Abstract
The results of extensive in vitro studies of DNA–lipid complexes allowed us to propose a model for the structure of such complexes and their involvement in the formation of DNA–membrane complexes (DMC). DMC seem to form the basis for such cellular structures as Bayer's junctions and nucleoid of bacteria, the nuclear pores, annulate lamellae and nucleoid of eucaryotes. The role of DMC in gene expression is discussed. Numerical density of mitochondria during cell aging correlates with the density of bacteria in batch culture. It is concluded that aging is caused by the unlimited growth of mitochondria and their subsequent degradation. The role of DMC in mitochondrial DNA damage at aging is discussed. The way of increasing the life span by controlling the density of mitochondria in a cell volume is likewise discussed. DMC formed between any two intracellular membranes can serve the basis for the membrane continuum in a cell.
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