Molecular mechanisms of the origin of chromosome aberrations and the structural organisation of eukaryotic DNA.

A new hypothesis on the appearance of exchange chromosomal aberrations has been suggested. According to this hypothesis, temporal duplex polynucleotide structure should arise during G1 and G2 phases during the correction of DNA. The size of the duplex, as a rule, should be restricted to the size of complementary nucleotide sequences in the regions of repetitions. Any polynucleotide break in a duplex zone would result in chromosome breakage and if complementary broken ends interact with each other, then exchange chromosome aberrations may be formed. This hypothesis would explain such previously obscure phenomena as extremely high frequencies of exchanges after mutagen treatment, the nature of mitotic crossing-over, negative interference, change of aberration types before replication, the low frequency of damaged structural genes during aberration formation, etc.