despite that....you still can't explain how mutations add up.
Still avoiding the explanations given to you, 57?
Previous count update/post 2012/03/25... Today is 2012/04/15
I'll stand in for him!
Recall please that the numbers show how many times this information has been posted for 57's benefit. Feel free to use all or part to continue to educate him.
31/21/20/14/14/13/10 <==== counts of number of times of 'presentation to 57' for each differenet explanation in a sub-part of this message
Dec 27, 2010 -- 3:13PM, d_p_m wrote:
Dec 26, 2010 -- 1:57PM, d_p_m wrote:
What part of 'every codon in the human genome is mutated every 20 years or less' have you
I've replied to that SEVERAL times but you just seem to keep forgetting.
Not with anything based in fact and logic.
Q)...HOW MANY OF THEM WILL BE BENEFICIAL?
A)...probably none. Sooooooooooo what's your point?
So nice of you to invent an answer for us. Fortunately it is
incorrect. You claim that there are no favourable mutations.
To falsify that all I have to do is point to one favourable human
mutation. I am not a geneticist, but I can point to several off the top
of my head.
1.Fair skin – an adaptation to northern latitudes.
2.Laplanders possess a mutation that allows their core body temperature
to drop without catastrophic hypothermia.
3.The recently discovered 'plague immunity gene' of European origin.
4.Adult lactose tolerance, European.
5.Adult lactose tolerance, African (different mutation, same effect)
6.Adult lactose tolerance (third mutation, same effect)
7.APO1 Milano, which confers immunity to bad effects of dietary
cholesterol Of course there are a myriad of others,
but that's enough that your assertion goes down in flames.
Oh, and if there just so happens to be two...what are the odds of them
effecting the same trait?
Oh, good! Let's do the math! Humans have about 3 x 10^9 base
pairs in their genome, encoding 2 – 2.5 x 10^4 proteins.
Protein coding represents about 1.5 x 10^-2 of the genome, with maybe .8
of it given over to regulatory code. Thus the average protein is coded
for by about 4.5 x 10^7 / 2.5 x 10^4 = 1800 codons. Now, more than one
protein is involved in any part of the body. Let's call it 10, thus coded
for by 18000 codons, on the average. In addition, gene expression is regulated
by roughly 2.7 x 10^9 codons. Let's assume that a similar proportion of
regulatory DNA is involved as protein DNA. Let us also assume that only
one regulatory area affects each protein... so we are looking at 1/2500
of the regulatory code... about 2.7 x 10^9 / 2.5 x 10^3 or roughly 10^6
codons. Thus the total codons involved in one of your ill-defined traits
is about 10^6 + 1.8 x 10^3, which is 10^6 codons. Now, each codon in the
human genome is mutated every 20 years, so each 'trait' (whatever that
is) is mutated 10^6 times every 20 years. We also know that the fixation rate
of neutral mutations is about 10^-5, so about 10 changes to any 'trait'
(sic) will be fixed each generation. Once that happens sexual
reproduction and continuing mutation both guarantee that the same 'trait'
(sic) will be the subject of multiple neutral mutations. Of course, any beneficial
mutations will fix more often, and spread more rapidly and thus add up
more rapidly. PS... on the rapid spread of beneficial mutations - note that
adult lactose tolerance is found in .98 of people in some of the Northern
European populations in only 10,000 years. The proportion is about .75
among the Fulani people in the Sahel, .... since domesticated cattle
reached this area just a couple of millennia ago.
Feb 5, 2011 -- 4:22PM, rsielin wrote:
This creationists shares the common *cdesign proponentsist*
misconceptions that genes are created de novo and that the odds of
randomly constructing an entire functioning gene from scratch are in some
way relevant to a debate over evolution. They aren’t, and they aren’t.
Evolution doesn’t work by building new genes for new proteins very often.
It works by sequentially modifying existing genes and proteins. It’s not
the odds of getting a specific sequence in isolation; it’s the odds of
getting a sequence that works. And working means interacting and
expression with the all other sequences that are present.
More about adding information:
me: Still waiting for the usually vocal YEC squad to present the YEC
explanation for why the addition of a partial or complete second 21st
chromosome (Down's syndrome) is NOT adding new information?
Still waiting for the usually vocal YEC squad to present the YEC
explanation for why the addition of a partial or complete second 21st
chromosome (Down's syndrome) is NOT adding new information?
You YEC guys keep dodging that one.(And yes, we know it isn't a
beneficial mutation, but it IS an addition of info.)Well?
What's your problem, 57? Where is the YEc explanation?
57: How do you figure?
How do you NOT figure?
It's one of those basic math concepts that I just assumed (erroneously,
evidently) that everyone posting here understood: 2 > 1.
