It is well-known that genetic changes are not directly manifested in phenotypic changes. Rather, a complex developmental machinery mediates between genetic information and phenotypic characteristics. It provides a certain robustness by filtering out genetic changes.
Canalization is a term that describes mostly hypothetical developmental mechanisms that reduce phenotypic variation, that is development is canalized against genetic perturbations. Hence canalization ensures sustainability of developmental pathways against perturbations by mutations. In other words, canalization gives "luft" for variability of intrinsic heritable characters without interruption of developmental trajectory. Such degree of freedom allows the organism to accumulate appropriate mutations without interruption of the development. When the volume of heritable changes achieving critical threshold, this can force out the development to a new higher-level trajectory.
Self-Regulation: It is known that gradients of morphogenetically active factors are used widely by organisms to co-ordinate the initial events of embryogenesis. In the modern developmental biology the system of reading of primary gradients is called primary morphogenetic field. It is apparent that the gradient contains positional information in an analogue form. Analogue information is less stable and hence more error-prone. If position needs to be specified more stable, it is important to convert the initial analogue positional information into a digital form. This conversion appears to be mediated by the genes from segmentation network.
However the problem remains regardless of the capabilities of the reading device used to discriminate concentration difference. Really, the stochastic nature of molecular motion is non-eliminated source of errors.
The key point here is that self-regulating mechanisms can be introduced at any of the early hierarchical levels to correct errors carried over from previous levels. The implication is that control systems dynamically structured to minimize error may be quite complex (Lacalli & Harrison, 1991). Known gene-gene interactions in limits of the segmentation net include cross-inhibition and autoregulation loops. These are sufficient to sharpen the concentration peaks, turning their graded slopes into step functions. Turing-like reaction-diffusion mechanisms are important in this respect because, though they respond to the cues provided by existing prepatterns, the new pattern they impose over these has its own intrinsic wavelength, independent of previous errors.
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