[Alamo-Girl]

For lurkers: I have been researching because it is now apparent to me that conditional operations at the genetic level requires symbolization (e.g. “if this [acquired data] is equal to that [symbol] then …”) Here are some things I’ve found, that might be of interest to anyone following this research:

Language-like features in junk DNA: Transposable element footprints in the genome?

The presence of extra-thymic selection processes for self/non-self discrimination is amply documented in the literature, though the mechanisms underlying these processes are still unclear. We postulated that peripheral self/non-self discrimination can be modelled by the response of a T cell to a rapid change in the number density of its MHC/peptide ligand. In this model changes in the concentration of MHC/peptide complexes that occur at a particular rate are regarded as being potentially 'dangerous' to the organism, and hence trigger T cell activation…

We are currently in the process of implementing a computer simulation of our model and will be testing its performance in distinguishing arbitrary non-self sequences from a pool of artificially generated self sequences. Our model, which effectively comprises a local definition of self / non-self could have profound implications for autoimmune diseases…

and … One of the most striking characteristics of many biochemical pathways is their complexity. This complexity is manifested principally through the number of routes connecting the various species in the pathway. In particular, it is often observed that there are various routes that an organism can use to manufacture a particular metabolite or species. This facility to switch biosynthetic routes confers considerable robustness to an organism since it is not reliant on a single route to some key compound. Robustness can be further increased by the presence of feedback loops within a biosynthetic pathway…

In addition to CCT there is compelling evidence in the literature that many enzymes involved in lipid biosynthesis are modulated by the membrane composition. This led us to postulate that feedback through membrane stored elastic energy could provide a common control mechanism that underlies the homeostatic control of membrane lipid composition/properties….

Our results show that introducing feedback does indeed increase robustness dramatically. We are currently comparing the type of feedback (i.e. positive or negative) which our models predict for the various steps, with literature data on the modulation of the individual enzymes by lipid composition. Once the model is validated against experimental data, we will conduct a series of 'what if' experiments aimed at understanding changes in membrane lipid composition following specific types of perturbation, e.g. the administration of anti-neoplastic ether lipids.

And here is a fascinating article, whose first conclusion is that junk DNA is not junk as it contains finite amount of algorithmic information. IMHO, that conclusion should be taken especially strong in light of the Chiatin definition of randomness:

Complexity International - Brief Comments on Junk DNA. Is it really junk? (pdf)

[gore3000]

This facility to switch biosynthetic routes confers considerable robustness to an organism since it is not reliant on a single route to some key compound. Robustness can be further increased by the presence of feedback loops within a biosynthetic pathway…

One of the most interesting examples of feedback loops is the one that controls cell replication. Let's consider this - right after conception cell replication occurs very quickly, after birth it still occurs and continues to add new cells to the body but at a slower pace. After adulthood cells are not added any more but they are replaced with new cells being created and old ones commiting suicide. At old age the process of replacement stops. We know how the last part of the loop works, the ends of the chromosomes get shorter at each replication and thus serve as 'counters' for when replication is to stop. This of course is totally symbolic, there is no purpose to those counters other than as counters.

[forsnax5]

Since you're interested in "Junk" DNA, you might appreciate this piece that was published today by the American College Of Neuropsychopharmacology.

Jewels That May Help Explain Behavioral Disorders Found Among "Junk" DNA

Scientists have been looking for genes that can explain behavioral disorders for 20 years without much success. According to L. Alison McInnes of Mt. Sinai School of Medicine, that may be because they have been concentrating their efforts in the wrong places in the genome.

Speaking on Dec. 8 at the annual meeting of the American College of Neuropsychopharmacology held in San Juan, Puerto Rico, McInnes advised that those interested in genetic links to behavior should start looking at places in the genome that produce special molecules called small non-messenger RNA (smnRNA) rather than concentrating on genes that code for proteins.

Current genetic screening techniques do not pick up these sequences because they are very small and not much is known about their structure. So McInnes and her colleagues at Mt. Sinai have created a computational and molecular screening technique designed specifically to look for smnRNA molecules produced by regions in the genome that have been associated with behavioral disorders. Furthermore, they have used this method to successfully identify such molecules in the first few genes that they investigated, she reported.

The existence of smnRNAs has been known for some time. Until recently, they have been generally dismissed as unimportant. New studies are finding that they are actually quite abundant and involved in a wide variety of biological processes. As a result, some scientists are beginning to speculate that they may represent an entirely new class of gene and type of gene activity.

McInnes cited the theoretical work of John Mattick and Michael Gagen at the University of Queensland in Brisbane. Last year they published a lengthy paper in Molecular Biology and Evolution in which they argued that, rather than being useless, smnRNAs and introns – the sequences in the genome between genes that code for proteins that have been called junk DNA – form a powerful network that can turn ordinary genes on and off at the proper times.

"It appears that smnRNA may be especially relevant for understanding behavioral differences," McInnes said, "because they appear to be particularly enriched in the brain. They represent a swift and energy efficient means of regulating gene expression and may be especially important for rapid regulatory events."

Lack of expression of an smnRNA has already been strongly associated with one neuropsychiatric disorder, Prader Willi syndrome, McInnes reported. Prader-Willi syndrome is characterized by abnormally poor muscle tone and feeding difficulties in early infancy, followed by excessive eating and gradual development of morbid obesity. It is also accompanied by cognitive impairment.

In the initial trial of their new screen, the Mt. Sinai researchers identified a possible smnRNA molecule produced by an intron of the human corticotrophin-releasing hormone gene. Corticotrophin releasing hormone (CRH) plays a key role in the response of humans and other mammals to external threats. It acts at a number of sites in the nervous system to control automatic, behavioral and immunological responses of stress. Alterations in CRH neural activity appear to contribute to a number of mental illnesses including depression, anxiety disorders and anorexia nervosa. In addition, the CRH smnRNA appears to form a complimentary match with a sequence in an untranslated region associated with a receptor, called the NMDA-glutamate receptor, which is widely implicated in schizophrenia and other degenerative neurological disorders.