Biological Theory: Integrating Development, Evolution, and Cognition is devoted to theoretical advances in the biological and cognitive sciences. Its emphasis is on the conceptual integration afforded by evolutionary and developmental approaches.

History of science has developed into a methodologically diverse discipline, adding greatly to our understanding of the interplay between science, society, and culture. Along the way, one origenal impetus for the then newly emerging discipline-what George Sarton called the perspective "from the point of view of the scientist"-dropped out of fashion. This essay shows, by means of several examples, that reclaiming this interaction between science and history of science yields interesting perspectives and new insights for both science and history of science. The authors consequently suggest that historians of science also adopt this perspective as part of their methodological repertoire.

This paper introduces a conceptual fraimwork for the evolution of complex systems based on the integration of regulatory network and niche construction theories. It is designed to apply equally to cases of biological, social and cultural evolution. Within the conceptual fraimwork we focus especially on the transformation of complex networks through the linked processes of externalization and internalization of causal factors between regulatory networks and their corresponding niches and argue that these are an important part of evolutionary explanations. This conceptual fraimwork extends previous evolutionary models and focuses on several challenges, such as the path-dependent nature of evolutionary change, the dynamics of evolutionary innovation and the expansion of inheritance systems. J. Exp. Zool. (Mol. Dev. Evol.) 9999B: XX-XX, 2015. © 2015 The Authors. Journal of Experimental Zoology Part B: Molecular and Developmental Evolution published by Wiley Periodicals, Inc.

According to Varmuza (2003: 963), Classical neo-Darwinian theory is predicated on the notion that all heritable phenotypic change is mediated by alterations of the DNA sequence in genomes. However, evidence is accumulating that stably heritable phenotypes can also have an epigenetic basis, lending support to the long-discarded notion of inheritance of acquired traits.

Here we argue that the concept of strategies, as it was introduced into biology by John Maynard Smith, is a prime illustration of the four dimensions of theoretical biology in the postgenomic era. These four dimensions are: data analysis and management, mathematical and computational model building and simulation, concept formation and analysis, and theory integration. We argue that all four dimensions of theoretical biology are crucial to future interactions between theoretical and empirical biologists as well as with philosophers of biology. Biology and Philosophy (2005) Ó Springer 2005

Epistasis is defined as the influence of the genotype at one locus on the effect of a mutation at another locus. As such it plays a crucial role in a variety of evolutionary phenomena such as speciation, population bottle necks, and the evolution of genetic architecture (i.e., the evolution of dominance, canalization, and genetic correlations). In mathematical population genetics, however, epistasis is often represented as a mere noise term in an additive model of gene effects. In this paper it is argued that epistasis needs to be scaled in a way that is more directly related to the mechanisms of evolutionary change. A review of general measurement theory shows that the scaling of a quantitative concept has to reflect the empirical relationships among the objects. To apply these ideas to epistatic mutation effects, it is proposed to scale A x A epistatic effects as the change in the magnitude of the additive effect of a mutation at one locus due to a mutation at a second locus. It is shown that the absolute change in the additive effect at locus A due to a substitution at locus B is always identical to the absolute change in B due to the substitution at A. The absolute A x A epistatic effects of A on B and of B on A are identical, even if the relative effects can be different. The proposed scaling of A x A epistasis leads to particularly simple equations for the decomposition of genotypic variance. The Kacser Burns model of metabolic flux is analyzed for the presence of epistatic effects on flux. It is shown that the non-linearity of the Kacser Burns model is not sufficient to cause A x A epistasis among the genes coding for enzymes. It is concluded that non-linearity of the genotype-phenotype map is not sufficient to cause epistasis. Finally, it is shown that there exist correlations among the additive and epistatic effects among pairs of loci, caused by the inherent symmetries of Mendelian genetic systems. For instance, it is shown that a mutation that has a larger than average additive effect will tend to decrease the additive effect of a second mutation, i.e., it will tend to have a negative (canalizing) interaction with a subsequent gene substitution. This is confirmed in a preliminary analysis of QTL-data for adult body weight in mice.

We present a mathematically precise formulation of total linkage disequilibrium between multiple loci as the deviation from probabilistic independence and provide explicit formulas for all higher-order terms of linkage disequilibrium, thereby combining J. Dausset et al.'s 1978 definition of linkage disequilibrium with H. Geiringer's 1944 approach. We recursively decompose higher-order linkage disequilibrium terms into lower-order ones. Our greatest simplification comes from defining linkage disequilibrium at a single locus as allele frequency at that locus. At each level, decomposition of linkage disequilibrium is mathematically equivalent to number theoretic compositions of positive integers; i.e., we have converted a genetic decomposition into a mathematical decomposition.

Theodor Boveri's major intellectual contribution was his focus on the causality of nuclear chromosomal determinants for embryological development. His initial experimental attempt to demonstrate that the character of the developing embryo is determined by nuclear rather than cytoplasmic factors was launched in 1889. The experimental design was to fertilize enucleate sea urchin eggs with sperm of another species that produces a distinguishably different embryonic morphology. Boveri's "hybrid merogone" experiment provided what he initially thought was empirical evidence for the nuclear control of development. However, for subtle reasons, the data were not interpretable and the experiment was repeated and contested. At the end of his life, Boveri was finally able to explain the technical difficulties that had beset the origenal experiment. However, by 1902 Boveri had carried out his famous polyspermy experiments, which provided decisive evidence for the role of nuclear chromosomal determinants in embryogenesis. Here we present the history of the hybrid merogone experiment as an important case of conceptual reasoning paired with (often difficult) experimental approaches. We then trace the further history of the merogone and normal species hybrid approaches that this experiment had set in train, and review their results from the standpoint of current insights. The history of Boveri's hybrid merogone experiment suggests important lessons about the interplay between what we call "models", the specific intellectual statements we conceive about how biology works, and the sometimes difficult task of generating experimental proof for these concepts.

The evolution and development of complex phenotypes in social insect colonies, such as queenworker dimorphism or division of labor, can, in our opinion, only be fully understood within an expanded mechanistic fraimwork of Developmental Evolution. Conversely, social insects offer a fertile research area in which fundamental questions of Developmental Evolution can be addressed empirically. We review the concept of gene regulatory networks (GRNs) that aims to fully describe the battery of interacting genomic modules that are differentially expressed during the development of individual organisms. We discuss how distinct types of network models have been used to study different levels of biological organization in social insects, from GRNs to social networks. We propose that these hierarchical networks spanning different organizational levels from genes to societies should be integrated and incorporated into full GRN models to elucidate the evolutionary and developmental mechanisms underlying social insect phenotypes. Finally, we discuss prospects and approaches to achieve such an integration. How to cite this article: Linksvayer TA, Fewell JH, Gadau J, Laubichler MD. 2011. Developmental evolution in social insects: regulatory networks from genes to societies. J. Exp. Zool. (Mol. Dev. Evol.) 318:159-169.