Re: Request


"Zoe" <muze10@xxxxxxx> wrote in message
news:79oif1l9d17qe44ck0i901p4og0coa7rr1@xxxxxxxxxx
> On Thu, 4 Aug 2005 22:23:34 -0500, "Steven J."
> <sjt1957NOSPAM@xxxxxxxxxxxxxxxxxxxx> wrote:
>
-- [snip]
>
> 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.
>
No, that is not the basis. The basis is this: if the last common ancestor
(LCA) of great apes had 23 pairs of chromosomes, then at least three
fissions (of the exact same chromosome, at the exact same place on that
chromosome) had to take place (once in the line leading from the LCA to
orangutans, and once again in the line leading to gorillas after the African
apes split off, and once yet again in the chimp line after the human-chimp
split). Meanwhile, no other chromosomes split or fused in any lineage -- so
why (if the LCA had 24 chromosome pairs) did chromosome 2 split at the same
place in every line except our own? But if the LCA had 24 pairs of
chromosomes, then we only have to account for one fusion in the line leading
to humans after the human-chimp split.
>
> 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.
>
Stephen J. Gould offered metaphor that became famous: picture a drunk,
starting at a wall and wandering randomly back and forth. The more time he
wanders, on average, the further he will get from the wall (simply because
he can't get closer to the wall than he was when he started, or go through
it), but any given step or set of steps may take him further from the wall
or further from it (you might want to think of a whole line of drunks, some
staying near the wall, some getting away from it and wandering back, and
others wandering further and further away). The wall represents the minimal
complexity needed to be a living cell (it might be possible for a lineage to
lose that minimal complexity -- but as Darwin pointed out, in a modern,
bacteria-filled world, a lineage that did so wouldn't be a "protocell;" it
would be lunch for the nearest bacterium).

Presumably, if life originated from simpler self-replicating molecules, then
the first life form (ca. four billion years ago) had fewer genes than most
(perhaps any) current species. But evolutionists don't think that evolution
is invariably progressive. Likewise, once complexity has evolved (once a
lineage is far enough away from the "wall" of minimal complexity), it can
perfectly well be lost again: indeed, evolution is replete with examples of
lost complexity (e.g. the hindlimbs of whales, or all the limbs of snakes).
For that matter, what evolutionist typically expect, with regard to number
of parts, is *reduction* of the number of parts, with the remaining parts
becoming more specialized (i.e. a lot of parts that look alike become a
smaller number of parts that look different from each other).

Of course, reducing the number of chromosomes through fusion no more reduces
the number of genes or the amount of "genetic information" than
consolidating three volumes of _Lord of the Rings_ into one makes the novel
shorter.
>
> 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.
>
Yes, as far as we know that is perfectly possible. However, to explain the
difference in chromosome numbers among the hominoid (great ape and human)
species through fission, you need, as noted aboe, three fissions in the
exact same place, with no other chromosome fissions or fusions taking place
among the hominoids during that time. That seems rather like bucking the
odds.
>
> 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).
>
Yes, *if* we had no idea of the order in which the various hominoid lineages
split off from one another, you would be correct. If it were reasonable to
accept common descent, but assume that, e.g. oranguatans were more closely
related to chimps than we are, then yes, a fission would be as "likely" an
explanation as a fusion (aside from the vestigial telomere and centromere in
chromosome 2)..

The trouble is, genetic sequences strongly indicate that gorillas split off
from the chimp-human line *before* chimps and humans split from each other.
And, of course, oranguatans are even more different, and therefore (it is
inferred) split off from the line leading to African apes before the
human-gorilla split. This is why I didn't bring up bonobos (pygmy
chimps): they also have 24 chromosome pairs, but they split off from chimps
after chimps split off from us, so if a chromosome fission took place early
in the chimp line (after it split from humans) it could be easily inherited
by both species. If you count in all the great ape species (not just the
splits that occurred between the great ape-lesser ape split and the
human-chimp split), then species with 24 pairs outnumber those with 23 pairs
by about six to one, not three to one -- but those splits that took place
after the human-chimp LCA don't "count" for this purpose.

By the way, while I don't think it's important to this discussion,
"mutations are random" does *NOT* mean "all mutations are equally likely,"
or "all mutations are equally likely to be selected" (while there's no
reason to believe fusions are more likely to become fixed in a population
than fissions, if they *were* more likely to be fixed, it would not mean
that these sorts of mutations were not random). "Random" means simply that
whatever causes mutations is not related to whatever causes mutations to be
beneficial, harmful, or neutral.
>
-- [large snip]
>
>>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.
>
Why would you not use random mutations? If you don't know how to make a
digestive system, making lots of copies of an initial cell, varying them in
small ways, and seeing which ways move you closer to a digestive system,
might be a better idea than trying to dream up a complete digestive system
from scratch. Note that, before there are any digestive systems, you can't
very well copy one that already exists (since none do).

