We have a number of genome segments which code for
similar genes.
ii) There are differences between these genes in different
organisms.
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 on
morphological grounds.
Conclusion::
The current organisms represent leaves of a 'tree of life', where
the 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 offspring
ii) 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 provide
a conclusion and assumption list for your view point.
Hopefully you will see (though you may claim sub-conscious bias) that
I have not assumed evolution in the first place, I have
concluded evolution.

This message is a reply to:
 Message 71 by peter borger, posted 01-23-2003 6:05 AM peter borger has not replied

Replies to this message:
 Message 77 by derwood, posted 01-23-2003 3:10 PM Peter has not replied

  
Peter
Member (Idle past 1479 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 82 of 95 (30511)
01-29-2003 2:04 AM
Reply to: Message 78 by peter borger
01-23-2003 7:48 PM


quote:
Peter Borger, he say::
And there is no such thing as MIS-interpretation. There are interpretations of data. (As if your interpretation is the right one, and anothers is MIS).
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 operates
in 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 itself
interpretative, which does not match the original intent
of the author is definitely mis-interpretation.

This message is a reply to:
 Message 78 by peter borger, posted 01-23-2003 7:48 PM peter borger has not replied

Replies to this message:
 Message 83 by derwood, posted 02-14-2003 12:39 PM Peter has replied

  
Peter
Member (Idle past 1479 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 84 of 95 (32781)
02-20-2003 9:05 PM
Reply to: Message 83 by derwood
02-14-2003 12:39 PM


bump

This message is a reply to:
 Message 83 by derwood, posted 02-14-2003 12:39 PM derwood has not replied

  
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