An evolutionary theory of clonal senescence (Q1897487)

Senescence is a standard feature in life histories of unitary animals with a well-defined distinction between germ and somatic cell lineages. However, it is still an open question to what extent senescence occurs among unicellular organisms and clonal and modular plants and animals that lack this separation of cell functions. Indeed, it has been argued that asexual production of rejuvenated offspring should preclude senescence in clonal organisms despite the death and decay of constituent organs and ramets. This notion is supported by the great age recorded for clones of some perennial plants and benthic invertebrates such as sponges and corals. Also there are several reports where no sign of clonal senescence was found in asexual populations cultured under laboratory conditions over tens or hundreds of generations. On the other hand, it is clear that asexual reproduction is not by itself sufficient for escaping senescene as there are also many reports of the deterioration of whole clones of plants, animals, and fungi as well as asexually derived colonies of unicellular organisms. The aim of this study is to follow the approach used by \textit{W. D. Hamilton} [J. Theor. Biol. 12, 12-45 (1966)] and formulate an evolutionary theory of senescence of clones. The clone is modeled as a group of independent lower-level reproductive units, here called ramets, and the Malthusian parameter or the intrinsic rate of increase is assumed to measure clonal level fitness. It is shown that the sensitivity of fitness with respect to changes in the life history parameters of ramets decreases towards zero with increasing age of the clone. Clonal senescence may therefore evolve through mechanisms at the clonal level.