PubMed · 14147456
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R L DEHAAN, J D EBERT. 1964. MORPHOGENESIS.. https://doi.org/10.1146/annurev.ph.26.030164.000311
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Cannibalistic polyphenism is observed in many fishes and amphibians. In the case of amphibian larvae, cannibal morph and typical morph coexist. Benefits and costs of the cannibal morph have been studied empirically but the mechanism of the maintenance of polymorphism is not well known. Here, we construct a game model of typical and cannibal morph strategies to obtain the condition of stable coexistence. Generally, once an individual succeeds in cannibalism, it grows very quickly, which facilitates the next cannibalism. In a model without this 'drastic growth effect', stable coexistence cannot occur. To represent drastic growth effect, it is assumed that cannibal/typical morph stage is followed by giant/normal stage. A cannibal morph that performs cannibalism in the first stage can become a 'giant' in the next stage. This model allows stable coexistence of cannibal and typical morphs. The condition for coexistence is that payoff of a giant is two times larger than normal individuals. As long as direct consumption of victim's body is considered as reward for successful cannibalism, coexistence cannot be explained. When the reward is considered as social standing of being outstanding size in a population, sympatric cannibalistic polymorphism is possible, without regard to the initial size variation or resource shortage.
Larval and adult urodeles and anuran tadpoles readily regenerate their limbs via a process of histolysis and dedifferentiation of mature cells local to the amputation surface that accumulate under the wound epithelium as a blastema of stem cells. These stem cells require growth and trophic factors from the apical epidermal cap (AEC) and the nerves that re-innervate the blastema for their survival and proliferation. Members of the fibroblast growth factor (FGF) family synthesized by both AEC and nerves, and glial growth factor, substance P, and transferrin of nerves are suspected survival and proliferation factors. Stem cells derived from fibroblasts and muscle cells can transdifferentiate into other cell types during regeneration. The regeneration blastema is a self-organizing system based on positional information inherited from parent limb cells. Retinoids, which act through nuclear receptors, have been used in conjunction with assays for cell adhesivity to show that positional identity of blastema cells is encoded in the cell surface. These molecules are involved in the cell-cell signaling network that re-establishes the original structural pattern of the limb. Other systems of interest that regenerate by histolysis and dedifferentiation of pigmented epithelial cells are the neural retina and lens. Members of the FGF family are also important to the regeneration of these structures. The mechanism of amphibian regeneration by dedifferentiation is of importance to the development of a regenerative medicine, since understanding this mechanism may offer insights into how we might chemically induce the regeneration of mammalian tissues.
Fifty years after Briggs and King first succeeded in obtaining normal tadpoles from transplanted embryo nuclei in vertebrates, two general principles have emerged from work in amphibia and mammals. One is the conservation of the genome during cell differentiation. A small percentage of adult or differentiated cells have totipotent nuclei, and a much higher percentage of cells committed to one pathway of cell differentiation have multipotent nuclei. The other is the remarkable reprogramming capacity of cell, and especially egg, cytoplasm. The eventual identification of reprogramming molecules and mechanisms could facilitate a route toward cell replacement therapy in humans.