Morphogenesis seems would be based on interactions between the genome and the "environment" (the multicellular layer) it finds itself in. Cells appear can test its local (bio)mechanical environment for sensing local changes of the layer geometry. After the cell cyto-mechanical sensors receive the signal about completion of appropriate morphogenetic movement, it transduces the "message" into the nucleus. The individual nucleus responds with the appropriate gene cascade for the cell's position. The initial signal is purely mechanical but the response is biochemically sensed, enhanced, and mediated by commonplace cell regulatory mechanisms (Bjorklund and Gordon, 1993). In this way the organism acquires the right cells, in the right place, and at the right time.
A simplest and effective mechanism of local cell respond on completion of appropriate morphogenetic movement consists of differentiation of intercellular contacts. In this case the feedback loop from the surface geometry to morphogen patterns is determined by change of the cell- to-cell conductivity (proportionally to local curvature in that part of the cell layer, wherein the morphogenetic movements have occurred). In our case it is natural to use as the key parameter the coefficient of cell-to-cell communication conductivity, since this is in a close agreement with known data about development of the system of cell-to-cell communications in sea urchin gastrula (Caveney, 1985).
Another way for effective feedback from pattern to form is assumed to be exploitation of the cell feature to sense the curvature of the substratum. According to Dunn and Heath (1976), fibroblasts movements across the substratum is inhibited if the curvature does not allow the cytoskeletal elements to retain linear integrity, because microfilament bundles cannot operate if bent. This hypothesis used by Nogawa (1983) in his curvature-increasing model of epithelial glands morphogenesis. I proceeded from Nogawa works for design of epithelial lobules morphogenesis, outlined below, in section 3.2.
Our concept of pattern-form interplay is closely similar to Cummings (1990; 1994) approach as well as Harrison and Kolar (1988) work. Cummings' pattern-form coupling model gives following "generic" gastrulation simulation. At first, blastula growth occurs as the radius of the middle surface increases in time, as the algorithm cannot be satisfied until a certain radius is attained. At the proper radius, growth slows as the blastula now attains a gradient of morphogen, given by the first Legendre polynomial. The geometrical response to this morphogen is the epithelial sheet deformation, the invagination at the region of lowest morphogen level, forming a "tube within tube". After the morphogenetic movement induced by the morphogen (gastrulation, here) the radius again increases until the morphogen has a second eigensolution, gene switching takes place in the delineated regions, and so on.
Similar self-organizing mechanism for extension of a single-cell marine alga surface by growth and branching of tips has working out by Harrison and Kolar (1988). Reaction-diffusion prepattern (Brusselator system) couples to expressed morphogenesis by catalysis of extension of the cell surface by one of the morphogens. It leads to a change in shape of the region in which the chemical prepattern continues to readjust. This version of chemistry-geometry feedback involves control by the morphogenetic mechanism of its own boundaries. Calculations of cell shape development give rough but still impressive similarities with real marine alga micrographs.
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