Re: Request
- From: Zoe <muze10@xxxxxxx>
- Date: Wed, 10 Aug 2005 03:12:21 GMT
On Thu, 4 Aug 2005 22:23:34 -0500, "Steven J."
<sjt1957NOSPAM@xxxxxxxxxxxxxxxxxxxx> wrote:
snip>
>> Steven, I'm talking about the usefulness of probability and statistics
>> in explaining how a cardboard box is put together or in determining
>> how chromosomes are consistently the same for any group of life forms.
>> It isn't useful for these purposes, is it?
>>
>Well, no. But before you were talking about the usefulness of probability
>in constructing cardboard boxes, you were talking about random mutations as
>though the laws of probability did not apply to them.
I trust your summarization of what went before, so will snip it.
If you say that I said that the laws of probability did not apply to
random mutations, then I take that back. I did not mean that. I agree
that probability and statistics can make a reasonable estimate as to
the chance of a certain random event happening, IF it gets the
background data right. It can predict the chances of fusion happening
if it knows that several populations have 24-chromosome members, or of
fission happening if a single population has 23-chromosome members.
But it seems to me that probability and statistics will be only as
good as its source information.
What is the source information for chromosome fission or fusion?
Apparently, the basis on which you decide that the last common
ancestor was more likely to have 24 chromosomes is because all apes
except humans have 24 chromosomes. You conclude that there is more of
a chance for fusion rather fission because there are (present tense)
more populations of 24's available for the random fusing mutation, and
less of a chance for the random fissioning mutation to hit a single
population of 23's. But the probability is calculated on what exists
today and not on the original population, which is what I think should
be used.
Besides that, I submit that, as an evolutionist, there is no reason to
reject or accept either scenario since, in principle, evolutionary
theory starts with a lesser number and evolves into greater numbers,
anyway. As well as, there is no predictability. Take, for instance,
a LCA that has 23 chromosomes. It may be probable that a chance
mutation can come along that causes fission in a chromosome, and a new
population eventually emerges (according to your theory) where its
members carry 24 chromosomes. And since mutations are random, meaning
that all possible mutations have equal probability of selection, then
humans (according to your theory) could have descended from the
original population that had 23 chromosomes, and the population with
the new 24th chromosome, through geographical isolation (according to
your theory) could be hit with other mutations (according to your
theory) that would cause the first 24-chromosome population to
continue to vary into your gorillas and other ape types (according to
your theory).
So, having sat inside of your evolutionary box for the last few
minutes, I don't see how you could use probability and statistics to
conclude that fusion is the more likely event when you don't know the
background of your proposed populations. You are assuming, without
grounds, that the LCA had 24 chromosomes, not 23. And this assumption
is based on the supposedly evolved populations of apes existing today,
instead of on the theorized first split in a population that could
have carried either 23 chromosomes or 24 chromosomes.
I think that probability and statistics is valid for known situations,
but not for the unknown. It has to be known that someone is
consistently, non-randomly flipping a coin thousands of times, and
only then can that background information be used in a probability and
statistics prediction of the chances of getting heads or tails. But
if someone is not consistently flipping a coin, but just randomly,
non-repetitively tossing a coin, a toss today, two tosses tomorrow, no
tosses for a week, a series of tosses in a single hour, and so on, is
there a way for probability and statistics to predict random behavior
that is based on random behavior?
I hope some statistician will clear that up for me, because right now
it doesn't make sense. I see the chances of a LCA having 23
chromosomes versus 24 as a totally random happening (according to your
theory). The random mutation could be hitting either a 23-chromosome
population or a 24-chromosome population, and there's no way to know
which. How does P&S predict realistically if the background
information is unknown?
And that is why, when it is claimed that random mutations can produce
the complexity seen in nature, and that, based on probability and
statistics, sooner or later you're going to get that lucky strike, I
tend to think to myself, What? NO WAY. Why no way? Because the
background information is such that it is impossible for P&S to work.
It is one thing to say that the probability of winning the lottery of
$20 million is X, but that is because the background data is a
reality. There is a pot of $20 million waiting to be won.
