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2 years ago  ::  Apr 29, 2012 - 9:19AM #11
amcolph
Posts: 16,282

Apr 29, 2012 -- 8:58AM, 57 wrote:


 


If it truly has been answered....like you claim....the answer should be readily available on the internet.  But guess what amcolph?  You evos can't answer the question...which explains why it is not readily available....and you claim I'm pretending?




Now you're just being silly.  There is quite a bit about it on the internet, for example:


bib.oxfordjournals.org/content/7/1/70.fu...


For a brush-up on the math used, got to

en.wikipedia.org/wiki/Stochastic_process

This post contains no advertisements or solicitations.
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2 years ago  ::  Apr 29, 2012 - 9:56AM #12
Midutch
Posts: 3,526

Apr 29, 2012 -- 8:46AM, 57 wrote:


Apr 29, 2012 -- 8:10AM, rsielin wrote:


Apr 29, 2012 -- 7:17AM, 57 wrote:

...any time you want too..feel free to show us how mutations add up.


Lookie, our creationist friend is back to drive by taunts and insults. He wears nary a stitch of empirical evidence, so he really can't compete on the clothed in knowledge academic level. This is all he's got. Clear sign of a defeated creationist.  ROTFLMAO


Pretty foolish and sophomoric MO, wouldn't you think.


I will present that question until it is answered.  


It truly is amazing how it has gone unanswered for so long.


So why don't you ever answer questions about YOUR side of the SCIENCE vs. bronze age myths, fables and fairy tales "debate".


Rather hypocritical of you, don't you think?


Here's a simple one: exactly how many nails and wooden pegs did Noah use in his wooden barge?


If you can't answer this question then Noah, Ham, Sham, Curly and their wooden barge aren't real ... which is the exact same conclusion behind your boring "how do mutations add up" question using your own logic.

"creationism" ... 2000+ years worth of ABYSMAL FAILURE ... and proud of it.
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2 years ago  ::  Apr 30, 2012 - 11:29AM #13
d_p_m
Posts: 9,013

Apr 29, 2012 -- 8:46AM, 57 wrote:


Apr 29, 2012 -- 8:10AM, rsielin wrote:


Apr 29, 2012 -- 7:17AM, 57 wrote:

...any time you want too..feel free to show us how mutations add up.


Lookie, our creationist friend is back to drive by taunts and insults. He wears nary a stitch of empirical evidence, so he really can't compete on the clothed in knowledge academic level. This is all he's got. Clear sign of a defeated creationist.  ROTFLMAO


Pretty foolish and sophomoric MO, wouldn't you think. 




I will present that question until it is answered.  


It truly is amazing how it has gone unanswered for so long.




It has been answered - directly to you - more than a hundred times, by actual counts.


What is truly amazing is that you seem to manage to forget this every time you start a new thread...  or when you haven't been answered in a given thread for a week or two.


The last time I answered you was three days ago, and the previous time was 12 days before that:


-----------------------------------------------------------------------------------------------


Previous count update/post 2012/04/27... Today is 2012/04/30







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.







33/23/22/16/16/15/12 <==== counts of number of times of 'presentation to 57' for each differenet explanation in a sub-part of this message


To save 57 the arithmetic, since we started keeping track, Slip and I have provide the explanation of mutations adding up in seven different ways or formats a total of more than 137 times (we didn't count every posting at first, and there were years of explanations before that).



-----------------------------------------------------------------------------------------------------------



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
forgotten?

I've replied to that SEVERAL times but you just seem to keep forgetting.



Not with anything based in fact and logic.

[author=33443027 post=479376853]

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.

[author=33443027 post=479376853]

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.






AND THIS



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:



McAtheist
Posts: 3,716
   

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
information.

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
genetic information.

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
information?

Yes or no, dude?





Original quote here: 

community.beliefnet.com/go/thread/view/4...

roves_Evolution?pg=142

and of course here's a whole thread dedicated to the subject:
community.beliefnet.com/go/thread/view/4...

hematical_basis_of_mutations_dont_add_up

community.beliefnet.com/go/thread/view/4...

k_up_their_claims_----_beneficial_mutational_math

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
individual).

 

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
generation."

"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."

-- sandwalk.blogspot.com/2007/07/mutation-r...

 

 

Now, I'm sure you will 'forget' this too, but don't say we didn't give it
to you.

PS: References: 

    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.
Science 277:1453-1474.

    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.
351:299-308.

