Genome sequencing leaves Creationists unable to respond

[Onlooker]

ToE does not assert this, as I have now said at least five times in this thread. ToE only describes HOW, of God created all things, He did so. It says nothing about whether He did so.

So we have yet another creationist who doesn't know what ToE says, and doesn't want to learn.
There is no science of ID. ID is not science.

Your system is a belief also.
Accept your belief.
Until you can show your proof like you stated earlier, all this is for naught.

 

[Onlooker]

And yet more evidence that you are ignorant of genetics and DNA.

Please give us all a primer.

 

[Autodidact]

All nice sites. Out of the millions of pages you can give, did you really need to site Berekely?
No doubt many pages explaining all the faith based beliefs and greater power and strength with mutations that may or may not have done something beneficial.

all my cites are from scientific sources. So you equate science with faith-based?

You need to read some elementary genetics and figure out the system.
How does proteins get made?
What is the rate of mutations that occur?
What does that mutation actually do?
How many of these improbable mutations can actually do anything constructive just on a "1 protein" model.
Now calculate on a simple organelle.
Just not probable.
Your system is faith based.You do the math.

Actually, you're the one making an assertion and challenging the entire structure of Biology--you do the math.

 

[Autodidact]

All nice sites. Out of the millions of pages you can give, did you really need to site Berekely?

You have a problem with scientific sources?

You made an assertion. You asserted that mutations cause disease. This assertion is false, as I have shown. Do you have a cite to support your assertion, or would you like to just admit your error?

 

[Autodidact]

So why do you ask for proof on ID.

I asked for proof on something? Please cite post; I'm skeptical.

Use the scientific method to study all possibilities.

We did that, over 100 years ago. We found that one of them is correct. Now you expect science to go back and unlearn, undo its foundations, as well as the last 100 years of progress in Biology.

Like Intelligent Design.
That is the scientific way.

Science cannot study ID, because it is not a scientific concept. It's philosophy or theology, which is where it belongs. Do you understand why, or do I need to explain it?

 

[Autodidact]

So why do you ask for proof on ID.
Use the scientific method to study all possibilities.
Like Intelligent Design.
That is the scientific way.

Your system is a belief also.

My belief is that science works. Do you agree or disagree?

Accept your belief.

Did that.

Until you can show your proof like you stated earlier, all this is for naught.

As I have now explained several times, science does not admit of proof. Proof is math. Science is evidence. The evidence supports ToE, which is why science accepts it. You have told us that you are not interested in the evidence, which does not surprise me. If you were, you too would accept ToE.

Science is empirical. It is evidence-based. It's all about the evidence--the one thing, for some reason, you do not want to talk about. Why is that?

 

[Onlooker]

Can you produce a scientific cite for this non-fact? Because what I get is: [UC Berkeley Evolution 101] and
[SIZE=-1]Genetics, Vol. 151, 1621-1631, April 1999, Copyright © 1999 [/SIZE]
Beneficial Mutations, Hitchhiking and the Evolution of Mutation Rates in Sexual Populations

Toby Johnson
Institute of Cell, Animal and Population Biology, University of Edinburgh, Edinburgh EH9 3JT, Scotland

and

BMC Evolutionary Biology
Research article Open Access
Identification and dynamics of a beneficial mutation in a long-term
evolution experiment with Escherichia coli
Mark T Stanek†1, Tim F Cooper†2 and Richard E Lenski*1

Would you show your math? thanks.

Are you serious.
What this tells me is you dont read your sources.
Some very, very basic genetic facts.
No citing.

Missense and nonsense mutations are point mutations: sickle cell and thalassemia.
Frameshift are non multiple of 3 (the codon remember) which can cause severe disease/death.

 

[Onlooker]

Saying "god did it" might make it easily explained but it isn't science. I could just as easily explain it all by saying the process was guided by super powerful aliens.

Read more into your faith based system. What I mean is the non God system believes in Big Bang from no guided force, abiogensis from no guided force or aliens, then evolution from no outside intelligent force.
The kicker is DNA co founder Crick. After thinking about the complex, cryptic and awesome DNA machinery, believed in Panspermia.
So join the club.
Aliens may have done it according to your faith system.

 

[micrurus]

Missense and nonsense mutations are point mutations: sickle cell and thalassemia.
Frameshift are non multiple of 3 (the codon remember) which can cause severe disease/death.

ah yes sickle cell, the fact that it gives people resistance to malaria is absolutly not positive.
in the rich spoiled west it may be a didease but when you go to places like......Africa, resistance to malaria is seen as a possitive thing. don't you think?

