DNA is an information storage molecule and DNA in and of itself does not have the ability to catalyze processes.
RNA by itself is a “living” precursor to DNA, and DNA “evolved” from RNA.
All cellular life requires ribosomal processes in order to translate out DNA codons.
Ribozymes are an example of how RNA bridge the metabolic gap between “living” and “non-living”.
When we use the term “DNA expression” or “genetic expression”, we are really talking about the process RNA uses to translate DNA, rather than the DNA itself. For example, trait/information can be encoded into DNA a particular way, but may have varied output depending on the specific process in ribosomes. How do individuals with the same trait have different expressions? Because of differences in RNA expression.
Cells communicate with each other via physical means. When any two cells interact, molecules are always involved.
“Genetic expression” is further complicated by mitochondion being effectively a different kind of “genetic” life with it’s own expression patterns.
DNA is poorly predictive of behavior because behavior is responsive and responsive means it’s going through two interdependent levels of RNA translation.
All multicellular organisms replicate and extend the same processes found in the most basic “life”. All multicellular organisms are individual cells with specializations, rather than an organism with cellular sub-units.
The “purpose” of biology is to fill metabolic niches.
Edit: It’s kind of crazy to think of life, in all it’s diversity as an unbroken metabolic cascade all the way back to that initial catalysis. Makes me wonder how many other independent chains of life got buried or subsumed under the landslide of our particular string/starting point.
Maybe the function of life/death is in ensuring species level responsiveness to an organisms metabolic niche. The more competitive the niche, the lower the lifespan? Human lifespans have been increasing because we’ve been carving out a metabolic niche with advancing success, recent losses due to epidemiology represents loss of effectiveness controlling metabolic niche.
Making me giggle a bit thinking that Giant Tortoises have (had) a far less competitive metabolic niche than humans under this conceit.
It’s interesting thinking about life requiring catalysis before replication, without the metabolic substrate in place “life” doesn’t happen. The more specialization in an organism, the more complex the initial metabolic environment needs to become to sustain that metabolic environment. Extremes like a womb compared to asexual replication mean that the metabolic cascade which ultimately results in behavior is way more flexible than I’ve imagined in the past, both in initiation and effect.
One upside to the past two months going down this path is that it it’s actually quelled a lot of anxiety about human initiated negative effects. I don’t think I had a grasp on just how profound and pervasively our evolution is guided by other organisms. Viruses alone have shaped and shifted evolution in exactly the sci-fi/mad scientist/genetic modification kind of way humans wish they were capable of at this point.
Guess over the next year the big deals will come from peptide A/B testing (e.g. tuning neuroligins) until we build a general map of which peptides bias toward being interpreted into which types of behavior. Rather double APOE4 for instance as a biomarker, we can use that as a starting point for treatments which modify RNA expression for proteins dealing with water transport, or even come up with more personalized guidelines (e.g. People with this phenotype should drink 4 glasses of water a day, people with this phenotype should not drink extra water, people with this phenotype should drink 8 glasses, etc.).
I’m still reasonably certain that the effect of fUS and other stimulation techniques is that they modify methylation of RNA guided products, so understanding current “production” rates of various peptides/proteins is probably going to represent a huge leap forward in pharmacology modified behavior.
Edit 2: I’m wondering if there is an association between organism specialization requirements and length of gestation periods? There seem to be gestation clusters for similar classes of organisms, and gestation period isn’t super coupled with size or specific features. Do we also consider the difference between organisms which have fully functional offspring (e.g. reptile) and those which require post natal nurturing (e.g. mammals)?
If this conceit is true, can we get to a better understanding of what is “complex” biologically? E.g. despite the more extreme sulci/gyri of dolphin brains, from a construction standpoint is there much of a difference? Are there classes of complexity we are completely missing, for example is there a ton of complexity we are missing in digestive systems or vascular systems because we’ve been so hyper focused on the brain part of nervous systems?
The really fascinating part of this is that genetic instructions aren’t just coded for sequential expression, they are coded for also coded temporal and environmental expression (and probably some modalities that I am missing). It suggests that as far as “nature” is concerned, there really isn’t much/any difference between these things, and the differences between them are probably just “perception” artifacts.
Something really surprising is just how subtle the differences are between many classes of proteins, despite the “visual” difference in expression.