    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????






Once more...

How many times do we have to tell you that 'beneficial' and 'harmful' are
context/environment dependent?

Fair skin is beneficial in Norway, and harmful in the Sudan.

Really, it's not that hard.





community.beliefnet.com/go/post/reply/43...

"e=498178865#post_input




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?




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
yourself?

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
studies.

You are fifty years behind the times. I would advise you to increase your
knowledge.

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.


community.beliefnet.com/go/thread/view/4...

.?pg=2



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
Biology).

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,
2008.








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
Futuyama)

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
460,000 animals.

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
mutations: 1200

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
occurring.

So, I look forward to you scientifically or mathematically demonstrating
that the above numbers are insufficient to explain the evolution of
dolphins.

And if you can not produce such a demonstration, then I look forward to
reading your farewell post.






community.beliefnet.com/go/post/reply/43...

_Disproves_Creationism"e=501836313#post_input

www.youtube.com/watch?v=mcAq9bmCeR0&feat...
Clock vid.  How mutations ADD UP!


PHARAOH IRY-HOR, FROM THE 3100s BC, IS THE FIRST HUMAN WHOSE NAME WE KNOW.

-- cool facts from xkcd


"As far as the laws of mathematics refer to reality, they are not certain, as far as they are certain, they do not refer to reality."

-- Albert Einstein
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2 years ago  ::  Apr 30, 2012 - 1:58PM #14
upsala81
Posts: 2,129

57,



Maybe all the math presented is too technical for you.  Hey, it's largely beyond me too.  So please look at the video here, no a non-mathematical "adding up" of mutations.



www.pbs.org/wgbh/evolution/library/01/1/...

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2 years ago  ::  Apr 30, 2012 - 3:26PM #15
Oncomintrain
Posts: 2,861

Apr 30, 2012 -- 11:29AM, d_p_m wrote:



It has been answered - directly to you - more than a hundred times, by actual counts.


What is truly amazing is that you seem to manage to forget this every time you start a new thread...  or when you haven't been answered in a given thread for a week or two.


The last time I answered you was three days ago, and the previous time was 12 days before that:


-----------------------------------------------------------------------------------------------


Previous count update/post 2012/04/27... Today is 2012/04/30




I would add that this is only a selection of the many answers 57 has received. Any sufficiently intrepid lurker could do a forum search for "mutations add up" and turn up a number more, dating back to 2007, when this forum switched formats. You do have to dig a little... there are about 3500 posts with that string, and probably about half are just 57 repeating his mantra.


But anyone with a long afternoon on their hands would get to witness 57 making things up, ignoring things he doesn't like, and declaring himself the arbiter of acceptable answers, despite the fact that he also displays a near constant inability to do the math, understand the concepts, or even comprehend what he's reading.


So if anyone is wondering why we DON'T just explain "how mutations add up," that's why. We already have. In dozens of different ways. 57 is just constitutionally unable to stomach it, so he just declares all answers invalid. His entire worldview depends on the Theory of Evolution being wrong, so he cannot under any circumstances admit even the possibility of his own error, ever.

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2 years ago  ::  Apr 30, 2012 - 4:08PM #16
d_p_m
Posts: 9,013

Apr 29, 2012 -- 8:58AM, 57 wrote:

If it truly has been answered....like you claim....the answer should be readily available on the internet.




Yes! Give the man a prize! Information on how mutations drive evolution IS READILY AVAILABLE ON THE INTERNET. Oddly, he seems to have problems finding it, so here is a little help:




An improved method for determining codon variability in a gene and its application to the rate of fixation of mutations in evolution


WM Fitch… - Biochemical genetics, 1970 - Springer

If one has the amino acid sequences of a set of homologous proteins as well as their
phylogenetic relationships, one can easily determine the minimum number of mutations
(nucleotide replacements) which must have been fixed in each codon since their common ...




Mutations and evolution


RR Gates - Nature, 1921 - adsabs.harvard.edu

Abstract THE article on my recent little book on``Mutations and Evolution''in NATURE of July
14, p. 636, shows such insight in the exposition of some of the views there set forth that it
may seem ungrateful of me to venture to reply to anything the reviewer has written. ...




MUTATIONS AND EVOLUTION.


RR Gates - New Phytologist, 1920 - Wiley Online Library

THE adoption of experimental methods of evolutionary study early in the present century
was accompanied by sanguine hopes that a general and universally applicable method of
evolution might thus be discovered. But two decades of intensive experimental work with ...