 

[Onlooker]

ah yes sickle cell, the fact that it gives people resistance to malaria is absolutly not positive.
in the rich spoiled west it may be a didease but when you go to places like......Africa, resistance to malaria is seen as a possitive thing. don't you think?

Ah yes,
that mutation that substitutes glutamic for valine.
Remember you guys dont believe that the environment caused it, it just selected out with a filter.
Think about this. These mutations killed everybody else (homozygous) prematurely, or gave them harsh limitations compared to not having it.
We found a population that may proportionally live longer in a malarial filled area. That is to say, without the life draining mutation, my life in this malarial filled area is 15 years old. Now that I have this crappy (but ToE says its a gift) mutation, I can live to 35 years old.
This is evolution at work. Excellent example to use.
My point, this mutation in other tribes/peoples living eleswhere, they died off. Only in a diseases filled area did it actually "lengthen" life.
So this random mutation selected a weaker human genome compared to the non mutated genome.
This weaker genome may have proportionally lived longer, along with lung disease, bone breaking pain, clotting in every capillary of your body, strokes, hemorrhages.
Yes, keep using this example, not very convincing.

Rich Spoiled West? You are "leaking" progressiveness.

 

[tumbleweed41]

Adaptation to High and Low Temperatures by E. coli.

A single clone of E. coli was cultured at 37 C (that is 37 degrees Celsius) for 2000 generations. A single clone was then extracted from this population and divided into replicates that were then cultured at either 32 C , 37 C, or 42 C for a total of another 2000 generations. Adaptation of the new lines was periodically measured by competing these selection lines against the ancestor population. By the end of the experiment, the lines cultured at 32 C were shown to be 10% fitter that the ancestor population (at 32 C), and the line cultured at 42 C was shown to be 20% more fit than the ancestor population. The replicate line that was cultured at 37 C showed little improvement over the ancestral line.Bennett, A.F., Lenski, R.E., & Mittler, J.E. (1992). Evolutionary adaptation to temperature I. Fitness responses of Escherichia coli to changes in its thermal environment. Evolution, 46:16-30.


http://www.gate.net/~rwms/EvoMutations.html
​

 

[tumbleweed41]

Adaptation to Growth in the Dark by Chlamydomonas.

Chlamydomonas is a unicellular green algae capable of photosynthesis in light, but also somewhat capable of growth in the dark by using acetate as a carbon source. Graham Bell cultured several clonal lines of Chlamydomonas in the dark for several hundred generations. Some of the lines grew well in the dark, but other lines were almost unable to grow at all. The poor growth lines improved throughout the course of the experiment until by 600 generations they were well adapted to growth in the dark. This experiment showed that new, beneficial mutations are capable of quickly (in hundreds of generations) adapting an organism that almost required light for survival to growth in the complete absence of light.

http://www.gate.net/~rwms/EvoMutations.html
​

 

[tumbleweed41]

Selection for Large Size in Chlamydomomas

Bell also selected clonal lines of Chlamydomonas for size by passing cultures through a fine filter and discarding the cells that were not retained on the filter. He reports that although this method was not very effective at retaining the largest cells (due to inconsistencies in the filter pore size), after forty generations of this selection technique, the cell diameter had increased by an average of about 1 phenotypic standard deviation.

http://www.gate.net/~rwms/EvoMutations.html
​

 

[tumbleweed41]

