Gavin Here is some more evidence, this time on Isochores
Erwin Chargaff identified two Rules governing DNA.
The first which gave Watson and Crick the necessary leg-up in identifying the structure of DNA.
These 4 nucleotide bases are Adenine (A
), Thymine (T
), Cytosine (C
), Guarnine (G
Chargaffs Rules govern two things.1
) Adenine(T) always pairs with Thymine (T) and are in equal amounts
Guanine (G) and Cytosine (C) always paired and are in equal amounts. 2
) The ratio of the amounts (G+C) and (A+T) varies from species to Species and is universal. (Chargaff's C+G% rule
In other words this ratio is species specific
There are large regions of DNA (greater than 300 KB) with a high degree uniformity in G-C and C-G (collectively GC) and these regions tend to have more genes, and important genome features are dependent on these isochore
regions or structures, e.g. genes are found predominantly in the GC-richest isochore classes.http://www.ncbi.nlm.nih.gov/pubmed/11591471
Here is an abstract from a paper that emphasises importance of these isochore structures.http://www.ncbi.nlm.nih.gov/pubmed/11433361
One of the most striking features of mammalian chromosomes is the variation in G+C content that occurs over scales of hundreds of kilobases to megabases, the so-called 'isochore' structure of the human genome. This variation in base composition affects both coding and non-coding sequences and seems to reflect a fundamental level of genome organization. However, although we have known about isochores for over 25 years, we still have a poor understanding of why they exist.
So an outstanding feature of eukaryote genomes is this segmentation of the DNA into these isochore r
egions, each with a distinctive species specific base composition.
Therefore to view the genome without reference to it’s isochore mosaic would be like describing, say, the Colorado River without any reference to the Grand Canyon, or the Grand Canyon National Park, Colorado desert or Horseshoe bend etc etc, the very structures that guide and direct the river to its destination into the gulf of California.
However the fact is that most of us view the genome in precisely this manner.
This means that although we acknowledge the fact of the genetic code, (how did that come about I wonder) we almost always are oblivious to this other level of information that organises the genome
, and another thing, remember also that each genome organisation is species specific.
If a graph is drawn of the relative densities of GC we would get an undulating line of hills and valleys, with the gene distribution being mainly around the hill sections of the genome
This type of graph is precisely what the authors of a paper appearing in Nature plotted.
The paper is entitledGenome sequence of the Brown Norway rat yields insights into mammalian evolution.
Rat Genome Sequencing Project Consortium*
*Lists of participants and afﬁliations appear at the end of the paperhttp://www.nature.com/nature/journal/v4 ... e02426.pdf
The principle author of this paper is Francis Collins,.along with some 150 or so other researchers.( I stopped counting after about 100)
Now why is this significant as far a evolutionary theory is concerned.?
Because it reaches directly into the issue of Darwinian speciation.
If you bring up the paper in a separate tab and scroll down to page 502
of this paper you will notice 4 graphs in figure 9
Let just examine the graph 9c labelled “Lineage specific SINE content”
The X axis represents some 110 million base pair segment of the Rat chromosome 10.
The Y axis Red line represents the Rat specific SINE distribution.
The Green line represents the corresponding distribution in the Mouse genome.
It is quite noticeable that the two demonstrate a remarkable similarity. In fact it could be argued that one is a copy of the other with a few minor amendments.
Each graph denotes only lineage specific mutational insertions affecting mostly the so called Junk DNA.Now here is the rub.
Evolutionary theory posits that the Rat and Mouse diverged from a common ancestor some 20 odd millions years ago.
So what we are seeing are two independent random mutational processes acting on Junk DNA over a period of some 20 million years and both processes randomly produce the same high order result.
What are the chances of an undirected random process producing this result?
If anyone wishes to believe in miracles, then you are staring at one.On page 509
Collins discusses this finding under the heading
Co-localization of SINEs in rat and mouse
Despite the different fates of SINE families, the number of SINEs inserted after speciation in each lineage is remarkably similar:,300,000 copies……Figure 9c displays the lineage-speciﬁc SINE densities on rat chromosome 10 and in the mouse orthologous blocks, showing a stronger correlation than any other feature. The cause of the unusual distribution patterns of SINEs, accumulating in gene-rich regions where other interspersed repeats are scarce, is apparently a conserved feature, independent of the primary sequence of the SINE and effective over regions smaller than isochores.
Notice how this reference to isochors is just glossed over. Why? Because Junk DNA is becoming an embarrassment It was used by Jerry Coyne amongst others as proof of Darwinian evolution. Now it is viewed as conserved
, but lets not dwell too loudly on that.
When looking for functionality the first thing geneticists try to spot is a distinct non random pattern. This is what we have here and we all know what non random functional patterns reveal.
However since an outside agent cannot be considered we are left with random mutations being the miracle worker.
So am I being selective. Well we can examine the other graphs if anyone wishes.
btw the Human genome produces the same pattern.
The whole genome is an organised entity as is being clearly demonstrated, not the cobbling together of random undirected mutations.