The only real question is how the YEC team is going to try to wriggle out
of their obvious problem --- a mutation that adds an entire new
chromosome to a person's genome can not be doing anything except adding
The YEC claim is that mutations don't add information. The mutation for
Down's syndrome adds a complete or partial chromosome.Therefore, the YEC
claim is provably wrong: mutations can --- and obviously do --- add
This is where the YEC team either ponies up evidence showing Down's
syndrome isn't accompanied by a full or partial extra 21st chromosome or
the YEC team admits that their claim about mutations not adding
information is complete crap.
If the YEC team is unable to grasp the concept of 2 > 1, then obviously
the YEC team is unable to grasp any part of the more complicated aspects
of any mainstream math or science, like addition.
So, 57 --- yes or no --- does the mutation responsible for Down's
syndrome, which adds a complete or partial 21st chromosome, add genetic
Yes or no, dude?
Original quote here:
and of course here's a whole thread dedicated to the subject:
And here's the mutation rate...
1. Humans each have on the average about 129 mutations (quoted figures
from various sources lie between about 125 and 135 mutations per
2. A more general metric, applicable from everything from E coli to
humans is that the overall error rate during DNA replication is 10^-10
nucleotides per replication. In order to get the mutations per
generation, look up the size of the organisms genome, and apply the post
repair mutation factor of 10^-10.
Thus for E coli, the estimate goes like this:
"Our model bacterium is Esherichia coli the common, and mostly benign,
intestinal bacterium. The entire genome was sequenced in 1997 (Blattner
et al., 1997) and its size is 4,200,000 base pairs (4.2 × 106 bp). Every
time a bacterium divides this amount of DNA has to be replicated; that’s
8,400,000 nucleotides (8.4 × 106).
* * *
This means one mutation, on average, every 1200 replications (8.4 × 106 ×
1200 is about ten billion). This may not seem like much even if the
average generation time of E. coli is 24 hours. It would seem to take
four months for each mutation. But bacteria divide exponentially so the
actual rate of mutation in a growing culture is much faster. Each cell
produces two daughter cells so that after two generations there are four
cells and after three generations there are eight cells. It takes only
eleven generations to get 2048 cells (211 = 2048). At that point you
have 2048 cells dividing and the amount of DNA that is replication in
the entire population is enough to ensure at least one error every
"I based my estimate of mutation rate on what we know about the
properties of the replisome and repair enzymes. Independent measures of
mutation rates in bacteria are consistent with this estimate. For
example, the measured value for E. coli is 5.4 × 10-10 per nucleotide per
replication (Drake et al., 1998). Many of these mutations are expected
to be neutral. The rate of fixation of neutral mutations is equal to the
mutation rate so by measuring the accumulation of neutral mutations in
various lineages of bacteria you can estimate the mutation rate provided
you know the time of divergence and the generation time. (Ochman et al.,
1999) have estimated that the mutation rate in bacteria is close to
10-10 assuming that bacteria divide infrequently.
The mutation rate in eukaryotes should be about the same since the
properties of the DNA replication machinery are similar to those in
eukaryotes. Measured values of mutation rates in yeast, Caenorhabditis
elegans, Drosophila melanogaster, mouse and humans are all close to 10^-10
(Drake et al., 1998).
The haploid human genome is about 3 × 109 base pairs in size. Every time
this genome is replicated about 0.3 mutations, on average, will be
passed on to one of the daughter cells. We are interested in knowing how
many mutations are passed on to the fertilized egg (zygote) from its
parents. In order to calculate this number we need to know how many DNA
replications there are between the time that one parental zygote was
formed and the time that the egg or sperm cell that unite to form the
progeny zygote are produced.
In the case of females, this number is about 30, which means that each
female egg is the product of 30 cell divisions from the time the zygote
was formed (Vogel and Rathenberg, 1975). Human females have about 500
eggs. In males, the number of cell divisions leading to mature sperm in a
30 year old male is about 400 (Vogel and Motulsky, 1997). This means
that about 9 mutations (0.3 × 30) accumulate in the egg and about 120
mutations (0.3 × 400) accumulate in a sperm cell. Thus, each newly
formed human zygote has approximately 129 new spontaneous mutations."
Now, I'm sure you will 'forget' this too, but don't say we didn't give it
Blattner,F.R., Plunkett,G., Bloch,C.A., Perna,N.T., Burland,V.,
Riley,M., ColladoVides,J., Glasner,J.D., Rode,C.K., Mayhew,G.F., egor,J., Davis,N.W., Kirkpatrick,H.A., Goeden,M.A., Rose,D.J., Mau,B.,
and Shao,Y. (1997) The complete genome sequence of Escherichia coli K-12.
Drake,J.W., Charlesworth,B., Charlesworth,D., and Crow,J.F. (1998)
Rates of spontaneous mutation. Genetics 148:1667-1686.
Ochman,H., Elwyn,S., and Moran,N.A. (1999) Calibrating bacterial
evolution. Proc. Natl. Acad. Sci. (USA) 96:12638-12643.
Tago,Y., Imai,M., Ihara,M., Atofuji,H., Nagata,Y., and Yamamoto,K.
(2005) Escherichia coli mutator Delta polA is defective in base mismatch
correction: The nature of in vivo DNA replication errors. J. Mol. Biol.