[PDF] On correlated mutations in evolution strategies



G unter Rudolph - M anner and Manderick, 1959 - ls11-www.cs.uni-dortmund.de

Originally Evolution Strategies (ESs) have been developed for experimental optimization, ie
optimization at the real object. Later they have been formulated as computer programs in
order to solve optimization problems given as mathematical models of the type minff (x) jx ...




Population genetics study of isoniazid resistance mutations and evolution of multidrug-resistant Mycobacterium tuberculosis



MH Hazbón, M Brimacombe… - Antimicrobial agents …, 2006 - Am Soc Microbiol

ABSTRACT The molecular basis for isoniazid resistance in Mycobacterium tuberculosis is
complex. Putative isoniazid resistance mutations have been identified in katG, ahpC, inhA,
kasA, and ndh. However, small sample sizes and related potential biases in sample ...




Stress‐directed adaptive mutations and evolution


BE Wright - Molecular microbiology, 2004 - Wiley Online Library

Comparative biochemistry demonstrates that the metabolites, complex biochemical
networks, enzymes and regulatory mechanisms essential to all living cells are conserved in
amazing detail throughout evolution. Thus, in order to evolve, an organism must overcome ...




… pattern of the nurse shark antigen receptor gene (NAR) is similar to that of mammalian Ig genes and to spontaneous mutations in evolution: the translesion synthesis …



M Diaz, J Velez, M Singh, J Cerny… - International …, 1999 - Jpn Soc Immunol

Abstract The pattern of somatic mutations of shark and frog Ig is distinct from somatic
hypermutation of Ig in mammals in that there is a bias to mutate GC base pairs and a low
frequency of mutations. Previous analysis of the new antigen receptor gene in nurse ...




… persistence in chronic inflammatory myopathy: viral RNA persists through formation of a double-stranded complex without associated genomic mutations or evolution



PE Tam… - Journal of virology, 1999 - Am Soc Microbiol

ABSTRACT Enterovirus infection and persistence have been implicated in the pathogenesis
of certain chronic muscle diseases. In vitro studies suggest that persistent enteroviruses
mutate, evolving into forms that are less lytic and display altered tropism, but it is less clear ...




A biochemical mechanism for nonrandom mutations and evolution



BE Wright - Journal of bacteriology, 2000 - Am Soc Microbiol

As this minireview is concerned with the importance of the environment in directing
evolution, it is appropriate to remember that Lamarck was the first to clearly articulate a
consistent theory of gradual evolution from the simplest of species to the most complex, ...




Mutually compensatory mutations during evolution of the tetramerization domain of tumor suppressor p53 lead to impaired hetero-oligomerization



MG Mateu… - Proceedings of the National …, 1999 - National Acad Sciences

Abstract We have measured the stability and stoichiometry of variants of the human p53
tetramerization domain to assess the effects of mutation on homo-and hetero-
oligomerization. The residues chosen for mutation were those in the hydrophobic core that ...


PHARAOH IRY-HOR, FROM THE 3100s BC, IS THE FIRST HUMAN WHOSE NAME WE KNOW.

-- cool facts from xkcd


"As far as the laws of mathematics refer to reality, they are not certain, as far as they are certain, they do not refer to reality."

-- Albert Einstein
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2 years ago  ::  Apr 30, 2012 - 4:18PM #17
d_p_m
Posts: 9,013

A bit-string model for biological aging



TJP Penna - Journal of statistical physics, 1995 - Springer

... Evolution in time of the fraction of individuals suffering mutations at ages 1 (O), 6 (E]), 12 (+),
and 30 (*). The data correspond to R=6, M=2, and T=4. Page 5. ... Starting from an uniform
distribution, Fig. 4 shows the evolution of the frequency of bad mutations. ...




Deleterious mutations and the evolution of sex



PD Keightley… - Science, 2000 - sciencemag.org

Abstract It has been suggested that sexual reproduction is maintained because it reduces
the load imposed by recurrent deleterious mutations. If rates of deleterious mutation per
diploid genome per generation (U) exceed 1, and mutations interact synergistically, then ...




evolution of human immunodeficiency virus type 1 in patients infected from the same source: rate of sequence change and low frequency of inactivating mutations.



P Balfe, P Simmonds, CA Ludlam… - Journal of …, 1990 - Am Soc Microbiol

ABSTRACT Direct sequencing of segments of the envelope gene of human
immunodeficiency virus type 1 proviruses in peripheral blood mononuclear cells has
revealed that a cohort of hemophiliacs who were infected after exposure to a single ...




