The miracle of gastrulation or how we grow from a mass of cells into a human being.

When humans and other animals are first conceived, they are nothing more than a fertilized egg, which is simply a single cell. This cell begins to divide very rapidly into clones of itself by a process called cleavage. This stage of embryonic development is called blastulation. This one large cell begins to divide so fast that the sizes of the clones become progressively smaller and smaller.

In the case of amphibians, this original cell is divided up into as many as 4,000 smaller cells with no significant change in the original volume of the fertilized egg. This eventually results in a hollow ball of cells which look very similar to more primitive colonies of organisms like the green algae, volvox. This is a classic example of ontogeny recapitulating phylogeny, i.e., the development of the individual is based upon how it’s ancestors evolved over eons of time. Then something very remarkable begins to happen, gastrulation: The cells begin to change into three basic kinds of cells, ectoderm, mesoderm, and endoderm which interact with each other to generate even more kinds of cells in an ever more complex, progressive cascade of events.

Something else happens as well: The origins of replication that were furiously cranking out DNA for these new cells begin to be “silenced”,  resulting in origins that replicate larger pieces of DNA.

Furthermore, as these origins begin to “die off”, gene expression begins to rise dramatically at the same time. So let’s take a moment to sort all of this out:

1) Origins are furiously replicating DNA during the blastula stage at the expense of cell   size. Gene expression is essentially nonexistent.

2)  During gastrulation, origins begin to functionally “disappear”, the remaining ones take over, replicating ever larger pieces of DNA.

3) Gene expression begins to increase rapidly.

Since a replicon is a piece of DNA with an origin associated with it, it appears these replicons are somehow fusing together, resulting in the silencing of one of the two origins.

How all of this happens is the crux of this blog. I will boil it down here in just a few statements:

Origins may be silenced either by fusing with another replicon in a manner similar to lambda phage site-specific recombination, or they may be deleted entirely from the genome as a circular replicon, leaving behind a “scar”.

In the first case, this “fusion” event is only partial, opening up a free end of DNA that can be used in transcription and, therefore, gene expression.

In the second case, the “scar” left behind on the genomic DNA can function as an enhancer of transcription.

In the case of splice sites, the partial fusion of the origin to the remaining replicon may be even more complete, thus converting a potential promoter into a splice site.

How all of this can be explained with a nontraditional, circular DNA model is illustrated throughout this blog.


About frankabernathy

I am a retired cell biologist and alumnus of Ohio State University. I became interested in chromosomes as far back as the 1960's when I wrote a term paper on the effects of radiomimetic drugs on chromosomes. I was fascinated at how they could break apart and reform new structures so easily. I became further involved in the early 1970's after taking a cytogenetics course at the University of Arkansas. I took that knowledge with me to Ohio State in 1980 where I eventually worked on my research and completed my Ph.D. dissertation, "Studies on Eukaryotic DNA Superstructure". My studies and later research suggested that the DNA within the eukaryotic chromosome is not the simple, linear molecular thread so widely suggested in all the classic textbooks published today. Instead, it may be the culmination of a geologically rapid set of endosymbiotic events where microorganisms plug into each other to create something greater than themselves. Feel free to contact me at
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