Excerpt: The sequencing of the human genome drove home the discovery that genes were just a small part of our total DNA—what made up much of the rest remained a big mystery. Now, a massive international project has begun to solve this mystery and bring us closer to understanding the links between genetics and disease. What is this other DNA doing? How much of the genome do we now understand? How can researchers use this information to understand disease better?
My comment (edited for concision): In the context of nutrient-dependent individual survival and pheromone-controlled reproduction, Bonasio (2012) reported that “Contrary to its original denomination as “junk” DNA, most of the 98% of the human genome devoid of protein-coding potential is transcribed, and a considerable fraction is also conserved in sequence among different species, more than would be expected by chance.”
Is there any reason to believe that the epigenetic effects of nutrient chemicals and pheromones do not exert the same control over our gene expression that has been modeled across species from microbes to man, as exemplified in the honeybee model organism? In vertebrates, for example, GnRH is conserved across 400 million years of evolution, and its secretion is epigenetically altered by nutrient chemicals and pheromones in my model. That suggests olfactory/pheromonal input epigenetically alters intracellular signaling and stochastic gene expression as is required to explain species diversity via ecological, social, neurogenic, and socio-cognitive niche construction. Presumably, species diversity results from de novo expression of receptors for olfactory/pheromonal input, which is an ever-present feature of any organism’s sensory environment.
From the archived text of the chat:
John A. Stamatoyannopoulos MD: ENCODE’s data provide a unique and powerful window through which to view evolutionary change. We can see those changes directly by lining up the genome sequences of many different organisms — these line-ups have revealed millions of regions where all the genomes agree, indicating sequences that have been specially preserved by evolution while others have decayed away (ie freely changed their letter codes). We now see that a large proportion of these ‘conserved’ regions are lighted up by ENCODE annotations, indicating that they are marking spots in the genome that contain important instructions for cell function.
My comment: It is the “…sequences that have been specially preserved by evolution…” that appear to refute random mutations theory since there is no explanation of how adaptive evolution “preserves” anything. For contrast, adaptive evolution appears to have preserved the ability of nutrient chemicals and pheromones to epigenetically effect intracellular signaling and stochastic gene expression, which is required for the wealth of species diversity that is seen. Their common molecular biology is used to achieve that diversity. Is their common molecular biology used by evolution? What I “see” is a pattern of design across what often can simply be viewed from the perspective of how common molecular biology is used across all of Creation (e.g., from a common man’s perspective).
From the archived text of the chat:
Ewan Birney: The DNA letters in our genome in some sense are clearly not random (for example, if I told you the chimpanzee’s genome, you could guess the human genome very well). However there are two scenarios where we use the word ‘random’ about the genome bases. Firstly there are random processes – such as mutational processes which often have some characteristics (a bit like the dice being loaded) but do seem to operate like a “dice”. Secondly in bioinformatics we very often have a random model of DNA as a way of “modelling” DNA bases, in other words trying to simulate what DNA “would look like” – these random models rarely are based on any mechanistic understandings of the DNA, rather they are a sort of statistically ok model.
So – there is no contradiction between the findings of ENCODE and the fact we use random models in our analysis (indeed – those random models are often critical in our analysis)
My comment: If the random processes were mutational processes akin to “loaded dice” in “…a sort of statically ok model…” we could not see any moving pattern of design. Instead, in a non-static model that may not be ok for some people, we see forward movement. The epigenetic effects of nutrient chemicals always precede the epigenetic effects of the metabolites of the nutrient chemicals, which are called pheromones. Moving away from any random model to a model of epigenetically driven forward movement akin to theistic Creation, we can then see that eco-evolution, which is the only type of biological evolution known to mankind, is driven by chemical ecology.
With eco-evolution, there is nothing random about the availability of nutrient chemicals in the sensory environment or their acquisition. The best adapted organisms eat and survive. The metabolism of what they eat to pheromones is the only clear indicator of the difference between self and non-self, which establishes the organism’s social niche. Unless cannibalism occurs, conspecifics are not eaten because they smell like each other. Heterospecifics are killed and often eaten because they do not smell like conspecifics. The nutrient-dependent ecological niche ensures pheromone-controlled reproduction in the pheromone-dependent social niche.
Are any ENCODE researchers concealing their perspectives on adaptive evolution to avoid the topic of theistic Creation? Minimally, I think attention should be focused on the model organisms Bonasio and others, like me, have used to detail precisely how the differentiation of species, brains, and behaviors is driven by nutrient chemicals and pheromones. If not, at some point in the near future we are going to see another clash of world views that might have been prevented by reviewing the available literature and modeling extant species for comparison to those that are extinct.