Evolution of hepatitis B virus polymerase gene mutations in hepatitis B e Antigen–negative patients receiving lamivudine therapy



ASF Lok, M Hussain, C Cursano, M Margotti… - …, 2000 - Wiley Online Library

Abstract Lamivudine has been shown to be effective in patients with hepatitis B e antigen
(HBeAg)-positive chronic hepatitis B, but its long-term efficacy and the rate of resistant
mutations in patients with HBeAg-negative chronic hepatitis B is less clear. Twenty-nine ...




A ruby in the rubbish: beneficial mutations, deleterious mutations and the evolution of sex



JR Peck - Genetics, 1994 - Genetics Soc America

This study presents a mathematical model in which a single beneficial mutation arises in a
very large population that is subject to frequent deleterious mutations. The results suggest
that, if the population is sexual, then the deleterious mutations will have little effect on the ...




Nucleotide sequence divergence and functional constraint in mRNA evolution



T Miyata, T Yasunaga… - Proceedings of the …, 1980 - National Acad Sciences

... Recently, from comparison of nucleotide sequences of adult a-globin genes from mouse and
rabbit with the sequence of mouse pseudo-a-globin gene (60, 61), which appears to have lost
its protein encoding ability due to frameshift mutations during evolution, we have found ...




Role of very slightly deleterious mutations in molecular evolution and polymorphism


T Ohta - Theoretical Population Biology, 1976 - Elsevier

Abstract Several models of multiple slightly deleterious alleles are reviewed and theoretical
consequences of slightly negative selection are discussed in conjunction with evolution and
variation at the molecular level. Facts are organized which may be satisfactorily explained ...




Evolution of the secondary structures and compensatory mutations of the ribosomal RNAs of Drosophila melanogaster.



JM Hancock, D Tautz… - Molecular Biology and Evolution, 1988 - SMBE

Abstract This paper examines the effects of DNA sequence evolution on RNA secondary
structures and compensatory mutations. Models of the secondary structures of Drosophila
melanogaster 18S ribosomal RNA (rRNA) and of the complex between 2S, 5.8 S, and 28S ...




Evolution by individuals, plant-herbivore interactions, and mosaics of genetic variability: the adaptive significance of somatic mutations in plants


TG Whitham… - Oecologia, 1981 - Springer

Differences in the pattern of organization of organisms may lead to different patterns of
evolution, genetics and ecology, Plants and animals differ in their fundamental patterns of
organization. Plants consist of a series of repeating units that compete with one another, ...




Adaptive evolution that requires multiple spontaneous mutations. I. Mutations involving an insertion sequence



BG Hall - Genetics, 1988 - Genetics Soc America

Escherichia coli K12 strain {chi} 342LD requires two mutations in the bgl ({beta}-
glucosidase) operon, bglR (0)-> bglR (+) and excision of IS103 from within bglF, in order to
utilize salicin. In growing cells the two mutations occur at rates of 4 X 10 (-8) per cell ...


PHARAOH IRY-HOR, FROM THE 3100s BC, IS THE FIRST HUMAN WHOSE NAME WE KNOW.

-- cool facts from xkcd


"As far as the laws of mathematics refer to reality, they are not certain, as far as they are certain, they do not refer to reality."

-- Albert Einstein
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2 years ago  ::  Apr 30, 2012 - 4:29PM #18
amcolph
Posts: 16,282

Apr 30, 2012 -- 1:58PM, upsala81 wrote:


57,



Maybe all the math presented is too technical for you.  Hey, it's largely beyond me too.  So please look at the video here, no a non-mathematical "adding up" of mutations.



www.pbs.org/wgbh/evolution/library/01/1/...




That's all very well, but it is 57's claim that it is the mathematics which disproves evolution.  Tongue Out

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2 years ago  ::  Apr 30, 2012 - 4:40PM #19
d_p_m
Posts: 9,013

Polyclonal evolution of multiple secondary KIT mutations in gastrointestinal stromal tumors under treatment with imatinib mesylate


E Wardelmann, S Merkelbach-Bruse, K Pauls… - Clinical cancer …, 2006 - AACR

Abstract Gastrointestinal stromal tumors (GIST) are characterized by a strong KIT receptor
activation most often resulting from KIT mutations. In a smaller subgroup of tumors without
KIT mutations, analogous activating mutations are found in the platelet-derived growth ...




