24/11/09 21:56 FractoGene explains the "Evolution Revolution" 99% of mouse genes have direct equivalents in human genes

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*** ARE YOU 99% MOUSE? THE EVOLUTION REVOLUTION ***
AS AN EMBRYO YES, YOU ARE. IN YOUR GENES, YES, YOU ARE.
IN YOUR INTRONS, NO, YOUR ARE NOT.
INTRONS HELP MAKING US HUMAN, BUT ... PLEASE EXPLAIN HOW?
Aspects of evolution of FractoGene utility patent are provided for illustrative purposes. From a patent the requirements are that it must
"theach new skills". FractoGene by measuring and comparing non-coding sequences of DNA as fractal sets, does that. However, from the
enormous publicity that FractoGene generated it is evident that there is a pressure from Academia to learn as much about the science
background of the patent as possible - without compromising the business interests. The author, having done his "homework" in Academia,
is open to all classic academic interests, presentations, publications, etc. This page is a preview to show that FractoGene is not only
consistent with prevailing scientific facts of evolution, but actually explains more, and the explanation is clearer (quantitative) - as it is
mathematical. Therefore, quantitative predictions will both stimulate experimentation as well as facilitate the profitability of a utility patent.
Thomas Edison used to say for the accomplishments of an inventor: "It takes 1% inspiration, 99% perspiration"
Given this classic slogan, we should not be overly surprised, that up to 97% of the human genetic information
(DNA) is seemingly needless, repetitive "junk" - only about 3% is known to generate proteins, deserving the name
"gene". The rest used to be called "junk DNA", lately renamed as "non-coding introns", sometimes labeled by the
mysterious, though not very explicit description that these self-similar strands "regulate gene expression".
This uncertainity if "junk DNA" is really "junk", that cought some scientists by surprise, is now history. Indeed,
scientists were never quite sure that any part of DNA could be discarded outright, and even the question was raised
if introns might play a role in evolution, see Mattick, 1994., Klyce, 2002). The bombshell of the 5th of December
issue of the highly reputed Nature 420, 509 (2002) revealed that the 99% of the genes of the mouse have
direct equivalents with the humane genes.
What does this mean?
1) It does not mean that homo sapiens is 99% identical to mouse. It has also been revealed, that the mouse DNA
is at least 10% less information, compared to the human DNA.
2) The significant difference is less visible in the "inspiration" to make a human out of a lower mammal. It is clearly
the "perspiration" that dominates the effort. It is the introns.
3) Are there any clear, maybe even mathematical explanations available how the repeated "non-coding sequences"
refine the basic "invention" expressed by a gene?
FractoGene, the patent application authored and submitted by July 31st, 2002, does provide the following
explanation:
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FractoGene patent (pending) pictures evolution as fractal elaboration of a gene
by its introns (the fractal model of Purkinje cell was published by Pellionisz, 1989)
The stem (as in "stem cell") in Fig. A. shows no differentiation. In Fig. B., the basic row of base-pair sequence,
composed of an ACTG jumble (a "gene") determines the fractal template of the bifurcation at the rudimentary, let's
call it "shark" stage. (The cerebellum is generally regarded to be the "invention" of the sharks about 400 million
years ago - but the evolutionary "root" has yet to be conclusively established, and as shark DNA has not been
sequenced, thus it is unknown if the "gene" determining the shape of Purkinje cells, contains much fewer or no
introns, compared to higher species). The repetition of the gene in a self-similar intron (which is not identical to the
gene, since the branchlets of the generated brain cell are replaced by the template in e.g. a smaller version as
shown in C). For the sake of simplicity, (given the compressed scheme of the diagram), let's call it "Frog stage".
