Re: Request
- From: Zoe <muze10@xxxxxxx>
- Date: Thu, 04 Aug 2005 01:41:11 GMT
On Sun, 31 Jul 2005 17:53:55 -0500, "Steven J."
<sjt1957NOSPAM@xxxxxxxxxxxxxxxxxxxx> wrote:
>
>"Zoe" <muze10@xxxxxxx> wrote in message
>news:igsne1tsdue4nfr1b8rgd1he8hq6cjtq3i@xxxxxxxxxx
>> On Wed, 27 Jul 2005 23:54:26 -0500, "Steven J."
>> <sjt1957NOSPAM@xxxxxxxxxxxxxxxxxxxx> wrote:
>>
>-- [snip]
>>
>>>For that matter, again, if random events had no order governing them, then
>>>probability as a field of mathematics could not exist. Your position as
>>>stated above is pure obstinant folly.
>>
>> probability and statistics does not explain how a cardboard box is put
>> together. Neither does it explain how a certain number of chromosomes
>> are consistently found in any particular life form. It merely
>> predicts the chances of a single, discrete action occurring. These
>> threads have had to do with how systems are put together.
>>
>Zoe, I thought that we had established that, in fact, a "certain number of
>chromosomes" is not found consistently in any particular species; there are
>species with varying numbers of chromosomes in different individuals.
>Heredity explains (to the extent that heredity is understood) why, in
>general, chromosome counts don't vary wildly from parent to offspring or
>individual to individual within a species.
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?
>> 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.
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.
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?
>>
>>>>
>>>-- [snip]
>>>>
>>>> if sequence similarity between genes were truly 99.75%, then
>>>> morphologically, we would be 99.75% similar to chimps. Reality is, we
>>>> are not 99.75% similar to chimps in our outward appearance. Outward
>>>> appearance is a result of those same genes that are considered to be
>>>> almost identical to chimps.
>>>>
>>>There is no one-to-one mapping between genotype and phenotype.
>>
>> I didn't mean genotype and phenotype here, but a one-to-one mapping
>> between genes and morophology. A specific gene will always produce
>> the same specific protein or proteins, and if there is another gene
>> that is identical to it, that identical gene will also produce the
>> same results. So if the claim is that gene similarity was 99.75%
>> between chimps and humans, you would expect to find 99.75% similar
>> morphology.
>>
>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.
Morphology has to do with individual characteristics, the form and
structure of individual animals and plants.
>Now, to be sure, to a biologist "phenotype" includes behavior
>(a pointer's tendency to point at birds is as much part of its phenotype as
>the shape of its ears), and may even include results of that behavior
>(Richard Dawkins has argued for treating, e.g. beaver dams and termite
>mounds as part of the phenotypes of these species), but it's basically "what
>the genes build, directly or indirectly, in a given environment."
>
>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?
>>> A tiny
>>>alteration in a gene can have an immense effect on how the organism
>>>develops, or, conversely, very large changes in multiple genes can have no
>>>effect at all.
>>
>> references, please, for the claim that large changes in multiple genes
>> can have no effect at all.
>>
>http://globin.cse.psu.edu/html/huisman/variants/contents.html
want to summarize or quote the section from this that describes very
large changes in multiple genes having no effect at all? Giving me
this link is tantamount to someone asking me a Biblical question and I
throw the whole Bible at them and say, "there's your reference."
>There are over 1000 documented variants in human hemoglobin. Granted, many
>of these produce very marked and generally deleterious phenotypic effects
>(e.g. sickle-cell anemia, thalassemia, etc.), but others have no apparent
>difference in function from normal human hemoglobin.
reference and quote, please? Not the whole library, but something
specific that you have read in the above.
> 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 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."
>>> It has been known for a long time (since well before the
>>>discovery of genes) that tiny changes in developmental rates (e.g. how
>>>long
>>>a particular structure continues to grow) can produce immense differences
>>>in
>>>how an organism looks -- and tiny changes in development rates can result
>>>from tiny changes in genes. OTOH, as noted, large sections of many
>>>proteins
>>>(and hence the genes that code for them) can be replaced with completely
>>>different sequences without affecting function.
>>
>> references, please?
>>
>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?
>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.
>>> Consider how many genetic
>>>disorders are the result of changing one amino acid in one protein (the
>>>result of changing one nucleotide in one gene). Equally drastic effects
>>>that are not disorders can be produced by equally small changes.
>>
>> examples of these equally drastic effects that are not disorders?
>>
>Does
>http://www.hindu.com/thehindu/seta/2002/03/07/stories/2002030700060300.htm
>count? It involves a mutation that drastically reduces the number of pairs
>of legs in a species of shrimp, without so far as I can tell actually
>crippling the shrimp.
so humans have learned how to manipulate the Hox gene to create
changes. One point for intelligence. How does this support
evolution? Indeed, do you have evidence that these fruit flies and
shrimp can successfully reproduce after their genes have been
manipulated to stop limb development?
