title: Developmental stability and signalling among cells.
abstract: The production of stable phenotypes depends from the earliest stages of development upon high levels of somatic cellular selection amongst cells or cell lineages. The signals exchanged amongst cells can reveal important aspects of a cell's phenotype, and might thereby be used in darwinian processes of developmental selection. Based upon an optimality model, we suggest that stable phenotypes require a substantial investment in two mechanisms of inter-cellular selection: "quality-selection" mechanisms regulate the average phenotype of a group of cells; "stability-selection" mechanisms regulate the variance in cell phenotypes. Variance in cell phenotypes may arise from developmental-error or other stochastic processes, or be generated as is true of the immune system, as part of a developmental strategy. The model shows that stability-selection mechanisms may exert the stronger effect on overall organ or body performance. Selection based upon reliable inter-cellular signalling of phenotypic properties may be the key way that bodies anticipate and then constrain variance in cell phenotypes around the optimal cellular attributes, and suggests an advantage of developmentally-selected systems over instructional ones. High levels of investments in stability mechanisms also ensure homogeneous collections of cells that can translate "upwards" into developmentally stable organ systems and phenotypes. Environmental and genetic factors, as well as the prevalent mode of selection, may all affect developmental stability and thereby give rise to varying of somatic selection.
authors.affiliation: Laboratoire d'Ecologie, CNRS URA 258, Université Pierre et Marie Curie, Paris, France.
authors.forename: A P
authors.initials: AP
authors.lastname: Møller
authors.forename: M
authors.initials: M
authors.lastname: Pagel
mesh_terms: D000818:Animals; D005075:Biological Evolution; D002450:Cell Communication / Q000502:physiology*; D002468:Cell Physiological Phenomena; D008954:Models, Biological; D010641:Phenotype; D015398:Signal Transduction