Joined: Oct. 2012
|Quote (sparc @ Nov. 16 2012,22:28)|
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|Quote (GaryGaulin @ Nov. 16 2012,19:59)|
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This would be the situation in a flask inocculated with a single E. coli cell susceptible to T2 phages.
|Quote (GaryGaulin @ Nov. 16 2012,09:04)|
|Quote (sparc @ Nov. 15 2012,23:22)|
Gary, what does theory say about the distribution of intelligence in a bacterial clone? Is theory assuming that all cells contain the same amount of intelligence?
As long as they were well isolated from external information from wild colony conjugation the molecular level intelligence of the clones would be essentially identical.
What does your theory predict will happen if a single T2 phage is added to the culture?
|But the cellular intelligence is the part it develops during its lifetime and depends on environment, resulting in tumblers, swarmers, or even sessile, resulting in very different cellular intelligence circuits.|
Thankfully I found another more normal question to work on:
After a phage inserts itself into the host genome to be replicated the molecular intelligence memory size increases. There are then additional molecular intelligence subsystems included. It makes sense that there is more intelligence there, even though the recent gain could later become harmful.
Where the phage is deactivated it's taken out of the molecular circuit, molecular intelligence is then the same as before. Where the phage starts quickly replicating inside, the molecular intelligence and/or (without help from host systems is) phage protointelligence continues to rise. The intelligence will not drop until the phage destroys the host.Where the phage is a beneficial mitochondria that just took up residence in a cell, the molecular intelligence of the cell increases, and the cellular intelligence would be more robust and responsive from the extra energy (but not have more cellular intelligence unless it also adds more cellular level circuitry/subsystem to its schematic).
T2 is a virulent phage that never integrates into the host genome.
Phages are virusses and have nothing to do with mitochondria which don't exist in bacteria and are actually a hallmark of eukaryotes. In addition, irrespective of the fact that they don't exist in bacteria and that the cell would be to small to harbor any what would make a mitochondrium beneficial for an E.coli cell?
Be that as it may be. How does your theory explain that the vast majority of infected cells die while some (very few indeed) survive? Remember that the bacteria are derived from a single cell and all phages in the system are derived from a single phage. How do the surviving cells differ from their relatives in terms of what you think is "intelligence"? And how does this "intelligence" make them survive?
The theory explains why the vast majority of infected cells die while some survive, by modeling it. And it looks like you're the one most into the T2 phage process. So model it as described in theory then show what you end up with for changing circuits and variables over the course of the infection cycle(s).
The theory of intelligent design holds that certain features of the universe and of living things are best explained by an intelligent cause, not an undirected process such as natural selection.