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-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 arefully transcribed.
•Transcription proceeds not just one way but both
•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].’
As many as 20% of transcripts range up to
more than 100 timesthe 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.
The non-protein-coding regions (previously thought
to be junk) are now calleduntranslated regions (UTRs)
because while they aretranscribed into RNA, they are
nottranslated into protein. Not only has the ENCODE
project elevated UTRs out of the ‘junk’ category, but it now
appears that they arefar more active than the translated
regions (the genes), as measured by the number of DNA
bases appearing in RNA transcripts.
Genic regions are transcribed on average in five different overlapping and
interleaved ways, while UTRs are transcribed on average
in seven different overlapping and interleaved ways. Since
there are about 33 times as many bases in UTRs than in
genic regions, that makes the ‘junk’ about 50 times more
DNA information normally
exists in a form similar to a closed book—all the chromatin coiling
prevents the coded information from coming into contact
with the translation machinery. When the cell wants some
information it opens a particular page, ‘photocopies’ the
information, then closes the book again.
The chromosomes in each cell are stored in the
membrane-bound nucleus. The nuclear membrane
has about 2,000 pores in it, through which molecules
need ‘permission’ to pass in and out. The required
chromosome is brought near to one of these nuclear pores.
One of the supposedly ‘knock-down’ arguments that humans
have a common ancestor with chimpanzees is shared
‘non-functional’ DNA coding. That argument is now out the window.
There are multiple information codes operating in living cells. The
protein code is the simplest, and has been studied for half
a century. But a number of other codes are now known, at
least by inference.
Cell memory code. DNA is wound up in four separate layers of
chromatinstructure. The first level
of this chromatin structure carries a ‘histone code’ that
contains information about the cell’s history (i.e. it is a cell
memory). Cell division is an opportunity for
changes in the nucleosomal composition of a specific DNA
region. Changes can also happen during the lifetime of a
cell due to chemical reactions allowing inter-conversions
between the different nucleosome types. The memory
effect of these changes can be that a latent capacity that was
dormant comes to life, or, conversely, a previously active
capacity shuts down.
In humans, there are about 300
different cell types in our bodies
All of these cells contain the same DNA, so how
does each cell know how to become a nerve cell rather
than a blood cell? The required information is written in
code down the side of the DNA double-helix in the form
of different molecules attached to the nucleotides that form
the ‘rungs’ in the ‘ladder’ of the helix. This code silences
developmental genes in embryonic stem cells, but preserves
their potential to become activated during embryogenesis.
The embryo itself is largely defined by its DNA sequence,
but its subsequent development can be altered in response to
lineage-specific transcriptional programs and environmental
cues, and is epigenetically maintained.
a large proportion of the
whole genome is required for the normal operation of the
cell—probably at least 50% in unspecialized body cells
and up to 70–80% in complex liver and brain cells—and,
of course, the whole genome is required during replication.
This creates a huge logistic problem—how to avoid clashes
between the transcription machinery (which needs to
continually copy information for ongoing use in the cell)
and the replication machinery (which needs to unzip the
whole of the DNA double-helix and replicate a ‘zipped’
copy back onto each of the separated strands).
Replication does not begin at any one point,
but at thousands of different points. But of these thousands
of potential start points, only a subset are used in any one
cell cycle—different subsets are used at different times and places.
•The pattern of replication in the late embryo and adult
is tissue-specific. This suggests that cells in a particular
tissue cooperate by coordinating replication so that
while part of the DNA in one cell is being replicated,
the corresponding part in a neighbouring cell is being
transcribed. Transcripts can thus be shared so that
normal functions can be maintained throughout the
tissue while different parts of the DNA are being
replicated. The early transcribed DNA is that which is needed
most often in cell function. The correlation between
transcription and replication in this early phase allows
the cell to minimize the ‘downtime’ in transcription
of the most urgent supplies while replication takes place.
Keeping the cell alive and functioning properly (transcription)
takes precedence over cell division (replication)
An obvious benefit of the pattern of replication initiation
being never the same from one cell division to the next
is that it prevents accumulation of any errors that are
Even if we granted that the first biological information
came into existence by a random process in an ‘RNAworld’
scenario, the meta-information needed to use that
information could not possibly come into existence by
the same random (independent) process because metainformation
is inextricably dependent upon the information
that it relates to.
Can natural selection save the day? No.
There are at least 100 (and probably many more) bits of
meta-informationin the human genome for every one bit of
primary (protein-coding gene) information. An organism
that has to manufacture, maintain and drag around with it
a mountain of useless mutations while waiting for a chance
correlation of relevance to occur so that something useful
can happen, is an organism that natural selection is going
toselect against, not favour!
According to Kirschner and Gerhart’s theory of
facilitated variation,14 DNA contains regulatorybased
modules which they liken to Lego® blocks.
That is, they have very strong internal coherence
and integrity (difficult to break) but are easily pulled apart
(during meiosis) and reassembled (during fertilization) to
produce a built-in capacity for variation.
The most surprising result of the ENCODE project,
according to its authors, is that 95% of the functional
transcripts (genic and UTR transcripts with at least one
known function) show no sign of selection pressure (i.e.
they are not noticeably conserved and are mutating at the
if 95% of the human
functional information shows no sign of natural selection
then it means that natural selection has not been a significant
contributor to our ancestry.
There are about 125 million single nucleotide differences
between humans and chimps, resulting from about 40
million mutational events.
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 inextricablydependent 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 Genetics8: 413–423, 2007.
JOURNAL OF CREATION21(3) 2007
Genetic Entropy & The Mystery of the Genome
Insert from an AiG article
Here are some other interesting differences between the human and chimp genomes which are often not reported:
The chimp genome is 12% larger than the human genome.
Only 2.4 billion bases have been aligned between the two genomes, leaving a maximum similarity of 68–77%.
In many areas of the genome, it appears major rearrangements of DNA sequences have occurred, accounting for another 10–20% dissimilarity.
Chimps have 46 chromosomes and humans have 44 chromosomes (excluding sex chromosomes for both species).
To save money and time, the chimp genome was assembled using the human genome as a template (because of the presupposition that humans evolved from the same line as chimps); it is currently unknown if the pieces of the chimp genome “puzzle” were put together properly.
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:
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. http://creationsafaris.com/crev200706.htm
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
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
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
genome. 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.
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