DHEA, DNA, Multicellularity and Tissue Formation, Form and Segmentation

 

Copyright 2005, James Michael Howard, Fayetteville, Arkansas, U.S.A.

 

It is my hypothesis that dehydroepiandrosterone (DHEA) was selected by evolution because DHEA optimizes replication and transcription of DNA.  Evolutionary phenomena regarding multicellularity and tissue formation may be derived from my primary hypothesis.

 

The ratio of DHEA to DNA may be involved in the ratio of DNA replication and transcription.  That is, when DHEA levels are sufficiently high, replication may predominate.  When DHEA levels are reduced, transcription should increase.  This is based on use of DHEA for “opening” of the DNA strand.  When a lot of DHEA is available, larger amounts of DNA may be separated and increase the probability of replication.  Hence, the ratio of replication and transcription of DNA relies on availability of DHEA.

 

In simple multicellular systems, the ratio of DHEA to DNA would be greater than that of complex multicellular systems.  As complexity increases with time, replication declines, followed by increased transcription as an organism grows.  Therefore, early growth is rapid followed by slowed growth.  This difference between simple organisms and complex organisms may explain tissue formation.

 

As an organism increases in growth, distribution of DHEA is controlled by absorption inherent in the form of the organism.  When DHEA is high, the genes of the organism organize the basic form.  As the form increases in size, further differences in distribution of DHEA are exerted.  This differential distribution of DHEA reduces overall availability of DHEA.  The ratio of DNA replication declines and transcription increases.  This differential distribution of DHEA exerts differential transcription of genes according to the form of the organism.  That is, with increases in the form of the organism, DHEA availability and cellular absorption of DHEA trigger differential transcription according to the basic plan of the form of the organism.  This is tissue formation.  Some tissues will acquire DHEA more rapidly than other tissues.  For example, I suggest the large brains of mammals represent this form of tissue competition (“Hormones in Mammalian Evolution,” Rivista di Biologia / Biology Forum 2001; 94: 177-184).

 

The foregoing explanation should also hold for competition for DHEA within tissues themselves.  That is, some cells within tissues should acquire DHEA at the expense of other cells within tissues.  I suggest this is the basis of growth and development of the organism as well as tissues, themselves.  This may explain the findings of Bengtsson, et al., (Genome Research 15:1388-1392, 2005) that gene activity of similar cells within tissues is not identical, in fact may be quiet different.

 

Segmentation is an evolutionary process we inherited from earlier animals.  The expression of segmentation is reduced with evolution.  I suggest the differences in expression of the genes controlling this process throughout evolution may be also be explained by the foregoing.  That is, as tissues were selected by evolution, they acquired DHEA at the expense of other tissues.  Hence, appendages, for example, disappear as less DHEA is available for their formation.  Segmentation is less pronounced during ongoing evolution because the hallmark characteristics of segmentation are not expressed as a result of competition for DHEA by other tissues.