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Dinoglyphs - Prehistoric Creatures Documented by the Ancient Man



About 93% of the genome is transcribed (not 3%,

as expected). Further study with more wide-ranging

methods may raise this figure to 100%. Because much

energy and coordination is required for transcription

this means that probably the whole genome is used by

the cell and there is no such thing as ‘junk DNA’.

Exons are not gene-specific but are modules that can

be joined to many different RNA transcripts. One exon

(i.e. a protein-making portion of one gene) can be used

in combination with up to 33 different genes located

on as many as 14 different chromosomes. This means

that one exon can specify one part shared in common

by many different proteins.

There is no ‘beads on a string’ linear arrangement of

genes, but rather an interleaved structure of overlapping

segments, with typically five, seven or more transcripts

coming from just one segment of code.

Not just one strand, but both strands (sense and antisense)

of the DNA are fully transcribed.

Transcription proceeds not just one way but both

backwards and forwards.

Transcription factors can be tens or hundreds of

thousands of base-pairs away from the gene that they

control, and even on different chromosomes.

There is not just one START site, but many, in each

particular gene region.

There is not just one transcription triggering (switching)

system for each region, but many.


‘An interleaved genomic organization poses

important mechanistic challenges for the cell. One

involves the [use of] the same DNA molecules for

multiple functions. The overlap of functionally

important sequence motifs must be resolved in time

and space for this organization to work properly.

Another challenge is the need to compartmentalize

RNA or mask RNAs that could potentially form

long double-stranded regions, to prevent RNARNA

interactions that could prompt apoptosis

[programmed cell death].’

more than 100 times the size of a typical gene region. This

would be like photocopying a page in a book and having

to get information from 10, 50 or even 100 other pages in

order to use the information on that one page.

to be junk) are now called untranslated regions (UTRs)

because while they are transcribed into RNA, they are

not translated into protein. Not only has the ENCODE

project elevated UTRs out of the ‘junk’ category, but it now

appears that they are far more active than the translated

regions (the genes), as measured by the number of DNA

bases appearing in RNA transcripts.

The vast majority of the information

stored in DNA is not primary protein-coding information but

secondary meta-information, demolishes the neo-Darwinian

argument that it arose by some random (independent)

process. Meta-information is inextricably dependent upon

the information it refers to so an independent origin is



Birney, E. et al., Identification and analysis of functional elements in 1%

of the human genome by the ENCODE pilot project, Nature 447: 799–816,


Kapranov, P., Willingham, A.T. and Gingeras, T.R., Genome-wide

transcription and the implications for genomic organization, Nature

Reviews Genetics 8: 413–423, 2007.




Genetic Entropy & The Mystery of the Genome

John Sanford



Insert from an AiG article 

Differences between humans and chimps

Here are some other interesting differences between the human and chimp genomes which are often not reported:

To address these concerns and others, comparisons of the human and chimp genomes will be a part of “GENE” project sponsored by the Institute for Creation Research (ICR).The bioinformatics team (of which I am a part) will be analyzing different aspects of the human genome with special emphasis given to the comparison of human and chimp genomes.



Human and chimp genomes differ markedly in:

  • Chunks of missing DNA

  • Extra genes

  • Number of chromosomes and chromosome structure

  • Altered connections in gene networks

  • Indels (insertions and deletions)

  • Gene copy number

  • Coexpressed genes

December 2006 paper from PLoS One where Matthew Hahn found a “whopping 6.4%” difference in gene copy numbers, leading him to say, “gene duplication and loss may have played a greater role than nucleotide substitution in the evolution of uniquely human phenotypes and certainly a greater role than has been widely appreciated.” But even that number is misleading. At the end of the article, Cohen quoted Svante Paabo, who said something even more revealing.  After admitting he didn’t think there was any way to calculate a single number, he said, “In the end, it’s a political and social and cultural thing about how we see our differences.1Jon Cohen, News Focus on Evolutionary Biology, “Relative Differences: The Myth of 1%,” Science, 29 June 2007: Vol. 316. no. 5833, p. 1836, DOI: 10.1126/science.316.5833.1836.

“For many, many years, the 1% difference served us well” ?!? Huh? Was it the millions of school children and laymen who were lied to? No!  “Us” refers to the members of the Darwin Party, the dogmatists who shamelessly lied to advance their agenda.  They had a strategy to portray humans and chimpanzees as similar as possible, in order to make their myth of common descent seem more plausible.  Now, 32 years later, they have come clean, without any remorse, only because the usefulness of that lie has run out, and needs to be replaced by new lies.  They had a political, social and cultural agenda that, in many cases, worked for 32 years.  “Truth be told,” he said.  Too late.


