Re: Possible vs. Likely
- From: Seanpit <seanpit@xxxxxxxxx>
- Date: Sun, 30 Nov 2008 07:59:12 -0800 (PST)
On Nov 29, 10:16 am, Ron O <rokim...@xxxxxxx> wrote:
On Nov 29, 9:45 am, "\(M\)-adman" <g...@xxxxxxxxxx> wrote:
Ron O wrote:
On Nov 28, 11:50 am, "'Rev Dr' Lenny Flank" <lfl...@xxxxxxxxx> wrote:
On Nov 28, 12:11 pm, Seanpit <sean...@xxxxxxxxx> wrote:
(snip)> Name a unique functional difference between humans and
chimps that
isn't just quantitative but qualitative . . . Then, once you have
done this, show the minimum number of genetic differences needed to
produce this novel functional difference.
(snip)
I'm a little curious here . . .
Humans and chimps are closer to each other, genetically, than many
other species are which creationists consider to be the same "kind"
-- horses and donkeys, for instance, or cheetahs and jaguars.
We don't know enough about the genetics of humans and apes to be
definitive in this matter. That's the point. However, there are
clues that humans and apes do not have the same kind of gene pool of
options as, say, horses and donkeys or cheetahs and jaguars. The most
obvious difference is that humans and apes cannot produce viable
offspring. And yes, this has been tested.
Another difference is the cellular and structural differences of major
organ systems like the brain. It seems like these differences are not
so much based on significant differences in coding genes or protein
building-block products, but in differences in non-coding DNA that
manipulates the coding portions of the genomes. A significant number
of non-coding DNA sequences have been discovered and this number and
percentage is growing.
"For example, miRNAs recently have been implicated in synaptic
development and in memory formation. As the species specific miRNAs
described here are expressed in the brain, which is the most complex
tissue in the human body, with an estimated 10,000 different cell
types, these miRNAs could have a role in establishing or maintaining
cellular diversity and could thereby contribute to the differences in
human and chimpanzee brain ... function."
Eugene Berezikov, Fritz Thuemmler, Linda W van Laake, Ivanela Kondova,
Ronald Bontrop4, Edwin Cuppen & Ronald H A Plasterk, "Diversity of
microRNAs in human and chimpanzee brain", Nature Genetics, Vol 38 |
Number 12 | December 2006 pp. 1375-1377.
http://www.detectingdesign.com/earlyman.html#Key
Why then do you consider it utterly absolutely completely impossible
for humans to have "micro-evolved" their genetic differencesd with
chimps, but NOT utterly absolutely completely impossible for members
of other "kinds" to have "micro-evolved" their LARGER genetic
differences with each other?
I've repeatedly explained in this forum that I do not think there is
enough evidence to adequately exclude human-ape common ancestry on a
genetic basis at this point. If you would have read the rest of my
comments on this topic instead of snipping them, you would have
understood this in this particular thread as well.
If the genetic differences between jaguars and cheetahs can have
evolved, then why do you insist that the SMALLER genetic differences
between chimps and humans, can not have?
Besides, of course, your religious opinion that humans are special
and simply cannot be related through descent to any other animal, no
matter what . . .
I've never said that . . .
================================================
Lenny Flank
"There are no loose threads in the web of life"
Editor, Red and Black Publishershttp://www.RedandBlackPublishers.com
It is worse than that for Sean because he seems to have this evidence
thing and backing up your own notions out of whack with reality. If
Sean wants to contend that he has something Sean has to come up with
examples that we can't explain. I haven't heard of any "qualitiative"
rather than "quantitative" difference that exist between humans and
chimps.
That's because no one knows enough about the genetics of either humans
or apes. We know that there probably are qualitative differences due
to the fact that humans and apes cannot produce viable offspring while
other species pairs, like donkeys and horses, can. Again, there are
hints of key qualitative genetic differences, especially now that we
are learning more about non-coding DNA. However, at this point, we
simply do not know enough about these differences to adequately
propose an overwhelming block to RM/NS.
Intellectually, chimps are about equivalent to 4 year old
humans. We share all our tissues and organs. Heck, we have about the
same number of hair follicles on our bodies as a chimp. The only
differences in our brains seems to be the size of the different
sections. We seem to share all brain parts. Sean has to demonstrate
that his type of gap exists.
