Hyperchirality: a mathematically convenient and biochemically possible model for the kinetics of morphogenesis
Two general problems in morphogenesis are discussed: (a) scaling of the repeating unit of a pattern to the overall size of the organism; (b) biochemically realistic mechanisms for highly localized autocatalysis to produce pattern on a wall or membrane of a single cell. These problems are approached by comparing the Mills (1932) model for spontaneous resolution by bimolecular autocatalysis in formation of a pair of enantiomers (D and L) with the Turing (1952) model for morphogenesis by catalytic and inhibitory interactions of two morphogens (X and Y) very unsymmetrically matched in kinetic properties. A model for a morphogen M is proposed in the form of a pair of enantiomers M D and M L , with the out-of-equilibrium morphogen concentration variable in the Turing equations being the optical asymmetry M = M D — M L . Formation of M out of a precursor (pro-morphogen A), with two reactions A → M D and A → M L to control the single variable M , allows the Turing theory to encompass a variety of ways in which pattern unit scales with overall size. To this end, formation of morphogens by parallel reactions exceeding in number the morphogen concentration variables is a general principle independent of the reality of this specific model. More tentatively, the model is put forward as a possible real structure for morphogens on a cell wall or membrane. Both M D and M L must be present. It is suggested that the lowest level of organization at which structures of two chiralities might be found, when their molecules are of one chirality only, is the attachment of an enzyme polymer, with definite quaternary structure, to the cell surface. The enantiomers may then be the same polymeric assembly facing inwards or outwards. The word hyperchirality is suggested for this kind of asymmetry. Some morphogenetic features of the single-celled desmid alga Micrasterias are discussed, to illustrate the geometrical problems of translating morphogen kinetics into development of shape, and to show that the number of active morphogens and the dimensionality of the space in which they act may decrease during development.