The idea has been percolating in my brain for a few weeks that our understanding of “how DNA works”, particularly in regard to expressed behavior, might rest on similar philosophical pitfalls that led to the over application of neuron function in the study of nervous systems. We’ve assumed that DNA construction guides expression because we could get an obvious expression result from DNA alone, much like we could get a sorta vague hint of what’s going on in a nervous system by measuring the interconnects (or neurons) between functional groups.
More recent understandings illustrate that the genes themselves matter a lot less than the total expression in a system. For example, an individual may have genes in their DNA which impart “predisposition” for a whole host of traits and expressions, everything from eye color to Huntington’s. Yet, expression still varies, even between monochorial twins. Why does this roulette of expression take place, even when we duplicate the DNA?
It’s always seemed really weird to me how unaffected by the expression differences in cloned animal models most research seems to be. The whole point of most neuro lab experiments is fix the number of variables possible to produce the same effect (reducing the possibility that the effect under study is occurring by “chance”), yet even in the same environment with the same DNA, trait and behavioral expression varies (and sometimes dramatically). We average all of this variance away into a statistical contrivance, but it’s still there.
Part of this effect is that (like many other things in the field) there’s a lot of discarded concepts which got transferred to new ideas, particularly in the case of DNA Mendellian expression. It is through the absorption of prior ideas that I think we came to overfocus on DNA itself rather than expression as the source of traits.
There’s no part of biological development which begins with DNA. Without the necessary expression framework, cells don’t multiply. They don’t perform metabolic tasks. They don’t signal. We can however induce and modify those same processes solely through the modulation of RNA expression. And that we have this unbroken chain of metabolic process transfer back through time, possibly all the way back to RNA world suggests to me that DNA does not provide the instructions to make RNA, but collective RNA expression provide the instructions to make DNA, and that DNA functions more as a substrate for the metabolic/catalytic chain, a data store for the entropic requirements of life.
A practical example of this difference would be that of “memory” performance, we have scoured DNA looking for particular genes which provide a particular impact on memory performance, however the wider the geography of our demographic pool, the less succinct these magic genes become. What if instead of thinking about traits in terms of an on rails regurgitation of DNA, we thought of “memory” as an artifact of RNA expression rates?
Thinking of the development cycle in mammals, when they are young they voraciously produce specific RNA which promote the write and encode of environmental data, this “memory/behavior” flexibility allows them the ability to establish cooperation and behavioral adaptation to their current world. This peaks just around the time of sexual maturity, and then “memory/behavior” flexibility/performance falls off at a rate consistent with the degradation of cellular ability to modify RNA methylation rates and produce the necessary quantity of peptides/proteins which form the substrate of memory/behavior.
By focusing on RNA expression rates, we may finally be able to advance through some of the many mysteries of DNA trait arbitrariness.
So let’s make a prediction here some low hanging fruit – For most phenotypes of “autism”, there is no DNA component. Most phenotypes are going to be purely the product of RNA expression guiding development along particular paths in response to environmental conditions, including the RNA transferred from parent organisms (and lets not forget that RNA reconfigures oocytes DNA on constant basis).
Testing this is kind of hard due to the multi-generationality of RNA guided transfer, but I propose that we should be able to find individuals who have drastically changed their environments, and as such gained/lost traits independent of any particular gene modification. Over a long enough time line, this is our assumption about how DNA works now, the difference here is that these changes can take place within a few generations via RNA expression rates.
Second proposal, is the “Flynn Effect” an artifact of mandatory public education attitudes modifying expression rates? Was the “smarter children” effect literally “smarter children”?