Eventually, sooner or later, someone will hit that jackpot. With
evolutionary theory, there is no pot of gold waiting to be won. There
is no concrete data in the pot. And you can't predict on what you
don't know. There is no chance of winning something out of nothing.
Okay, so detour's over. May I now revert to the original intent of my
threads, which is to establish how mental activity is recognized? And
I believe the last thing I requested was for an explanation of how,
absent mental activity, random mutations are expected to achieve the
formation of a digestive system, going from a single cell (which is an
overly generous "given") to a system within systems that includes the
digestive system.
>>>> So now, are you saying that random events are credited with pulling
>>>> together a digestive system or a circulatory system or a cardboard
>>>> box? Or are you taking a fully-formed reproductive system and
>>>> applying your evolutionary theory of mutations to it? I am really
>>>> interested in the construction of the system, not in the mutations
>>>> that can happen to the construction.
>>>>
>>>No, I am not saying that random events are credited with putting together
>>>a
>>>digestive system (at least, not by themselves); random events in
>>>combination
>>>with natural selection (reproduction, variation, and differential
>>>reproductive success) put complex structures together.
>>
>> and this is the process that has not yet been explained by posters to
>> TO -- not one. Please describe a scenario, based on facts, not
>> fantasy, of how a digestive system comes together through random
>> events in combination with natural selection. And you cannot use
>> reproduction, variation, and differential reproductive success unless
>> you are willing to concede that the machinery was already in place,
>> fully functioning, after which comes along your mutations and
>> selection.
>>
>I suspect you're asking me for a mutation by mutation, selective regime by
>selective regime, account of how the human digestive tract evolved from a
>single-celled organism. I cannot, of course, provide any such thing.
and why not? Based on your scientific, observed data of how mutations
behave, surely you can plug that data into your evolutionary scenario
and scientific observations of how mutations and selection work in
describing a realistic step-by-step pathway on how a digestive system
can come into existence. If you can't do this, then I must take your
declaration on faith...which I am not inclined to do.
> I
>also suspect that you have neither the intention nor the ability to tell us
>how "intelligence" (other, perhaps, than human intelligence) implements any
>"design" or change in design in living organisms.
I cannot make a digestive system, so I cannot tell you how to do it.
But if I were to try to recreate something that works like the
digestive system, I certainly would not try to do it by random
mutations. Would you? I would take note of the steps taken in a
what-you-see-is-what-you-get system, and attempt to copy those, as far
as possible. And that would be a useful, scientific venture, learning
from nature, copying its processes, rather than speculating on its
history.
>> So, okay, we have a simple common ancestor consisting of a single
>> functioning cell (and even that is a generous given) that replicates
>> (we know not how that started). Take it from there and describe a
>> realistic scenario, using factual, scientific observations, as to how
>> this single cell develops a digestive system, based on random
>> mutations and selection.
>>
>> Can't do it? Then evolutionists need to be a little humbler about
>> their position. To say "We know the digestive system evolved," but go
>> silent when the question of "how?" is asked, is to ask thinking minds
>> to take your word on faith.
>>
>Don't be silly, Zoe. It is perfectly possible to demonstrate that something
>happened, without having a complete description of how it happened. Your
>position is tantamount to saying that if we can't figure out how someone
>died, we are not justified in inferring that he is dead.
the issue is not about whether someone is dead or whether something
happened. It is about HOW something happened. My position is
tantamount to saying that if we can't figure out how someone died, we
are not justified in making up stories about how he died. There is no
controversy over whether the person is dead. Neither is there
controversy that we exist.
>You have, in the consistent nested hierarchy of homologies,
you have yet to demonstrate that nested hierarchies always mean common
descent. If they do not always mean common descent, then on what
basis do you decide that only the nested hierarchies of nature mean
common descent?
> in biogeography,
why does biogeography mean common descent, unless there is a
preconceived notion in place?
