Sometimes scientists focus on their little corner of the world so intently that they fail to see the forest for the trees. Alternatively, they may be afraid to see the forest because of the ramifications. In any case, however, any biologist worth his salt understands the central dogma: DNA makes RNA which makes protein.
Here’s another “central” dogma that I believe merits further investigation: Origins of replication make origins, promoters, enhancers, and splice sites
Duplication of origins
Origins make new origins through a process of DNA amplification that generates new replicons. This is what viruses do on a regular basis. I believe this occurs when circular viruses (a form of replicon) binds to another origin on host DNA and physically attaches to it in some manner that generates a double origin of replication (see blog for details). This double origin is the mating of two different replicons, one of which may be considered as the remainder of the entire genome. They would be interlocked together into a four-strand complex in a frozen state of recombination and covalently linked together by interstrand bridges, preventing complete fusion of the two replicons. This allows the viral DNA to spin off copies of itself which are then bound up into viral particles by proteins in a cascade of events well known in virology. These viral clones make seek out other areas of the genome in which to attach as well.
Conversion of an origin of replication into a promoter of transcription
During cellular differentiation, a portion of the interior of the four-strand complex may be clipped out leaving an interior gap with exposed ends available for transcription of RNA. The ability to function as a replicon ceases to occur, resulting in a functionally larger replicon via a nearby double origin on the remaining genome. This partial fusion of the replicons makes this site more susceptible to breakage and fusion during laboratory DNA isolation.
Conversion of an origin of replication into an enhancer of transcription
The bonds holding the two replicons are split, causing the smaller replicon to be released from the genome. The single origin remaining on the genome becomes an enhancer of transcription. Unless altered further in some way, it provides a means for a new replicon to join the genome.
Conversion of an origin of replication into a splice site
This may happen in one of two ways, directly or indirectly: The double origin is clipped even more than what occurs to generate a promoter, or a promoter is clipped further, generating a splice site. In either case, the partial fusion of two replicons remains intact.
Whether this dogma has merit or not can only be determined through rigorous scientific investigations that leave absolutely no stones unturned.