title: [Redusome aging: commentaries].
abstract: The redusome hypothesis of aging and biological age control (Olovnikov, Biochemistry (Moscow) 2003, vol. 68, pp. 2-33; http://protein.bio.msu.su/biokhimiya/contents/v68/ToC6801.htm.) is discussed. Though the main part of telomere-related predictions (Olovnikov, 1971, 1973) have successfully been confirmed (end under-replication of linear DNA molecules; explanation why bacterial genome is circled to avoid this problem; telomerase existence in sex and cancer cells; correlation of telomera shortening with the number of cell doublings already performed by somatic cells that divide and age in vitro), I state that telomere model of cell aging should be abandoned, since a telomere-dependent signal of cellular senescence does not exist. Instead, it is postulated that so called redusomes are involved in control of biological time and aging. Redusomes are postulated nuclear organelles which are presented by small linear double helix DNA molecules of different specificities which are covered by proteins and located at special chromosomal nests. Each redusome has its own ori for replication, as well as promoter for transcription, but it has no centromere. Hence redusomes are distributing in mitoses among daughter cells only due to the behavior of chromosomes as their specific carriers. Transcripts from redusomes (both micro RNAs and so called fountain RNAs) participate in chromatin remodeling and chromosomal structural genes expression. Regular and consecutive losses of repeated genes from chronomeres (DNA of redusomes of neuroendoclinal and neurotrophic cells of a brain) are perceived by cells of brain's biochronometer as a course of biological time. Continuation of shortening of redusomal DNA molecules in the organism that has already achieved its physiological maturity is responsible both for cellular senescence and the organism aging. Telomere attrition is only a bystander process of aging, while the genuine cause of the cell and organism aging is the redusome DNA shortening.
authors.affiliation: Institute of Biochemical Physics of RAS, ul. Chernyakhovskogo, 5-94, Moscow, 125319, Russia. olovnikov@dol.ru
authors.forename: A M
authors.initials: AM
authors.lastname: Olovnikov
mesh_terms: D000375:Aging / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D001683:Biological Clocks; D016922:Cellular Senescence / Q000502:physiology*; D002875:Chromosomes / Q000378:metabolism*; D006801:Humans; D015388:Organelles / Q000378:metabolism*; D016615:Telomere / Q000378:metabolism