[PDF] Adaptive protein evolution at the Adh locus in Drosophila



JH McDonald, M Kreitman - Nature, 1991 - ib.berkeley.edu

... Thus, the rate of adaptive protein evolution seen at the Adh locus may not be unusually high,
and selective fixation of adaptive mutations may be a viable alternative to the clocklike
accumulation of neutral mutations as an explanation for most protein evolution. ...




The role of compensatory neutral mutations in molecular evolution



M Kimura - Journal of Genetics, 1985 - Springer

Abstract A pair of mutations at different loci (or sites) which are singly deleterious but restore
normal fitness in combination may be called compensatory neutral mutations. Population
dynamics concerning evolutionary substitutions of such mutants was developed by ...




Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate- …



S Branford, Z Rudzki, S Walsh… - …, 2003 - bloodjournal.hematologylibrary.org

... patients acquired imatinib resistance, and mutations were detected in 6 (86%) of 7. There was
no significant difference in the frequency of mutations in patients with clonal evolution as the
sole criterion for AP compared with the patients with other criteria for classification as AP. ...




Evolution of mutations conferring multidrug resistance during prophylaxis and therapy for cytomegalovirus disease



S Chou, G Marousek, S Guentzel… - Journal of Infectious …, 1997 - jid.oxfordjournals.org

Abstract In a human immunodeficiency virus-infected subject, cytomegalovirus (CMV)
isolated 9 months after the patient began oral ganciclovir prophylaxis was resistant to
ganciclovir and cidofovir and contained mutations in both UL97 and Pol coding regions. At ...




Rapid evolution of cis-regulatory sequences via local point mutations



JR Stone… - Molecular Biology and Evolution, 2001 - SMBE

Abstract Although the evolution of protein-coding sequences within genomes is well
understood, the same cannot be said of the cis-regulatory regions that control transcription.
Yet, changes in gene expression are likely to constitute an important component of ...




The effects of Hill-Robertson interference between weakly selected mutations on patterns of molecular evolution and variation



GAT McVean… - Genetics, 2000 - Genetics Soc America

Associations between selected alleles and the genetic backgrounds on which they are
found can reduce the efficacy of selection. We consider the extent to which such
interference, known as the Hill-Robertson effect, acting between weakly selected alleles, ...




Deleterious mutations, variable epistatic interactions, and the evolution of recombination



SP Otto… - Theoretical population biology, 1997 - Elsevier

Abstract In this paper, we examine the conditions that allow increased recombination to
evolve in the presence of recurrent deleterious mutation. We focus on a three-locus model
first studied by Feldmanet al.(1980), which follows the dynamics of a modifier locus that ...




Adapting arbitrary normal mutation distributions in evolution strategies: The covariance matrix adaptation



N Hansen… - Evolutionary Computation, 1996., …, 1996 - ieeexplore.ieee.org

... the result of a principle component analysis of (exponentially decreasing weighted) evolution
paths. We give a geometrical idea of the resulting distribution change, ignoring the initial
distribution: A mutation step at generation g + 1 is composed by g line mutations along certain ...




Mitochondrial DNA sequences of primates: tempo and mode of evolution



WM Brown, EM Prager, A Wang… - … of molecular evolution, 1982 - Springer

... Guanine Thymine Cytosine (2) multiple substitutions occur at the same site when the time is long,
obscuring the record of transitions. This last point is illustrated by the following hypothetical case
of evolution by 10 point mutations at the same site along two diverging lineages: ...


PHARAOH IRY-HOR, FROM THE 3100s BC, IS THE FIRST HUMAN WHOSE NAME WE KNOW.

-- cool facts from xkcd


"As far as the laws of mathematics refer to reality, they are not certain, as far as they are certain, they do not refer to reality."

-- Albert Einstein
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2 years ago  ::  Apr 30, 2012 - 4:45PM #20
d_p_m
Posts: 9,013

The really funny thing is, if I put 'for 57' at the start of the message, almost always the formatting screws up... It's at least partly an issue here, of course, but it is amusing.

PHARAOH IRY-HOR, FROM THE 3100s BC, IS THE FIRST HUMAN WHOSE NAME WE KNOW.

-- cool facts from xkcd


"As far as the laws of mathematics refer to reality, they are not certain, as far as they are certain, they do not refer to reality."

-- Albert Einstein
Quick Reply
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