Vogel,F. and Motulsky,A. (1997) Human Genetics: Problems and
Approaches. (Berlin, New York: Springer-Verlag).
Vogel,F. and Rathenberg,R. (1975) Spontaneous Mutation in Man. Adv.
Hum. Genet. 5:223-318.
Jun 7, 2011 -- 11:16AM, d_p_m wrote:
Jun 6, 2011 -- 10:34PM, 57 wrote:
DPM I noticed you STILL didn't answer the question.
HOW MANY WERE BENEFICIAL????
How many times do we have to tell you that 'beneficial' and 'harmful' are
Fair skin is beneficial in Norway, and harmful in the Sudan.
Really, it's not that hard.
Jun 8, 2011 -- 6:46PM, rsielin wrote:
Jun 8, 2011 -- 3:21PM, 57 wrote:
What percent are considered as
beneficial? You act like just about every mutation is beneficial. Then
again it only takes one to turn a fin into a leg. Right?
Since only 2% of mutations can be harmful, for the remaining 98%,
eventually all be become beneficial given deep time.
Development is regulated through cascades of gene expression with
proteins interacting with DNA, RNA and other proteins in order to create
morphogenic fields that direct development and produce morphological
structures. This has been determined through thousands of careful
experiments involving immunogenetics techniques as well as genetic
engineering and knock out experiments.
I have provided you with references, you have ignored them. Why do you
cling to your ignorance? Why not take the opportunity to educate
The notion that all animals are related and share almost all of the same
genes is supported by hundreds of comparative genomic studies. The fact
that differences in morphology arise primarily through changes in
regulatory regions is supported by hundreds of comparative genomic
You are fifty years behind the times. I would advise you to increase your
One last time. No one cares if you believe it or not. Either provide a
testable alternative, or STFU. You cannot ignore the conclusion of
hundreds of years of research without providing any alternative and
expect anyone to take you seriously. No one cares what you think. Provide
a testable alternative with evidence or accept the consensus of an entire
field of science. Those are your only options.
Dec 13, 2009 -- 8:57AM, Ridcully wrote:
There have been a number of experiments on evolution in vitro. Here's my
layman's summary of one by Kramer, et al. (1974 - Journal Of Molecular
In this particular study a RNA sequence of 221 nucleotides was allow to
evolve in a series of transfer experiments (moving the molecules from one
environment to another that differs in some way) after being exposed to
ethidium bromide (EtBr). In essence, the EtBr binds to the RNA making it
more difficult for it to replicate, and thus creating stress for the RNA.
One interesting thing in this case was that since there are a small
number of nucleotides, the researchers can examine the changes that occur
over time at a minute level. The bottom line is that after a number of
generations, 3 mutations occur that increase the survivability of the
RNA. Further, the scientists know exactly which 3 nucleotides changed
(say for A to U) and the sequence of the change.
In other words, this is a case where the reserachers could literally
watch the mutatins "add up."
Sorry, but I couldn't find a free link to the research on-line, but any
univerity library should have it I would think. I got my info on this
research from the book Selection: the mechanism of evolution by Bell,
Jul 7, 2011 -- 1:14PM, McAtheist wrote:
57: If anyone here can show me where a post has been presented that shows
how mutations could possibly add up...I WILL NEVER POST HERE AGAIN.
Size of dolphin genome: 3 billion base pairs
General rate of mutation: 350 per individual (Evolution, 2005, Douglas
Rate of beneficial mutations for terrestrial population heading back into
the ocean, ie --- an unfit population: 16% (Understanding the
Evolutionary Fate of Finite Populations: The Dynamics of Mutational
Effects, POLS Biology, Olin K. Silander, Olivier Tenaillon, Lin Chao)
Size of population: 23,000 dolphins are killed by Japan yearly. Assume
that this represents 5% of the world-wide population, then there are
Total number of mutations per generation: 1.61 x 107
Total number of beneficial mutations in the unfit population changing
from terrestrial to marine: (1.61 x 107) x (1.6 X 10-1) = 2.576 x 106 or
around 2.5 million beneficial mutations per generation
Number of generations needed to replace entire genome with beneficial
So, every 1200 generations, the entire genome of our proto-dolphin was
replaced by beneficial mutations. The task for you then, 57, is to show
mathematically or using demonstrated biology that this rate is
insufficient to explain the features of today's dolphins.
Remember that natural selection will eliminate deleterious mutations and
fix beneficial mutations in the population --- this aspect of natural
selection has been observed, as with mosquitoes when organophosphate
pesticides were introduced: the mutations for resistance for the new
pesticides spread rapidly and quickly became fixed in those populations
so exposed, even though (one assumes) deleterious mutations were also
So, I look forward to you scientifically or mathematically demonstrating
that the above numbers are insufficient to explain the evolution of
And if you can not produce such a demonstration, then I look forward to
reading your farewell post.
Clock vid. How mutations ADD UP!