>in vestigial structures at the genetic and morphological level,
the term "vestigial structures" is a term arising out of preconceived
notions. Some may call the appendix vestigial, but there are uses for
the appendix. Some may call the tailbone vestigial, but there are
uses for the tailbone...and so on. To call something vestigial
because it seems to have no use is a misunderstanding of and
egotistical dismissal of structures that are really not vestigial at
all.
> in the
>fossil record,
the fossil record is subject to interpretation.
>in the jury-rigged and improvised nature of many adaptions
>(e.g. Darwin's remark on "similar structures for dissimilar functions and
>dissimilar structures for similar functions"), compelling evidence for
>common descent with modification.
nothing compelling so far to this creationist.
>You have, furthermore, an demonstrated mechanism of mutation and natural
>selection.
this is a mechanism that fails to produce a digestive system, so how
has it been demonstrated? Instead, you want your systems to be fully
in place and operating a la creation, and then you begin to apply your
theory of random mutations to these ready-made systems. You can't
have this head start unless you acknowledge that the system was in
place, fully functioning, from the beginning -- which is the position
of creation theory.
> It has produced, in the lab, bacteria resistant to poisons never
>found in nature,
the ability to respond to changes in the environment, including
poisons never found in nature, is an inherent ability.
> bacteria that *eat* poisons never found in nature,
as long as the bacterium is programmed to respond to alien influences,
including poisons never found in nature, it will adapt to these alien
influences, or die, depending on its health.
>multicellular colonial organisms evolved from single-celled ancestors,
I submit you are observing a programmed ability to divde, and are
mistakenly calling it evolution.
> and
>similar examples of striking novel traits. It seems to me that you are not
>being asked to accept anything on "faith," but on the basis of considerable
>evidence regarding both the fact and the proposed mechanism for it.
faith is called upon to rely on your interpretation of the above data,
Steven.
>> So, here we go.
>>
>> A single cell exists, replicating itself repeatedly. Along comes a
>> random "beneficial mutation." What happens next, based on your
>> selection principle? How does the digestive system develop?
>>
>It becomes a multicellular organism.
could you be a little less vague? So you think that a single cell
becoming multicellular is how a digestive system forms? Have you
accounted for the changes in DNA sequences that are needed to produce
the particular types of proteins needed to construct an esophagus, a
stomach, duodenum, jejunum, small intestines, and all the attendant
parts that make a digestive system work?
> http://www.gate.net/~rwms/EvoMutations.html
>
>Starting from single celled animals, each of which has the capability to
>reproduce there is no sex in the sense that we think of the term. Selective
>pressure has been observed to convert single-cellular forms into
>multicellular forms. A case was observed in which a single celled form
>changed to multicellularity.
>Boxhorn, a student of Boraas,writes:
>Coloniality in Chlorella vulgaris
>Boraas (1983) reported the induction of multicellularity in a strain of
>Chlorella pyrenoidosa (since reclassified as C. vulgaris) by predation. He
>was growing the unicellular green alga in the first stage of a two stage
>continuous culture system as for food for a flagellate predator, Ochromonas
>sp., that was growing in the second stage. Due to the failure of a pump,
>flagellates washed back into the first stage. Within five days a colonial
>form of the Chlorella appeared. It rapidly came to dominate the culture. The
>colony size ranged from 4 cells to 32 cells. Eventually it stabilized at 8
>cells. This colonial form has persisted in culture for about a decade. The
>new form has been keyed out using a number of algal taxonomic keys. They key
>out now as being in the genus Coelosphaerium, which is in a different family
>from Chlorella. "
>
>Boraas, M. E. 1983. Predator induced evolution in chemostat culture. EOS.
>Transactions of the American Geophysical Union. 64:1102.
okay, so far you've gotten your single cell to become multicellular.
Is this the digestive system?
>There are, of course, an immense number of steps along the way: the
>development of multiple layers (starting with something cnidarian-like with
>two layers of cells, and gradually evolving (in some lineages) a third
>layer), the innermost of which may be devoted to digesting food (note that
>the single cell, and its simple colonial descendants, already can take in
>food through their surface, so what we are talking about here is having some
>fraction of the body cells specialize in a function they already have).
and how do you propose selected random mutations achieve the
conversion of some cells into specialized functions? If you have no
pathway, then merely saying "it evolved" is asking thinking minds to
take your word by faith.