Adaptation to a Low Phosphate Chemostat Environment by a Clonal Line of Yeast

P.E. Hansche and J.C. Francis set up chemosats to allow evolution of a single clonal line of beer yeast in a phosphate limited (due to high pH) environment. (A chemostat is a device that allows the propagation of microorganisms in an extremely constant environment.) The yeast clones grew slowly for about the first 180 generations when there was an abrupt increase in population density. This was later shown to be due to better assimilation of the phosphate, presumably due to an improvement in the permease molecule. (Permease is an enzyme that controls what is allowed to come into the cell through the yeast's cell membrane.) After about 400 generations, a second improvement in cell growth rates occurred because of a mutation to the yeast's phosphatase (an enzyme that improves the cells ability to use phosphate). The phosphatase became more active overall, and its optimal pH (the pH where it is most active) was raised. Finally, a third mutant appeared after 800 generations that caused the yeast cells to clump. This raised the population density in the chemostat because individual cells were no longer being washed out of chemostat (which is one of the methods that the chemostat uses to maintain very uniform conditions) as quickly as they had prior to the mutation. (This is just speculation on my part, but I wonder if it wasn't under some similar conditions that multi-cellularity became favored over unicellularity - perhaps on a sea bed or river bottom.)This experiment was repeated, and the same mutations occurred, but in different orders. Also, in one replication, the processing of phosphate was improved by a duplication of the gene that produces phosphatase. This is experimental evidence of an extremely important mechanism in evolutionary history! It is also a particularly elegant experiment because not only was all of this adaptation shown to occur in clonal lines (descended from a single individual), but the authors also determined the exact mutations that caused the improved adaptations by sequencing the genes and proteins involved.
Francis, J.E., & Hansche, P.E. (1972) Directed evolution of metabolic pathways in microbial populations. I. Modification of the acid phosphatase pH optimum in Saccharaomyces cervisiae. Genetics, 70: 59-73.
Francis, J.E., & Hansche, P.E. (1973) Directed evolution of metabolic pathways in microbial populations. II. A repeatable adaptation in Saccharaomyces cervisiae. Genetics, 74:259-265.
Hansche, P.E. (1975) Gene duplication as a mechanism of genetic adaptation in Saccharaomyces cervisiae. Genetics, 79: 661-674.


http://www.gate.net/~rwms/EvoMutations.html
​

 

[tumbleweed41]

Evidence of genetic divergence and beneficial mutations in bacteria after 10,000 generations

Papadopoulos, D., Schneider, D., Meier-Eiss, J., Arber, W., Lenski, R. E., Blot, M. (1999). Genomic evolution during a 10,000-generation
experiment with bacteria. Proc. Natl. Acad. Sci. U. S. A. 96: 3807-3812Edited by John R. Roth, University of Utah, Salt Lake City, UT, and approved February 3, 1999 (received for review July 21, 1998)
Molecular methods are used widely to measure genetic diversity within populations and determine relationships among species. However, it is difficult to observe genomic evolution in action because these dynamics are too slow in most organisms. To overcome this limitation, we sampled genomes from populations of Escherichia coli evolving in the laboratory for 10,000 generations. We analyzed the genomes for restriction fragment length polymorphisms (RFLP) using seven insertion sequences (IS) as probes; most polymorphisms detected by this approach reflect rearrangements (including transpositions) rather than point mutations. The evolving genomes became increasingly different from their ancestor over time. Moreover, tremendous diversity accumulated within each population, such that almost every individual had a different genetic fingerprint after 10,000 generations. As has been often suggested, but not previously shown by experiment, the rates of phenotypic and genomic change were discordant, both across replicate populations and over time within a population. Certain pivotal mutations were shared by all descendants in a population, and these are candidates for beneficial mutations, which are rare and difficult to find. More generally, these data show that the genome is highly dynamic even over a time scale that is, from an evolutionary perspective, very brief.


http://www.gate.net/~rwms/EvoMutations.html​

 

[tumbleweed41]

Etc, etc, etc.....

 

[Onlooker]

Adaptation to High and Low Temperatures by E. coli.

This is homework I can read (just one example from that website would have been enough).
Before reading, its not disproving my hypothesis.
That an intelligent design created a database for all organisms. This is shown by such similarity among a huge diverse species.
No one knows what all this junk DNA that we share does.
No one knows what all the junk DNA in bacteria represents.
Again, before I read the above, know one knows that bacteria's DNA already has codons ready to be read if temp/pH/osmotic/uv/etc. changes.
Just dont know yet, but its awesome isnt it.

 

[tumbleweed41]

This is homework I can read (just one example from that website would have been enough).
Before reading, its not disproving my hypothesis.
That an intelligent design created a database for all organisms. This is shown by such similarity among a huge diverse species.
No one knows what all this junk DNA that we share does.
No one knows what all the junk DNA in bacteria represents.
Again, before I read the above, know one knows that bacteria's DNA already has codons ready to be read if temp/pH/osmotic/uv/etc. changes.
Just dont know yet, but its awesome isnt it.

I am not here to disprove your hypothesis.

It is up to you to provide objective, empirical evidence that it is viable.

Rather than your current speculative musings.

 

[David M]

Please give us all a primer.

Wikipedia details the different types of mutations that have been observed, and shows there are mutations of more than single codons.

Mutation - Wikipedia, the free encyclopedia

 

[Onlooker]

I am not here to disprove your hypothesis.

It is up to you to provide objective, empirical evidence that it is viable.

Rather than your current speculative musings.

speaking of musings, did you read your 1st study. Im almost done.
ready to discuss some science?