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Chickenasaurus
5 months ago  ::  Jan 11, 2012 - 2:20AM #38
Blü
Posts: 17,544

Would the last creationist to leave the Discovery Institute please turn off the power and water, lock the doors and set up the For Sale sign.

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5 months ago  ::  Jan 10, 2012 - 10:29PM #37
MMarcoe
Posts: 8,414


Read it and weep, creos:


 


Evolution of complexity recreated using 'molecular time travel'


 


Scientists find that small, high-probability mutations can produce complex system


Much of what living cells do is carried out by "molecular machines" – physical complexes of specialized proteins working together to carry out some biological function. How the minute steps of evolution produced these constructions has long puzzled scientists, and provided a favorite target for creationists.


In a study published early online on Sunday, January 8, in Nature, a team of scientists from the University of Chicago and the University of Oregon demonstrate how just a few small, high-probability mutations increased the complexity of a molecular machine more than 800 million years ago. By biochemically resurrecting ancient genes and testing their functions in modern organisms, the researchers showed that a new component was incorporated into the machine due to selective losses of function rather than the sudden appearance of new capabilities.


"Our strategy was to use 'molecular time travel' to reconstruct and experimentally characterize all the proteins in this molecular machine just before and after it increased in complexity," said the study's senior author Joe Thornton, PhD, professor of human genetics and evolution & ecology at the University of Chicago, professor of biology at the University of Oregon, and an Early Career Scientist of the Howard Hughes Medical Institute.


"By reconstructing the machine's components as they existed in the deep past," Thornton said, "we were able to establish exactly how each protein's function changed over time and identify the specific genetic mutations that caused the machine to become more elaborate."


The study – a collaboration of Thornton's molecular evolution laboratory with the biochemistry research group of the UO's Tom Stevens, professor of chemistry and member of the Institute of Molecular Biology – focused on a molecular complex called the V-ATPase proton pump, which helps maintain the proper acidity of compartments within the cell.


One of the pump's major components is a ring that transports hydrogen ions across membranes. In most species, the ring is made up of a total of six copies of two different proteins, but in fungi a third type of protein has been incorporated into the complex.


To understand how the ring increased in complexity, Thornton and his colleagues "resurrected" the ancestral versions of the ring proteins just before and just after the third subunit was incorporated. To do this, the researchers used a large cluster of computers to analyze the gene sequences of 139 modern-day ring proteins, tracing evolution backwards through time along the Tree of Life to identify the most likely ancestral sequences. They then used biochemical methods to synthesize those ancient genes and express them in modern yeast cells.


Thornton's research group has helped to pioneer this molecular time-travel approach for single genes; this is the first time it has been applied to all the components in a molecular machine.


The group found that the third component of the ring in Fungi originated when a gene coding for one of the subunits of the older two-protein ring was duplicated, and the daughter genes then diverged on their own evolutionary paths.


The pre-duplication ancestor turned out to be more versatile than either of its descendants: expressing the ancestral gene rescued modern yeast that otherwise failed to grow because either or both of the descendant ring protein genes had been deleted. In contrast, each resurrected gene from after the duplication could only compensate for the loss of a single ring protein gene.


The researchers concluded that the functions of the ancestral protein were partitioned among the duplicate copies, and the increase in complexity was due to complementary loss of ancestral functions rather than gaining new ones. By cleverly engineering a set of ancestral proteins fused to each other in specific orientations, the group showed that the duplicated proteins lost their capacity to interact with some of the other ring proteins. Whereas the pre-duplication ancestor could occupy five of the six possible positions within the ring, each duplicate gene lost the capacity to fill some of the slots occupied by the other, so both became obligate components for the complex to assemble and function.


"It's counterintuitive but simple: complexity increased because protein functions were lost, not gained," Thornton said. "Just as in society, complexity increases when individuals and institutions forget how to be generalists and come to depend on specialists with increasingly narrow capacities."


The research team's last goal was to identify the specific genetic mutations that caused the post-duplication descendants to functionally degenerate. By reintroducing historical mutations that occurred after the duplication into the ancestral protein, they found that it took only a single mutation from each of the two lineages to destroy the same specific functions and trigger the requirement for a three-protein ring.


"The mechanisms for this increase in complexity are incredibly simple, common occurrences," Thornton said. "Gene duplications happen frequently in cells, and it's easy for errors in copying to DNA to knock out a protein's ability to interact with certain partners. It's not as if evolution needed to happen upon some special combination of 100 mutations that created some complicated new function."