>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.
snip>
>> so how do you determine whether an adaptation is inherent or a result
>> of beneficial mutations? You haven't answered that yet.
>>
>You weren't asking that question.
I thought I was.
> With bacteria or fruit flies, watching
>evolution in real time, one can sequence individuals at the start and end of
>the experiment and spot the mutations.
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?
> In the case of humans and chimps,
>one can only note that certain alleles that are ubiquitous in humans are
>unknown in chimps, and infer that either humans or chimps have experienced a
>mutation since the LCA.
see, you're basing your conclusions on a preconceived notion that any
differences have to be a result of change over time from some LCA.
There is no evidence for this other than a just-so story. Since the
faulty premise is that change is always a sign of mutations, then when
something that was built to change, changes, the conclusion is that,
see, mutations did it. The problem is with the premise.
snip>
>> as long as you are consistently categorizing the same items, whether
>> books or cars or life forms, you will always get nested hierarchies
>> for whatever traits are chosen to be used as a categorizing tool. For
>> any category chosen, you WILL get the same nested hierarchy because
>> you are dealing with the same category of things.
>>
>But pretty clearly ear bones and mammary glands are not the same things.
>Having hair and having a single (left) aortic arch (as opposed to having two
>aortic arches like many reptiles, or a single right arch like birds) are not
>the same thing either. So why, if you create a category of all vertebrates
>that have three bones in the inner ear, have you also, automatically,
>created a category of all vertebrates with mammary glands, a single left
>aortic arch, and fur?
doesn't mean a thing. Why, if I create a category of all cars that
have four doors, don't I also automatically create a category of all
cars with windshields, a steering wheel, and wheels?
>If I create a category of all cars with automatic transmissions and four
>doors, that will not the the same as, or entirely contain, or be entirely
>contained within, a category of, e.g. "all Ford cars with CD players."
because you have created a category that doesn't fit, is all. If I
create a category of all vertebrates with three bones in the inner
ear, it will not be in the same category as vertebrates with wings and
beaks.
It's all subjective.
>Consistent nested hierarchies which arise independently from comparisons of
>many different sets of traits are not found in designed artifacts.
I can make them consistent if I choose the right qualities. It's
subjective.
snip more of the same>
>>>but one can see the same thing just be comparing, say, anatomical
>>>features.
>>>All organisms with one bone in the lower jaw and three in the middle ear
>>>also have mammary glands, and none have feathers. There's no obvious
>>>reason, assuming separate origins, for that feature -- why not bats with
>>>feathers, or penguins with mammary glands? *Consistent* nested
>>>hierarchies
>>>do not arise through known methods of design -- human engineers cross-copy
>>>components into very different designs (e.g. CD players installed in both
>>>GM
>>>sedans and Ford trucks). Nature does not: pterosaurs and bats, although
>>>both used furry membranous wings, use different ways of modifying
>>>forelimbs
>>>to produce those wings.
>>
>> are you saying that similarity, wherever observed, must always be
>> evidence of common roots and never evidence of cross-copying? On what
>> basis do you decide that certain similarities cannot be the result of
>> cross copying and other similarities are the result of cross-copying?
>>
>I was talking, in this case, about *dissimilarity*.
you're not answering my question, you know. Why is similarity
evidence of common roots only and never evidence of cross-copying?
> Pterosaurs and bats
>clearly aren't examples of cross-copying, because their shared features are
>all shared with the larger category of amniote vertebrates, and their
>derived features -- e.g. wings and other flight adaptions -- are different
>from each other. Just as a tape player in one truck isn't cross-copied from
>a CD player in another, so bird, bat, and pterosaur wings don't seem to be
>examples of cross-copying.
yet the same intelligence can choose to make a tape and make a CD
player, right?
> Conversely, we see that small, insect-eating
>birds have the same basic wing structure as large birds like eagles (or
>ostriches, for that matter), while small, insect-eating bats have the same
>basic wing structure (as well as many other anatomical similarities to)
>large fruit bats. If wings aren't cross-copied between bats and birds in
>similar ecological niches, and both bats and birds fall into the consistent
>nested hierarchies expected from common descent, isn't it reasonable to
>ascribe the shared wings of bats to common roots?
only if the starting premise is validated that similarity always means
relationship and common roots. You have to establish that premise on
a firm foundation of facts. What facts do you have that will
establish a fundamental rule that similarity always means common
descent or common roots? And if there are exceptions, then on what
basis do you decide that certain similarities mean common root and
other similarities don't?
snip>
.
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