Abstract
Cell proliferation depends on the fission (or budding) of cells that have duplicated all of their constituents and divided them more or less equally between daughter cells. Most constituents are synthesised continuously throughout the cell cycle and their segregation does not require great care either because they are sufficiently numerous or because they can be synthesised de novo using directions supplied by the genome. Chromosomes and possibly also microtubule organizing centres are exceptions to this rule. Each gene within the genome must be replicated using itself as a template once and only once per cycle and each sister chromatid must be segregated away from each other to opposite poles of the cell.1 Because most of the instructions for building a cell reside within chromosomes, their duplication and segregation must occur with a fidelity which far exceeds that of other biosynthetic processes. Nuclear division must be avoided when sister chromatids have not properly aligned on the mitotic spindle, when one chromatid has been damaged and needs repairing using its undamaged sister, or when DNA replication has not yet been completed. Cells therefore possess surveillance mechanisms2 that detect these sorts of accidents and induce inhibitors of chromosome alignment on the mitotic spindle (metaphase) and/or disjunction of sister chromatids (anaphase).
A related article on this subject was published in Trends in Genetics in October 1996.
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Nasmyth, K. (1997). A Eukaryotic Cell Cycle. In: Mihich, E., Hartwell, L. (eds) Genomic Instability and Immortality in Cancer. Pezcoller Foundation Symposia, vol 8. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5365-6_11
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