Thornton proposes that the accumulation of simple, degenerative changes over long periods of times could have created many of the complex molecular machines present in organisms today. Such a mechanism argues against the intelligent design concept of "irreducible complexity," the claim that molecular machines are too complicated to have formed stepwise through evolution.


"I expect that when more studies like this are done, a similar dynamic will be observed for the evolution of many molecular complexes," Thornton said.


"These really aren't like precision-engineered machines at all," he added. "They're groups of molecules that happen to stick to each other, cobbled together during evolution by tinkering, degradation, and good luck, and preserved because they helped our ancestors to survive."


###


The paper, "Evolution of increased complexity in a molecular machine," appears in the January 18, 2012, issue of Nature [doi: 10.1038/nature10724]. The work was a collaboration of Thornton's molecular evolution lab with the research group of Tom Stevens, a yeast geneticist at the University of Oregon. Other authors include Gregory C. Finnigan and Victor Hanson-Smith, of the University of Oregon.


Funding for this work was provided by the National Institutes of Health, the National Science Foundation, and the Howard Hughes Medical Institute.


 


eurekalert.org/pub_releases/2012-01/uocm-eoc010512.php


editing altered format only. RK

Moderated by rangerken on Jan 11, 2012 - 01:42AM
There are three sides to every story: your side, my side, and the truth.
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5 months ago  ::  Jan 10, 2012 - 6:15PM #36
Namchuck
Posts: 7,773

'Scientists find that small, high-probability mutations can produce complex systems.'



eurekalert.org/pub_releases/2012-01/uocm-eoc010512.php



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5 months ago  ::  Jan 10, 2012 - 5:05PM #35
wohali
Posts: 8,763

More wit and wisdom from Ian Juby:


creationistidiocy.blogspot.com/2008_09_0...

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5 months ago  ::  Jan 10, 2012 - 11:57AM #34
wohali
Posts: 8,763

Juby's bio, no education:


www.tccsa.tc/notices/juby_bio.html

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5 months ago  ::  Jan 09, 2012 - 11:16PM #33
Ken
Posts: 30,467

Jan 9, 2012 -- 9:40PM, McAtheist wrote:


Thanks for the links, wohali.


My question is how this Juby person (anyone know what his educational background is?  I can't find diddly...)


High school. Maybe. When you can't find diddly, that means there isn't diddly. Not even a mail-order degree in Christian Education.

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5 months ago  ::  Jan 09, 2012 - 9:40PM #32
McAtheist
Posts: 4,975

Thanks for the links, wohali.


My question is how this Juby person (anyone know what his educational background is?  I can't find diddly...) knows that the misidentified dinosaur supposedly laying eggs while fleeing (cool trick) is running from Noah's flood and not from a T-REX or similar predator?


These guys get sillier all the time.

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5 months ago  ::  Jan 09, 2012 - 8:33PM #31
wohali
Posts: 8,763

Ian Juby's "creation science"


www.youtube.com/watch?v=PLpCwhwO0_g


doubtingmarcus.tumblr.com/post/703815698...

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5 months ago  ::  Jan 09, 2012 - 1:56AM #30
Slipnish
Posts: 3,772




I'll wait over here in logic corner, while 57 tries to make this, "add up."

I don't believe it. Prove it to me and I still won't believe it.

~Any Creationist~
(But honestly Douglas Adams)

"Anti-intellectualism has been a constant thread winding its way through our political and cultural life, nurtured by the false notion that democracy means that 'my ignorance is just as good as your knowledge.'" - Isaac Asimov
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5 months ago  ::  Jan 08, 2012 - 1:01PM #29
d_p_m
Posts: 5,006

Jan 7, 2012 -- 4:58PM, 57 wrote:


Jan 7, 2012 -- 2:26PM, F1fan wrote:


Jan 7, 2012 -- 1:08PM, 57 wrote:

I don't really care what came first...because we all know evolutionism is impossible.  



You believe it is "impossible" becuase you don't care about facts and knowledge.





No, I know it is impossible.  


Reason 1. No evo has ever demonstrated how mutations add up. 







Previous count update/post 2011/11/21... just under 4 weeks ago. Today is 2011/12/17





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.





29/19/18/12/12/11/08 <==== 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
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!


"I am the soul of nature that gives life to the universe."

-- The Charge of the Goddess
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