CDC2-KINASES, CYCLINS, AND THE SWITCH FROM PROLIFERATION TO POLYPLOIDIZATION [Review]

摘要

Almost all organisms, from protists to humans, and from algae to orchids, display somatic polyploidy, including polyteny. In insects and higher plants, nearly all normal, differentiated cells are polyploid, corresponding to the majority of living matter. So far, no universal mechanism controlling the switch from proliferation to polyploidization has been proposed. However, recent progress in understanding regulation of the mitotic cell cycle by protein kinases and cyclins allows some unifying ideas which can be experimentally tested to be put forward. The key events are the abolishment of the dependence of DNA replication on mitosis, and changes in the expression and activity of the complexes formed by cyclin-dependent kinases and cyclins. In addition, repression of further cell cycle control genes may allow underreplication of DNA, characteristic of endo-cycles in many insects and angiosperms. Change to a different checkpoint may be responsible for gene amplification. The switch in cell cycle control is developmentally regulated by signal transduction cascades, which are briefly discussed. Polyploidy is also known from many cancers, where genetic and metabolic disturbances lead to a similar switch to that in normal cells. The related literature is reviewed and some possible lines of future research are suggested. [References: 92]