We do not share certain features of cellular structure and
organization within the brain - for example. Again, such differences
are understood well enough at this point to say anything definitive.
We know far more about less complex systems, like subcellular systems,
that do show very clear limitations to the mechanism of RM/NS.
What probably gets to Sean is how his bogus 1000 aa argument breaks
down with closely related species like chimps and humans. Sean comes
face to face with one obvious fact. Any change in any gene, protein,
whatever, has to work within the whole. Whether some new change is
part of a large existing complex or the start of some future large
complex it has to work within what already exists.
That's right . . .
If it doesn't it
has to limp along and exist against selection to remove it, and most
likely it is lost.
Right again . . .
What we see are the changes that fit well enough
to make it. Sean can't cope with that fact.
Where have I said anything else but this? This is a big part of my
own position on this topic.
His whole 1000 aa bull
pucky is based on some stupid reality that doesn't exist.
There are lots of known systems that require far more than 1000 fsaar
at minimum to work. Tell me, how can you make a flagellar system with
less than 1000 fsaar? Think you can do it? How?
He comes
face to face with that reality with chimps and humans, and has to
demand that his opposition provide what he cannot. Sean has to
demonstrate that his type of gaps ever existed. He can't do that with
the human and chimp example.
You guys hide behind creatures and systems which are largely unknown
instead of even trying to deal with those systems that are much better
known and understood. What a crock . . .
Ron Okimoto
If a gene can "limp along and exist against
selection to remove it" as you say, then that kinda
shoots evolution down to ZERO.
We know of examples of this. You can go into any extant population
and find deleterious mutations segregating. Just look up any paper on
mutation selection balance. We have examples where gene knockouts
have been fixed in populations and those species have had to deal with
loss of the gene. The gene responsible for vitamin C defficiency in
humans and other primates down to Monkeys is due to the knock out of a
single gene. The common ancestor of monkeys including the lineage
that evolved into humans is descended from a population where this
gene knock out got fixed due to genetic drift or founder effects or
some combination of such factors. Scurvy is the result of not having
enough vitamin C in our diets due to this gene loss. Evolution
doesn't necessarily allow only good things to happen. If it did
extinction would not be as common as it is.
That's right . . . In fact, "devolution" or significant ongoing
genetic losses are a real problem to the overall ToE.
http://www.detectingdesign.com/dnamutationrates.html#Detrimental
How can random mutations take
place if a gene can limp along and exist against selection to
remove it?
Really, just look up mutation selection balance and learn something.
Populations can exist with quite a load of deleterious mutations. It
isn't just theory, we have done genetic analysis of populations like
flies and even population studies of humans to demonstrate it. What
do you think it means when they estimate that every human carries a
genetic load of around 2.5. This means that the average human has the
equivalent of 2.5 recessive lethals in their genomes.
It is actually worse than that when one considers all the non-lethal
deleterious mutations that are present in the genomes of humans and
all other slowing reproducing creatures.
This isn't all bad. There are plenty of examples of where a second
mutation can "fix" the detrimental effects of another mutation. Look
up papers on second site reversions.
That's right. It is fairly easy to step back onto a beneficial island
which a population has taken a very short step off of in the past.
This increases the evolutionary
potential of any population since Sean's gaps of 2 or 3 mutations can
obviously be crossed under such conditions.
It is one thing to step off of an island that one was already on in
the past. It is quite another think to find a novel beneficial island
to begin with.
Just ask Sean why he went
from demanding examples of 3 mutation gaps to his 1000 aa bull pucky.
He did the calculations himself and figured out that 3 mutation gaps
aren't that much of a problem. So he had to go into gap inflation.
It went from 3 to 20 and then 40 fairly quickly and then he settled on
the 1000 aa junk.
It is just amazing to me that you still do not understand, despite my
explaining it to you dozens and dozens of times, that the structural
threshold of 1000 fsaar is NOT a measure of the gap distance. It is
the measure of a level of functional complexity. Functional
complexity is not the same thing as the likely gap distance. The
likely minimum gap distance is always smaller than the level of
functional complexity - always. The smallest gap distance between an
existing starting point and a potential target at the 1000 fsaar level
is likely to be only a few dozen mutational changes wide.
I've been explaining this for over ten years now. There's been no
"inflation" here. That's just your strawman misrepresentation.
< snip >
Sean Pitman
www.DetectingDesign.com
.
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