Suppose, that Mother Nature is content with such a primitive rendering, e.g. for the frog. In this case the lower-
ranking animal only needs two self-similar strands of base-pair sequences (one gene and one intron). Let's assume
for the sake of a little more complexity, that evolution does not stop at the "frog stage". A third row of base-pair
sequence replaces each terminal branchlet of C with the fractal template itself (in an even smaller version, plus e.g.
with a higher density of synapses). This could result in the Purkinje cell of a creature somewhat higher on the
evolutionary ladder from the "frog", let us call it symbolically "a mouse". For this to happen, a third repetition, one
gene and two introns, "non-coding sequences" are needed, generating D. With yet another round of "perspiration",
the outer branchlets of D are replaced by the tiny version of the basic fractal template shown in A, and thus E
arises. For the sake of this diagram, let's figuratively call it "Human stage" (although a Purkinje cell at this level of
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complexity approximates only the guinea pig). As shown the bottom Purkinje cell (and in the original publication),
this is a strinkingly accurate fractal model of a fairly sophisticated Purkinje neuron (E).
Why is FractoGene called here to help an "evolution revolution"? Because a paradigm-shift is happening, a
transition from the classic notion that the main drivers of evolution are the "genes". Apparently, the primary drivers
are the repetitive, "non-coding" introns, constantly improving on the "performance" of the basic "inventions" of the
genes. In view of this schematic diagram of fractogenesis (evolution expressed in fractal geometry), it is evident that
the "gene pool" of the mouse and human is 99% identical (as found by the Consortium, and reported by Nature,
Dec. 5th, 2002) - while there is a fairly significant difference of the total volume of the DNA, it is an experimentally
established trend that the higher ranking species contain significantly more "introns".
From the schematic diagram based on the FractoGene patent, it is also evident why the development of the embryo
"mimics" the development of species through the evolution, both embryogenesis repeating phylogenetic
development in general, (see excerpt Figure below), and research is intensifying to explore this phenomenon at
genomic and also at the molecular levels.
(Fig. and Legend from the Nobel e-museum)
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Here is the original lead-article of Nature:
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Nature 420, 509 (2002)
Human biology by proxy
Chris Gunter, Chief Biology Editor and Ritu Dhand, Associate Biology Editor
Since the publication of the human genome, the scientific community has been eagerly awaiting the results of the
mouse genome sequencing project.
This week's issue contains a landmark publication from the Mouse Genome Sequencing Consortium that many say
holds more promise for our future than even the human genome itself. But why? The laboratory mouse is hailed as
holding the experimental key to the human genome. Working on mouse models allows the manipulation of each and
every gene to determine their functions, and this will give us detailed insights into many aspects of human disease
as well as basic human biology. It is our pleasure to present this special section of Nature on the mouse genome.
We hope it will provide a comprehensive overview of the future of mouse, and by extension human, genetics and
genomics.
The 2.5-Gb mouse genome sequence reported on page 520, from the C57BL/6J strain, reveals about 30,000
genes, with 99% having direct counterparts in humans.
To further understand physical gene structures, a second consortium describes in a companion paper 37,086
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individual 'transcriptional units' (page 563). This cDNA resource is freely available as physical clones and will
advance the pace of research. Humans appear to have about the same number of genes, with similar sequence,
and we both like cheese. So why aren't mice more like us? The answer probably lies in the regulation of those
genes.
In a third paper, Dermitzakis et al. directly compare sequences on human chromosome 21 with their counterparts in
mice (page 578). Surprisingly, even gene-poor regions of the chromosome show extensive similarity between the
two organisms, suggesting that further exploration into the non-coding regions of both genomes will be required to
explain the differences between us. In a separate study, Wade et al. compare two inbred mouse strains to map
regions of high and low polymorphism (page 574). Distinguishing areas of high polymorphism will be extremely
useful for mapping quantitative trait loci, and thus possibly identifying genes that contribute to the inheritance of
complex diseases. Finally, in an effort to gain functional information, two groups report large-scale analyses of gene
expression in both adult and embryonic tissues of mouse orthologues of the genes on human chromosome 21
(pages 582 and 586). The expression patterns of these genes provide a first step in generating information on
specific gene function.
As the sequence has been deposited in public databases, the mouse genome and resources included here provide
a huge boost to genetic researchers.
Given the bonanza of information they have just received, scientists may now consider the laboratory mouse to be
'man's best friend.
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(For more detailed explanation of FractoGene, click here)

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