Science. 2005 Apr 1;308(5718):107-11. Epub 2005 Feb 10. Comparison of fine-scale recombination rates in humans and chimpanzees. Winckler W, Myers SR, Richter DJ, Onofrio RC, McDonald GJ, Bontrop RE, McVean GA, Gabriel SB, Reich D, Donnelly P, Altshuler D.
    We compared fine-scale recombination rates at orthologous loci in humans and chimpanzees by analyzing polymorphism data in both species. Strong statistical evidence for hotspots of recombination was obtained in both species. Despite approximately 99% identity at the level of DNA sequence, however, recombination hotspots were found rarely (if at all) at the same positions in the two species, and no correlation was observed in estimates of fine-scale recombination rates. Thus, local patterns of recombination rate have evolved rapidly, in a manner disproportionate to the change in DNA sequence.


10-10-2008 17:12 | Dr Richard Buggs

From 1964 to 2004, it was believed that humans are almost identical to apes at the genetic level.

Ten years ago, we thought that the information coded in our DNA is 98.5% the same as that coded
in chimpanzee DNA. This led some scientists to claim that humans are simply another species of
chimpanzee. They argued that humans did not have a special place in the world, and that
chimpanzees should have the same ’rights’ as humans.

Other scientists took a different view. They said that it is obvious that we are very different
from chimpanzees in our appearance and way of life: if we are almost the same as chimpanzees in
our DNA sequence, this simply means that DNA sequence is the wrong place to look in trying to
understand what makes humans different. By this view, the 98.5% figure does not undermine the
special place of humans. Instead it undermines the importance of genetics in thinking about what
it means to be a human.

Fortunately (for both the status of human beings and the status of genetics) we now know that the
98.5% figure is very misleading
. In 2005 scientists published a draft reading of the complete DNA
sequence (genome) of a chimpanzee. When this is compared with the genome of a human, we find
major differences.

To compare the two genomes, the first thing we must do is to line up the parts of each genome
that are similar. When we do this alignment, we discover that only 2400 million of the human
genome’s 3164.7 million ’letters’ align with the chimpanzee genome - that is, 76% of the human
. Some scientists have argued that the 24% of the human genome that does not line up with
the chimpanzee genome is useless ”junk DNA”. However, it now seems that this DNA could contain
over 600 protein-coding genes, and also code for functional RNA molecules

Looking closely at the chimpanzee-like 76% of the human genome, we find that to make an exact
alignment, we often have to introduce artificial gaps in either the human or the chimp genome.
These gaps give another 3% difference. So now we have a 73% similarity between the two genomes.

In the neatly aligned sequences we now find another form of difference, where a single ’letter’
is different between the human and chimp genomes. These provide another 1.23% difference between
the two genomes
. Thus, the percentage difference is now at around 72%.

We also find places where two pieces of human genome align with only one piece of chimp genome,
or two pieces of chimp genome align with one piece of human genome. This ”copy number variation”
causes another 2.7% difference between the two species
. Therefore the total similarity of the
genomes could be below 70%.

This figure does not take include differences in the organization of the two genomes. At present
we cannot fully assess the difference in structure of the two genomes, because the human genome
was used as a template (or ”scaffold”) when the chimpanzee draft genome was assembled

Our new knowledge of the human and chimpanzee genomes contradicts the idea that humans are 98%
chimpanzee, and undermines the implications that have been drawn from this figure. It suggests
that there is a huge amount exciting research still to be done in human genetics.

The author is a research geneticist at the University of Florida.


DNA Chunks, Chimps And Humans: Marks Of Differences Between Human And Chimp Genomes

ScienceDaily (Nov. 6, 2008) — Researchers have carried out the largest study of differences
between human and chimpanzee genomes, identifying regions that have been duplicated or lost
during evolution of the two lineages. The study, published in Genome Research, is the first
to compare many human and chimpanzee genomes in the same fashion.

The team show that particular types of genes - such as those involved in the inflammatory
response and in control of cell proliferation - are more commonly involved in gain or loss
They also provide new evidence for a gene that has been associated with susceptibility to
infection by HIV.

"This is the first study of this scale, comparing directly the genomes of many humans and
chimpanzees," says Dr Richard Redon, from the Wellcome Trust Sanger Institute, a leading
author of the study. "By looking at only one 'reference' sequence for human or chimpanzee,
as has been done previously, it is not possible to tell which differences occur only among
individual chimpanzees or humans and which are differences between the two species.