>-- [snip]
>>
>>>What is your definition of "phenotype," and how does "phenotype" differ
>>>from
>>>"morphology?"
>>
>> phenotype has to do with group characteristics, psychological and
>> anatomical, resulting from both heredity and environment. It refers
>> to characteristics of organisms collectively, or a group of organisms
>> having like characteristics.
>>
>Where did you get this definition? I cannot find a definition of
>"phenotype" that limits it to *group* characteristics; most sources define
>it as either the physical expression of the genotype, or the observable
>characteristics of the individual organism, or simply anything you can find
>out about the organism without sequencing its genes.
I got my definition from a standard dictionary.
>> Morphology has to do with individual characteristics, the form and
>> structure of individual animals and plants.
>>
>-- [snip]
>>
>>>http://w3.fiu.edu/milesk/genetics.htm
>>>
>>>Let's take a simple case and question: are chihuahuas and St. Bernards
>>>99+%
>>>similar in morphology (note that not merely size, but proportions and even
>>>toe number may vary between these breeds)? Domestic dogs differ from grey
>>>wolves by only about 0.2% of their mitochrondrial DNA (and mitochrondrial
>>>DNA mutates faster and is more variable than nuclear DNA, which is what we
>>>were comparing with humans and chimps above), so the degree of genetic
>>>difference between any two dog breeds must be very tiny indeed. I'm not
>>>sure how you'd quantify the difference between, e.g. the St. Bernard and
>>>the
>>>chihuahua, or a greyhound and a dachsund, but I think you'd easily come up
>>>with less than 99.9% similarity in appearance, for all that their genetic
>>>similarity can be that great.
>>
>> nuclear DNA produces morphological similarity. MtDNA has to do with
>> energy transfer, not morphological similarities. So why are you using
>> MtDNA as an example of morphological similarity?
>>
>I am not; please read more carefully. I am stating that if mtDNA
>differences are so tiny, then presumably nuclear DNA differences are even
>smaller, so that two dogs can be 99.8% or more genetically identical, and be
>as morphologically different as chihuahuas and St. Bernards.
this is an assumption without foundation. Just because mtDNA
differences are tiny, there is no reason to presume (your word),
without evidence, that nuclear DNA differences are even smaller.
Indeed, as mentioned earlier, after chimp/human genome comparison, it
has been noted that the differences are 83%, so definitely not
smaller.
>-- [snip]
>
>Let me reargue this entire section (i.e. my assertion that major changes in
>DNA sequence can have little or no effect on morphology).
>
>The genetic code (the correspondence of three-nucleotide codons to amino
>acids that make up proteins) is "degenerate:" rather than having one codon
>per amino acid and one for punctuation, most amino acids correspond to
>multiple codons (up to six), and there are three separate stop codons. From
>this it follows that one could, in principle, make massive changes (ca. 30%
>of the sequence) in the genome of any species without making any changes at
>all in the proteins produced or the way the organism grows.
I'm not sure what you mean by "massive" here. That these codons allow
for the morphing of a species into another? What exactly are these
massive changes?
> This are
>"silent mutations" -- they have no phenotypic effects at all. Therefore,
>logically, one cannot assume that changes in the genome must translate to
>changes in the phenotype at all, much less must map one-for-one onto the
>changes in the phenotype.
these variations of codons for protein don't vary the proteins to the
point where you have change in morphology, so why use them as evidence
at all then?
>>> Or consider this:
>>>there is a gene, Pax-6, which triggers eye development in fruit flies.
>>>Humans also have a form of Pax-6 (which controls development of the iris
>>>of
>>>the human eye), which is not identical to the fruit fly version, but
>>>experimenters have induced fruit fly eyes to grow on fruit fly wings by
>>>introducing *human* Pax-6 genes into the wings (there are, of course,
>>>already fruit fly Pax-6 genes in the wings, but they are deactivated).
