The world of genetics is moving so fast it is hard to keep up. Luckily one of my favorite writers on the subject Robert Plomin (together with Oliver Davies) has written an update on the genetics of child psychology and psychiatry in the Journal of Child Psychology and Psychiatry. There is a lot of information in the article regarding the latest genetic findings but the issue that stuck me most was about how our understanding about how genes work is changing. My understanding of genes was the classic model described succinctly by Plomin and Oliver as “a gene is a sequence of DNA that is transcibed into messenger RNA which is then translated into amino acid sequences, the building block of protein”. The proteins then build to form brain structure, neurotransmitters etc.

The hunt has been on to find the genes that affect behavior and illness using this classic DNA process. There have been successes with a number of single gene neurological disorders identified such as Huntington’s Chorea and PKU. For these conditions the gene has been located and the sequence from gene to protein to behavior is well documented. Unfortunately this process has not worked in discovering the genes for most other psychological/ psychiatric disorders or for behavior in general. Although it is clear that there is a substantial genetic component in behaviors such as IQ, reading and language and disorders such as ADHD and Autism, as shown by twin studies, the actual genes responsible have not been found. Recent arguments have focused on the idea that many genes may be involved in combination to influence such behaviors. Plomin’s article however also raises another difficult issue. There may also be a problem with the standard DNA model as an explanation for gene- behavior effects. There are a number of puzzles regarding the standard coding DNA model. Firstly there are far fewer of these traditional genes than expected (about 24,000 in humans). Also they only make up about 2% of DNA, the other 98% were said to be junk, a byproduct of evolution. Another factor is how little these traditional genes vary between individuals and species for example simple worm like creatures called called nematodes have 19000 genes compared to the 24000 in humans. Are we not that much different to nematodes? Chimpanzees share 99.4% of DNA coding genes with humans.

Plomin and Oliver show that part of the problem may be that we have not focused on the way that RNA works. Out of the 98% thought to be junk DNA about 1/2 does produce RNA but not the type of RNA that codes for amnio acids. Instead the non coding RNA ‘plays an important role in regulating the expression of the protein coding DNA‘. RNA is also much more complicated than once thought and many different types of RNA have now been identified, including microRNA, tRNA, snRNA, rasiRNA, snoRNA, etc. How RNA works is explained in detail in the article but that explanation is too detailed to describe here other than to say that there is much more variation between individuals and species in terms of their RNA profile and that it is the RNA that may hold the key to understanding more complex gene behavior effects. The implication of these findings according to Plomin and Oliver is that we should be analyzing the whole genomes of individuals rather than searching for individual genes. This is becoming cheaper and easier to do but so far the results are still very limited.

My take home message from the article was that genes and their effects are not as simple as most people believe and as much of the media describes. It is very unlikely that we will find the gene for Autism, for IQ or for being gay. Instead such behavior is likely to be the result of a complex interaction of many different genes, with different types of RNA dictating how the genes are expressed which in turn will probably be influenced by factors in the environment. Hugh discoveries are being made all the time but I think the more that is known the more complex it all seems.