Eidetic Analysis of the Premature Chromosome Condensation Process

Abstract

An exact transfer of genetic information depends on the accuracy of mechanisms duplicating DNA molecules in the S-phase and the precise division sister chromosomes during mitosis. The regulation systems of these processes (checkpoints) not only control the activation course of the factors imposing different metabolic specificity on each of the cell cycle phases, but first of all – supervising the proper chronology of events – they condition the behavior of the structural and functional genome integrity. Checkpoints receive signals of all abnormalities or structural damages to DNA and in response evoke reactions inhibiting successive transitions through the cell cycle to enable the expression of specific genes and activation of DNA repair factors. One of the easily perceptible effects of disorders in this signaling system is the induction of premature chromosome condensation (PCC). The present chapter is a review of the ways and mode of the induction of PCC. The term ‘PCC’ is inseparably associated with Johnson & Rao (1970) and their experiments on the premature mitosis induced by fusion of interphase and mitotic HeLa cells (G1/M, S/M and G2/M) which were originally carried out using Sendai virus. PCC process can be also induced by chemical signals. Drug-induced PCC provides the new knowledge that DNA replication is tightly coupled with the premature chromosome condensation and that the genome stability results first of all from the alternation of the S-phase and mitosis. The main objective of this review is to show that the PCC induction is possible from various subperiods of cell cycle. Moreover, it has been shown that there are cause-and-effect relationships between the chromosome structure defining ‘PCC phenotype’ and subperiods, e.g. of the S-phase, initiating the biosynthesis of ‘early’ or ‘late’ replicons. Attempts have been made to find answers to questions such as: How to force cells to break out of the rules being developed by Nature for billions of years? How – despite the interrupted, still unterminated process of genome replication – to force a cell to initiate its division? What mechanisms annihilate the subordination principle verified in the course of evolution: first create (DNA-duplicating Sphase) and then divide (mitosis – a stage of DNA condensation and formation of sister