>>>Evidently, fruit flies could develop normally if some of their genes were
>>>replaced by their human homologues, which implies, again, that large
>>>changes
>>>in multiple genes could have little or no noticeable effect.
>>
>> I don't know how you can draw such a sweeping conclusion from an
>> experiment that shows that fruit fly eyes can grow on fruit fly wings.
>> Until you present fruit flies that are reproducing successfully with
>> eyes on their wings, how can you say that there is no apparent
>> difference in function with these changes?
>>
>The issue is not whether the flies can successfully reproduce
it most certainly is the issue. You are asserting that changes such
as seen done in the fruit fly are evidence for evolution of the
species. If the flies cannot successfully reproduce, then you don't
have a species that can continue to morph. End of the line. No
macroevolution along that fruit-fly line.
> (and the
>changes to their wings would not be reproduced; these are aquired traits
>that do not affect the germ-line DNA).
worse yet. Then that's the end of that genetic change for sure.
> The issue is whether a a PAX-6 gene
>that differs from the fruit fly version can do the same job in cells and
>tissues that the fruit fly version can. The fact that human PAX-6 triggers
>the same effects as fly PAX-6 argues that the fly version of PAX-6 could
>mutate to match the human version, without affecting the way fruit flies
>develop.
can't happen, not if the species with this gene cannot reproduce.
Indeed, if it is an acquired trait, as you state above, then it's
certainly not going to be passed down to eventually form a new
species, even if the fly could still reproduce.
>They would neither lose their eyes nor start growing
>vertebrate-style eyes. Again, a change to genes would *not* map one-to-one
>onto a change in morphology.
but neither would the changes carry on into future generations. What
good is this to the evolution of a new species? Your whole point is
becoming more and more moot.
>>> The large
>>>variations in sequence between cytochrome-c in various species, together
>>>with the similarity in function of the enzyme in different species,
>>>likewise
>>>suggests that changes in genes don't map one-to-one directly to changes in
>>>morphology or behavior.
>>
>> first of all, you need to demonstrate that these variations in
>> sequence are really a result of changes over time and not a result of
>> original makeup. It's like an ant looking at the differences between
>> a car and a plane and saying, "see these differences? They are a
>> result of changes that occurred over millions of years." A second ant
>> says, "how can you tell this?" The first ant says, "because, can't
>> you see that changes occur as a normal course of events? See here,
>> rust builds up on this car, and the fender falls off eventually.
>> Therefore, given enough time, the car will end up being a plane."
>>
>First of all, my argument does not depend on the assumption that the
>differences between, e.g. human and pine tree cytochrome-c evolved in the
>course of descent from a common ancestor. It depends only on the assumption
>that human and pine tree cytochrome-c do the same job, engaging in the same
>chemical reactions.
it makes sense, based on the behavior of creative mental activity,
that a particular gene would be used in the master plan for all life
forms, but switched on for some life forms and switched off for other
life forms. When switched off, it is not even recognizable as a gene,
but is just part of the material that is presently called junk. Why
switch this gene off? I might want to give certain life forms the
ability to enjoy citrus fruit and therefore switch off that gene so
that there is not an overload of vitamin C?
> If this is correct, a mutation or series of mutations
>which did change human cytochrome-c to pine tree cytochrome-c would not
>alter the way our metabolisms worked or our morphology. That is, not only
>can silent mutations produce, in principle, large changes in DNA with no
>changes in phenotype, even non-silent mutations could produce very tiny,
>inconsequential changes in phenotype. This was one of the points under
>contention.
meaning you can have it working for you all ways, coming and going --
sounds very much like a sweeping "mutationsdidit" with no further
explanation.
