Focusing on the opposing ways of thinking of philosophers and scientists to explain the generation of form in biological development, I show that today\'s controversies over explanations of early development bear fundamental similarities to the dichotomy of preformation theory versus epigenesis in Greek antiquity. They are related to the acceptance or rejection of the idea of a physical form of what today would be called information for the generating of the embryo as a necessary pre-requisite for specific development and heredity. As a recent example, I scrutinize the dichotomy of genomic causality versus self-organization in 20th and 21st century theories of the generation of form. On the one hand, the generation of patterns and form, as well as the constant outcome in development, are proposed to be causally related to something that is \"preformed\" in the germ cells, the nucleus of germ cells, or the genome. On the other hand, it is proposed that there is no pre-existing form or information, and development is seen as a process where genuinely new characters emerge from formless matter, either by immaterial \"forces of life,\" or by physical-chemical processes of self-organization. I also argue that these different ways of thinking and the research practices associated with them are not equivalent, and maintain that it is impossible to explain the generation of form and constant outcome of development without the assumption of the transmission of pre-existing information in the form of DNA sequences in the genome. Only in this framework of \"preformed\" information can \"epigenesis\" in the form of physical and chemical processes of self-organization play an important role.

The debate about what causes the generation of form and structure in embryological development goes back to antiquity. Most recently, it has focused on the divergent views as to whether the generation of patterns and form in development is a largely self-organized process or is mainly determined by the genome, in particular, complex developmental gene regulatory processes. This paper presents and analyzes pertinent models of pattern formation and form generation in a developing organism in the past and the present, with a special emphasis on Alan Turing\'s 1952 reaction-diffusion model. I first draw attention to the fact that Turing\'s paper remained, at first, without a noticeable impact on the community of biologists because purely physical-chemical models were unable to explain embryological development and often also simple repetitive patterns. I then show that from the year 2000 and onwards, Turing\'s 1952 paper was increasingly cited also by biologists. The model was updated to include gene products and now seemed able to account for the generation of biological patterns, though discrepancies between models and biological reality remained. I then point out Eric Davidson\'s successful theory of early embryogenesis based on gene-regulatory network analysis and its mathematical modeling that not only was able to provide a mechanistic and causal explanation for gene regulatory events controlling developmental cell fate specification but, unlike reaction-diffusion models, also addressed the effects of evolution and organisms\' longstanding developmental and species stability. The paper concludes with an outlook on further developments of the gene regulatory network model.

The ability of developmental systems to produce constant phenotypes, even in a wide range of different environments, and the longstanding stability of species are among the most remarkable phenomena in biology. I argue that understanding the longstanding constancy and stability of species or the constant outcome of development in different environments are also prerequisites for explaining stable change (i.e., change that does not consist of random plasticity). Various approaches to account for stable changes in development are based on the causal role of genes and an organized genome, mathematical-physical-chemical models, or a combination of both. I argue that the constancy of developmental outcome and the longstanding stability of species are associated with organisms\' structural and organizational hierarchies, particularly highly organized gene-regulatory networks and genetic causality, which are fundamental principles of life. Mathematical-physical-chemical models that marginalize these principles cannot convincingly account for the observed constancy in development and evolution. However, an integration of physical-chemical processes such as reaction-diffusion mechanisms and genome-based mechanisms of form generation has recently proved fruitful in explaining the development of some periodic structures. Constancy and change were also major topoi in ancient Greek philosophy, in which prominent philosophical schools such as the atomists attempted to bridge the antinomy between them by basing stable change on constant entities. I argue that the idea of change, that is, change without losing complexity or even increasing it, being based on modifications of the otherwise reliable transmission of genomes over long periods of time has a historical parallel in the writings of these ancient speculative thinkers, notwithstanding the fundamental differences between the two thought systems.

The existence of discrete phenotypic traits suggests that the complex regulatory processes which produce them are functionally modular. These processes are usually represented by networks. Only modular networks can be partitioned into intelligible subcircuits able to evolve relatively independently. Traditionally, functional modularity is approximated by detection of modularity in network structure. However, the correlation between structure and function is loose. Many regulatory networks exhibit modular behaviour without structural modularity. Here we partition an experimentally tractable regulatory network-the gap gene system of dipteran insects-using an alternative approach. We show that this system, although not structurally modular, is composed of dynamical modules driving different aspects of whole-network behaviour. All these subcircuits share the same regulatory structure, but differ in components and sensitivity to regulatory interactions. Some subcircuits are in a state of criticality, while others are not, which explains the observed differential evolvability of the various expression features in the system.

Sea urchin embryos begin zygotic transcription shortly after the egg is fertilized.  Throughout the cleavage stages a series of transcription factors are activated and, along with signaling through a number of pathways, at least 15 different cell types are specified by the beginning of gastrulation.  Experimentally, perturbation of contributing transcription factors, signals and receptors and their molecular consequences enabled the assembly of an extensive gene regulatory network model.  That effort, pioneered and led by Eric Davidson and his laboratory, with many additional insights provided by other laboratories, provided the sea urchin community with a valuable resource.  Here we describe the approaches used to enable the assembly of an advanced gene regulatory network model describing molecular diversification during early development.  We then provide examples to show how a relatively advanced authenticated network can be used as a tool for discovery of how diverse developmental mechanisms are controlled and work.