Note that developmental biologists are attempting to learn from nature and
discover the processes at work (why copy them? we already have digestive
systems). As yet, only the broad outlines and a few isolated details of how
genes and the other molecular systems in a cell build an organism are well
understood; the exact number of genes in a human or chimp has not been
counted yet, and still less is the exact function of all those genes (many
still unknown) discovered.
>
>>> 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.
>
One of the things that have been inferred to have happened is common
descent.
>
>>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?
>
I have argued that *consistent* nested hierarchies -- seen if families of
hand-copied manuscripts, families of languages, and clades of living
organisms -- imply common descent. Your supposed counterexamples involve
sets of entities that fall into very different hierarchies depending on what
traits one chooses to examine and compare.
>
>> in biogeography,
>
> why does biogeography mean common descent, unless there is a
> preconceived notion in place?
>
If, e.g. the various genera of the hominoids are not related, why do the two
living genera most genetically similar to humans share a continent with [a]
the greatest genetic diversity of humans (indicating humans have lived on
that continent longer than they've lived on other continenets), and [b] with
the australopiths, the extinct great ape genus most similar to our own genus
_Homo_. On the assumption of separate creation, gorillas might as well be
in Asia along with orangutans -- or even in Central America alongside howler
monkeys. Separate origins offers no reason for similar "kinds" to be found
in the same geological region as one another or extinct "kinds" similar to
them.
>
>>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.
>
"Vestigial structures" are defined as having *reduced* function, not *no*
function, and can be recognized without regard to evolutionary notions.
Indeed, they can be recognized where evolution is rejected as an
explanation: the shortened simplified limbs of a thalidomide baby are
vestigial according to definition (that is, they lack some of the function
of homologous structures in related or allied organisms), but the vestigial
limbs aren't caused by any genetic change (the genes are unchanged), and
therefore cannot be an example of evolution. However, when vestigial
features are not the result of developmental derangement, it is reasonable
to ask why they share so many details of structure with organs with which
they do not share details of function, in species otherwise very similar to
the one with the vestigial structure.

Saying that the appendix is vestigial does not mean it does nothing; it
means that it occupies the location and shares embryological and anatomical
features with the caecum, a pouch used to digest leaves in many monkeys.
Since it doesn't digest leaves in humans, why does it have this location and
these traits? Why does the human tailbone, whatever its uses, share so many
homologies to actual tails in other primates (and other mammals)? Vestigial
structures are simply an extreme case of the problem of "parahomology:"
similar designs for dissimilar functions. It's one thing to use commn
design for common purposes, but what logic (other than evolutionary logic,
in which the function of a structure can evolve over time, without erasing
all traces of the structure's history) is there to common design for
different purposes (especially when there is also -- consider bat, bird, and
pterosaur wings -- different design for common purposes).
>
>> in the
>>fossil record,
>
> the fossil record is subject to interpretation.
>
Yes, and when some creationists say that ER1470 is "fully human" and others
say it is "fully ape," then something is wrong with the creationist
interpretation (that all fossils are fully one "kind" or another, with no
intermediates) can possibly be correct.
>
>>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.
>
There is no creation theory, and your ramblings have not changed that.
There was a creation theory once. It predicted that no genus would ever go
extinct, that human artifacts would turn up under the lowest level of
sediments, and that scientific dating methods would show the Earth to be
thousands of years old. After all of these predictions failed, creation
theory was replaced with the assertion that evidence means nothing, if it
contradicts religious dogma, because God could have created the world and
subsequently intervened in it in any manner that struck His fancy.
Elaborating this position with every "god of the gaps" argument that springs
to mind does not make creationism a theory.

And you, please note, have not demonstrated that natural selection of
mutations "fails" to produce a digestive system. Above, you argue that we
cannot assert that some structures are functionless "junk" because we don't
know all the details of how biology works. Here, you seem to ignore you own
point and argue that we know so much about all the details of biology that
if it were possible to give a mutation-by-mutation, selective
regime-by-selective regime evolutionary history of the digestive tract, any
supporter of mainstream science could pull one out of his hat. I do not
think you can logically adhere to both positions at once.
>
>> 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.
>
Zoe, you are being obstinate here. You are simply assuming that you, in
abject ignorance of biology, know more about how living things work that
thousands of scientists who've spend decades studying these systems.
>
>> 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.
>
You are wrong. You are stringing words together and mistaking this for an
argument.
>
>>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?
>
Multicellularity preceeds specialization of the cells in question. For that
matter, formation of a digestive system preceeds all those specialized
subcomponents you mention.
>
>> 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]
>
>>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.
>
I would assume this on the evidence that mtDNA differences are larger than
nuclear DNA differences both within species (e.g. humans) and between
species (e.g. humans and chimps). This is pretty much common knowledge.
Again, you seem to be confusing percentage of sequence similarity with the
percentage of genes that have some difference. Having 83% of *genes*
different is not the same as having 83% of the sequence of nucleotides
different, and indeed one could in principle have 99% sequence similarity,
with 100% of genes each being 1% different in the two species. If you don't
understand this, what in this discussion are you capable of understanding?
>
>>-- [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?
>
Zoe, as a rule, when I include a parentheses that says "ca. 30% of the
sequence" after "massive," you are justified in assuming I meant, by
"massive," "about 30% of the sequence." This is far greater than the
sequence difference between humans and, say, monkeys. And when I say that
these changes could be made "without making any changes at all in the
proteins produced or the way the organism grows," I thought you would deduce
that, in fact, the species would not "morph" at all, even though the genetic
changes are larger than those separating dogs from cats.
>
>> 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?
>
We were discussing whether 98.4% sequence similarity had to mean 98.4
percent morphological similarity. There are two aspects to that question:
do tiny changes in the genome automatically mean tiny changes in the
organism, and do large changes in the genome automatically mean large
changes in the organism. We were discussing, above, the latter point.
>
-- [snip]
>
>>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.
>
No, we are discussing what different forms of the same gene can do, as part
of an attempt to show you that large changes in the genome do not have to
mean large changes in the phenotype. Can the human gene do the same job as
the fly gene, even though it is not identical to the fly gene? If it can
trigger eye development, there is reason to suppose it can.
>
-- [snip]
>
>>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?
>
No, Zoe, genes are recognizable as genes whether they are "turned on" or
not. And, by the way, we were discussing cytochrome-c, not the GULO
pseudogene (which I think is not found in pine trees).
>
>> 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.
>
Frankly, I'm beginning to think I could have a more productive discussion of
evolution with an ant.
>
-- [snip]
>
-- Steven J.


.

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