The hormones--a model for a new understanding of cell differentiation process. Part II. Why does mitosis avoid those...

This new replicative model here explained is the result of the fact that, even if replication and transcription are distinct events during the cell evolution, they are functionally correlated, being responsible both for the main features of the cell, and for hormones affinity, too. This model of replication suggests the spreading of replication, in both directions symmetrically from the origin site of each replicon, as well as a simultaneous replication of both DNA strands, despite the fact that one of them was until now called "lagging" strand. These two events are explained by initiation of each DNA catena with distinct RNA polymerase forms depending on the presence or absence of the sigma 70 recognition factor (or its beta gamma analogous eukaryotic factor). The arguments sustaining these events were gathered from many already known genetic studies, some of them being here supposed to new interpretations (for instance, the phi x 174, M13 phages replication models). The disposition of both DNA strands during replication allows the intervening of both RNA polymerase types only in RNA primer synthesis. However, other physical restrictive interactions suggested theoretically prevent the going on of RNA polymerases activity like they do during transcription. This is the main reason that determines the exposure of DNA conformational changes occurring in the replication. These explanations may bring a possible new light about the "mystery" of the phenomenon producing the "replicative eye" inside the double helical structure of DNA.