"This is our first view of those two important legacies of evolution."

Rather than examining single-letter differences in the genomes (so-called SNPs), the
researchers looked at copy number variation (CNV) - the gain or loss of regions of DNA
CNVs can affect many genes at once and their significance has only been fully appreciated
within the last two years. The team looked at genomes of 30 chimpanzees and 30 humans: a
direct comparison of this scale or type has not been carried out before.

The comparison uncovered CNVs that are present in both species as well as copy number
differences (CNDs) between the two species. CNDs are likely to include genes that have
influenced evolution of each species since humans and chimpanzees diverged some six million
years ago. (Suom. Huom. Ihanko totta!)

"Broadly, the two genomes have similar patterns and levels of CNVs - around 70-80 in each
individual - of which nearly half occur in the same regions of the two species' genomes,"
continues Dr Redon. "But beyond that similarity we were able to find intriguing evidence
for key sets of genes that differ between us and our nearest relative."

One of the genes affected by CNVs is CCL3L1, for which lower copy numbers in humans have
been associated with increased susceptibility to HIV infection. Remarkably, the study of 60
human and chimpanzee genomes found no evidence for fixed CNDs between human and chimp and
no within-chimp CNV. Rather, they found that a nearby gene called TBC1D3 was reduced in
number in chimpanzee compared to human: typically, there were eight copies in human, but
apparently only one in all chimpanzees.

The authors suggest that it might be evolutionary selection of CNDs in TBC1D3 that have
driven the population differences. Consistent with this novel observation, TBC1D3 is
involved in cell proliferation (favoured category) and is on a core region for duplication
- a focal point for large regions of duplication in human genome.

"It is evident that there has been striking turnover in gene content between humans and
chimpanzees, and some of these changes may have resulted from exceptional selection
pressures," explains Dr George Perry from Arizona State University and Brigham and Women's
Hospital, another leading author of the study. "For example, a surprisingly high number of
genes involved in the inflammatory response - APOL1, APOL4, CARD18, IL1F7, IL1F8 - are
completely deleted from chimp genome
. In humans, APOL1 is involved in resistance to the
parasite that causes sleeping sickness, while IL1F7 and CARD18 play a role in regulating
inflammation: therefore, there must be different regulations of these processes in

"We already know that inactivation of an immune system gene from the human genome is being
positively selected: now we have an example of similar consequences in the chimpanzee."

CNVs in humans and chimpanzees often occur in equivalent genomic locations: most lie in
regions of the genomes, called segmental duplications, that are particularly 'fragile'.
However, one in four of the 355 CNDs that the team found do not overlap with CNVs within
either species - suggesting that they are variants that are 'fixed' in each species and
might mark significant differences between human and chimpanzee genomes.

DNA Samples and analysis

The project used DNA samples from 30 chimpanzees (29 from W Africa, one from E Africa): the
chimpanzee reference was produced using DNA from Clint, the chimpanzee whose DNA was used
for the genome sequence.

Human DNA samples were obtained from following participants: ten Yoruba (Ibadan, Nigeria),
ten Biaka rainforest hunter-gatherers (Central African Republic) and ten Mbuti rainforest
hunter-gatherers (Democratic Republic of Congo). The human reference is a European-American
male from the HapMap Project (NA10852).

CNVs and CNDs were detected using a whole-genome tilepath of DNA clones spanning the human
genome used previously to map human CNVs: this platform can reveal structural variants
greater than around 10,000 base-pairs in size.

This work was funded by the Wellcome Trust, the LSB Leakey Foundation, the Wenner-Gren
Foundation for Anthropological Research, the National Institutes of Health, The University
of Louisiana at Lafayette-New Iberia Research Center and the Howard Hughes Medical

The authors thank the Human Genome Diversity Project, the Coriell Institute for Medical
Research, the Integrated Primate Biomaterials and Information Resource, New Iberia Research
Center, and the Primate Foundation of Arizona for samples.

1. The Chimpanzee Sequencing and Analysis Consortium. Initial sequence of the chimpanzee
genome and comparison with the human genome. Nature, 2005; 437 (7055): 69 DOI:
2. Perry et al. Copy number variation and evolution in humans and chimpanzees. Genome
Research, 2008; 18 (11): 1698 DOI: 10.1101/gr.082016.108
Adapted from materials provided by Wellcome Trust Sanger Institute.

How to See the Handcraft of the Creator in Nature?

Drawings from the Finnish Nature

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