Robustness of embryonic spatial patterning in Drosophila melanogaster.

Publisher Summary Mathematical models of embryonic development can provide insights into the complex interactions between spatial variations in morphogens, signal transduction, and intracellular response in patterning processes. Mechanistic models of specific processes based on our current understanding of them provide an additional tool to help in understanding the complex regulation of development. The chapter discusses a number of different aspects of robustness in Drosophila embryonic patterning, and have shown how the models lead to new insights concerning scale-invariance in AP patterning, the role of network topology and signature in the switching network used for control of the segment polarity genes, and the role of signaling via heterodimers in dorsal–ventral (DV) patterning. The modular decomposition of DV patterning described in the chapter is based on the current understanding of the kinetic interactions between morphogens and inhibitors in the perivitelline (PV) space, and incorporates the various dimeric forms of inhibitors and signaling the bone morphogenetic proteins (BMPs). Scale-invariance is a basic feature of a number of developmental processes. A rather surprising result is that the robustness of DV spatial patterning can essentially be predicted from an analysis of the local dynamics. The analysis of the spatially distributed system corroborates the earlier results and provides further evidence for the selective advantage of using heterodimers for signal transduction and morphogenesis.