Saturday, July 07, 2012

Quantity and Quality .

Quantity and Quality
Andre Willers
7 Jul 2012
“Quantity has a Quality of its own “ Stalin
Synopsis :
A few simple rules translates quantity into quality . This is extensively used in genetic systems .
Discussion :
Rules are boundary conditions .
Genetic Systems :
A long string of instructions (DNA) is chopped up into genes and chromosomes . This immediately increases the complexity of the system (see “Dark matter update” June 2012 ) . The Complexity of the Universe is also a measure of the degree of complexity .
N = 2^4592.7933 . A large number
Upper boundary of complexity for human genetic systems = 2^n , where n = number of basepairs in DNA . For Humans , n~3x10^9 .
You have the delicious result that the complexity of a subset of system is greater than the complexity of the system if we use the axiom of delineation . This is merely a restatement of the Godel principles ,
You might as well call it the Bootstrap Principle . Entropy is pumped into a virtual dimension . You can do this because the number of possibilities of chopped-up (ie quantum) systems are larger than the number of possibilities in smooth systems . So much for the General Theory of Relativity .

The Genome Problem :
Why so few human genes ?
Duplication of genes obviously increase fitness. The old gene continues to function , but the duplicates can experiment (like cancers) . But there are limits and boundaries , which can be calculated from basic principles .
What is the human mechanism limiting the number of genes to about 23 000 ?
It is the chromosome mechanism . To put it very simplistically , genes are defined by a START and a STOP codon sequence .
Similarly , chromosomes have START and STOP markers .But these are also part of the DNA instruction (all those pesky introns, etc) . See Appendix IV
Epigenetics :
What happens to these bits and pieces that don’t quite make it to the duplication process ?
We would like to think that they simply disappear , but number 2 , 3 ,4 etc are not that obliging . They have sufficient relevance that large numbers of these structures (remember ,these are unsuccessful duplicates) remain as a back-up reservoir . We call this the epigenetic system .
Prions and Speciation :
Prions specialize in masking DNA coding at the various STOP stages . Hence the duplication of genes . But the physical process of cell-division limits the cut-off points , unless there is a simultaneous mutation in the chromosome markers . See Appendix III .
Thus you can expect marked new levels of speciation due to global warming .
Gaia is inside your decision loop .

Appendix I
The haploid human genome contains about 23,000 protein-coding genes, which are far fewer than had been expected before sequencing.[1] In fact, only about 1.5% of the genome codes for proteins, while the rest consists of non-coding RNA genes, regulatory sequences, introns, and noncoding DNA (once known as "junk DNA").[2]
Appendix II
Rapid and asymmetric divergence of duplicate genes in the human gene coexpression network.
Chung WY, Albert R, Albert I, Nekrutenko A, Makova KD.
Department of Biology, Penn State University, University Park, PA 16802, USA.
While gene duplication is known to be one of the most common mechanisms of genome evolution, the fates of genes after duplication are still being debated. In particular, it is presently unknown whether most duplicate genes preserve (or subdivide) the functions of the parental gene or acquire new functions. One aspect of gene function, that is the expression profile in gene coexpression network, has been largely unexplored for duplicate genes.
Here we build a human gene coexpression network using human tissue-specific microarray data and investigate the divergence of duplicate genes in it. The topology of this network is scale-free. Interestingly, our analysis indicates that duplicate genes rapidly lose shared coexpressed partners: after approximately 50 million years since duplication, the two duplicate genes in a pair have only slightly higher number of shared partners as compared with two random singletons. We also show that duplicate gene pairs quickly acquire new coexpressed partners: the average number of partners for a duplicate gene pair is significantly greater than that for a singleton (the latter number can be used as a proxy of the number of partners for a parental singleton gene before duplication). The divergence in gene expression between two duplicates in a pair occurs asymmetrically: one gene usually has more partners than the other one. The network is resilient to both random and degree-based in silico removal of either singletons or duplicate genes. In contrast, the network is especially vulnerable to the removal of highly connected genes when duplicate genes and singletons are considered together.
Duplicate genes rapidly diverge in their expression profiles in the network and play similar role in maintaining the network robustness as compared with singletons.

Appendix III
The idea of gene duplication is not new; the striking evidence for earlier suggestions for at least limited occurrence has come from the degree of similarity of amino acid sequences among different, although related, proteins. The probable relation between gene duplication and the rate of evolution is also of interest. Once a gene has been duplicated, the risk of deleterious mutation is decreased. Further, if we may consider one copy (the effective gene) as being conserved relatively unchanged as a result of selection pressure, so that the function it specifies is neither lost nor adversely modified, other copies would be free to mutate as long as deleterious gene products did not result. These copies would initially have the capacity to specify a complete gene product-for example, an enzyme or part of a physiological system. As mutations occurred in the copies some elements might be lost or modified and other elements maintained. The development of a gene specifying a new function from remaining elements of an older gene that had been protected from adverse selection pressure by copying seems to be far more probable than its development de novo from a random nucleotide sequence. A great source of variety in new structures might result from the combination. of elements from several preexisting genes.
Appendix IV
A special DNA base sequence in the region of the kinetochores provides, along with special proteins, longer-lasting attachment in this region. The microtubules then pull the chromatids apart toward the centrosomes, so that each daughter cell inherits one set of chromatids. Once the cells have divided, the chromatids are uncoiled and DNA can again be transcribed. In spite of their appearance, chromosomes are structurally highly condensed, which enables these giant DNA structures to be contained within a cell nucleus


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