>
>By the way, even if you don't accept (or, I suspect, understand) the
>argument about consistent nested hierarchies as evidence for common descent,
>at least you could acknowledge that it has been presented to you. The ant
>in your little parable offers no argument, not even a bad one, for cars
>evolving into aircraft or for the common ancestry of cars and aircraft (of
>course, cars and aircraft reproduce rather differently from living things).
the ant is an apt example of human thinking in relation to the things
we don't understand. The ant might think, if it could think, that it
has a great argument for how a car changes into an airplane. It is an
ant's perspective. Relatively speaking, humans are like ants.
snip>
>>>The classic examples of small changes in genes producing large phenotypic
>>>effects are things like four-winged fruit flies (the rear wings are
>>>produced
>>>by a single mutation modifying the growth of the halteres behind the
>>>front -- and in normal flies, only -- wings), or achondroplasty in humans
>>>or
>>>dogs (a mutation that shortens the limbs).
>>
>> and these four-winged fruit flies, do they reproduce successfully?
>>
>Yes. Why should they not? They don't *fly* very successfully, which is the
>usual creationist retort at this point, but they reproduce.
is there a growing population of four-winged fruit flies in existence
somewhere? What are they called? Are they out and surviving in the
wild or cultured only in a lab?
>>>It is well-known that some homologous proteins between different species
>>>are
>>>very different in sequence (e.g. the aforementioned cytochrome-c, or the
>>>even more widely varying fibrins, while others (e.g. the histones that
>>>form
>>>the backbones of chromosomes) differ very little between species. And
>>>I've
>>>mentioned that there are variants in hemoglobin within the human species,
>>>some of which don't seem to have much in the way of effects. The
>>>inference,
>>>of course, is that nearly all alterations to histones prevent them from
>>>working properly, while hemoglobin and cytochrome-c can vary much more
>>>without affecting function.
>>>
>>>http://alpha2.bmc.uu.se/~lars/biowww/Proteinevol.html
>>
>> the mistake made here is to assume that differences in sequence arose
>> as a result of external mutational change instead of recognizing that
>> beneficial differences were there from the beginning.
>>
>*boggle* That is not right.
that's all you got to say, Steven? That's not right? Okay, then I
will respond that it is, too, right. :-\
snip>
>>>http://www.talkorigins.org/faqs/mutations.html#Q2 has a list of favorable
>>>mutations in various species, which would certainly seem to answer your
>>>request.
>>
>> please, not the same old tired list of six examples. In any event,
>> what you call favorable mutations, I call inherent ability to vary or
>> adapt to environmental stimuli. How are we going to demonstrate which
>> is correct? I'm betting there is no predictability test or
>> explanatory test that will demonstrate that these responses to the
>> environment are really favorable mutations from the outside. However,
>> creation theory would predict that favorable adjustments to
>> environmental stimuli (what you call favorable mutations) can be
>> traced to an internal program that allows for such variations.
>>
>*boggle* Apparently bacteria have spent their entire history on Earth
>(granted, in your view, that's a much shorter history than in mainstream
>science's view) hiding untold myriads of spare beneficial alleles (and a
>program for calling them forth) in hyperspace, since neither of these show
>up when the bacterial genes are sequenced, but the bacteria keep coming up
>with really weird beneficial adaptions (why should a bacterium have the
>ability to adapt to eat nylon? is this a problem that's likely to come up in
>the natural environment?).
life forms are programmed to adapt to foreign influences, and that
would include stuff that is not likely to come up in the natural
environment.
snip>
>> and how do you determine that what you are observing are mutations
>> from the outside or inherent ability to vary, coming from the inside
>> of the genetic system?
>>
>> It's like watching figures morph in a computer program and claiming
>> that the changes are a result of random external mutations when, all
>> along, the ability to change was programmed into the morphing figures.
>> Have you tracked the source of these changes to determine if they are
>> external or internal?
>>
>Personally, no, though as noted some of these bacterial changes have been
>sequenced. And, again, what on earth would lead a reasonable person to
>suppose that bacteria had a built-in "ability to adapt" (unless that ability
>consisted of the potential to undergo random mutations and natural
>selection) for, e.g. the ability to digest poisons not found in nature?
it is not unreasonable to suppose that a programmer will make his
program with protections from external stimuli that could affect how
the program operates. If a life form is indeed the result of mental
activity, then it is to be expected that built into such a form would
be the ability to protect itself -- a situation that is clearly
evident in how the body's immune system operates, for instance.
snip>
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