How biological form is generated remains one of the most fascinating but elusive challenges for science. Moreover, it is widely documented in contemporary literature that development is tightly coordinated. The idea that such development is governed by a coordinating field of force, the morphogenetic field, and its position in embryology research paradigms, is traced in this article. Empirical evidences for field phenomena are described, ranging from bioelectromagnetic effects, morphology, transplantation, regeneration, and other data. Applications of medical potential including treatment of (...) cancer, birth defects, and wound healing are highlighted. The article hypothesizes that distinct morphological forms may have distinct field parameters. Experimentally tractable field parameters may thus provide an exciting research program for probing morphogenesis and phylogenetic diversity. (shrink)

In describing the flawless regularity of developmental processes and the correlation between changes at certain genetic loci and changes in morphology, biologists frequently employ two metaphors: that genes ‘control’ development, and that genomes embody ‘programs’ for development. Although these metaphors have an admirable sharpness and punch, they lead, when taken literally, to highly distorted pictures of developmental processes. A more balanced, and useful, view of the role of genes in development is that they act as suppliers of the material needs (...) of development and, in some instances, as context‐dependent catalysts of cellular changes, rather than as ‘controllers’ of developmental progress and direction. The consequences of adopting this alternative view of development are discussed. (shrink)

We argue that the physics of complex materials and self-organizing processes should be made central to the biology of form. Rather than being encoded in genes, form emerges when cells and certain of their molecules mobilize physical forces, effects, and processes in a multicellular context. What is inherited from one generation to the next are not genetic programs for constructing organisms, but generative mechanisms of morphogenesis and pattern formation and the initial and boundary conditions for reproducing the specific traits of (...) a taxon. There is no inherent antagonism between this “physicalist” perspective and genetics, since physics acts on matter, and gene products are essential material components of living systems whose variability affects the systems’ parameters. We make this notion concrete by summarizing the concept of “dynamical patterning modules” (DPMs; Newman and Bhat, Phys Biol 5:1–14, 2008; Int J Dev Biol 53:693–705, 2009), an explicit physico-genetic framework for the origin and evolution of multicellular form in animals, as well as (when differences in interaction toolkit genes and applicable physical processes are taken into account) in multicellular plants (Hernández-Hernández et al., Int J Dev Biol 56:661–674, 2012). DPMs provide the missing link between development and evolution by revealing how genes acting in concert with physics can generate and transform morphology in a heritable fashion. (shrink)

The “DNA is a program” metaphor is still widely used in Molecular Biology and its popularization. There are good historical reasons for the use of such a metaphor or theoretical model. Yet we argue that both the metaphor and the model are essentially inadequate also from the point of view of Physics and Computer Science. Relevant work has already been done, in Biology, criticizing the programming paradigm. We will refer to empirical evidence and theoretical writings in Biology, although our arguments (...) will be mostly based on a comparison with the use of differential methods (in Molecular Biology: a mutation or alike is observed or induced and its phenotypic consequences are observed) as applied in Computer Science and in Physics, where this fundamental tool for empirical investigation originated and acquired a well-justified status. In particular, as we will argue, the programming paradigm is not theoretically sound as a causal(as in Physics) or deductive(as in Programming) framework for relating the genome to the phenotype, in contrast to the physicalist and computational grounds that this paradigm claims to propose. (shrink)

In this paper, I discuss the neo-Aristotelian approaches, which usually reinterpret Aristotle’s ideas on form and/or borrow the notion of formal cause without engaging with the broader implications of Aristotle’s metaphysics. In opposition to these approaches, I claim that biosemiotics can propose an alternative view on life’s form. Specifically, I examine the proposals to replace the formal cause with gene-centrism, functionalism, and structuralism. After critically addressing these approaches, I discuss the problems of reconciling Aristotelianism with the modern view of life’s (...) organization. I claim that the notion of the final cause proposes a cosmological hierarchy and that this is the main problem with applying the formal cause to biology. An alternative categorization of conceptualizing life’s form involves the processual identity, relational property clusters, and context-dependent transmission of representational units. The third category points to a semiotic basis of the form of life. In this context, I offer to readjust the focus of the problem of matter-form duality by pointing out that form is primarily an issue of the subject-object relation. Biosemiotics helps to understand the constructive role of symbolic representation in living systems, which is crucial to extend the analysis of the form from cognitive representations to external phenomena. Emergence of subjectivity and perspectivity of interactions are key elements to bridge the form and actual processes within a non-hylomorphic account. To demonstrate transitions from the physical influence of shapes to the organic recognition of forms, I address the biological studies on the synchronization of coincidental inputs and enzyme specificity. (shrink)

The logic of genetic discovery has changed little over time, but the focus of biology is shifting from simple genotype–phenotype relationships to complex metabolic, physiological, developmental, and behavioral traits. In light of this, the traditional reductionist view of individual genes as privileged difference‐making causes of phenotypes is re‐examined. The scope and nature of genetic effects in complex regulatory systems, in which dynamics are driven by regulatory feedback and hierarchical interactions across levels of organization are considered. This review argues that it (...) is appropriate to treat genes as specific actual difference‐makers for the molecular regulation of gene expression. However, they are often neither stable, proportional, nor specific as causes of the overall dynamic behavior of regulatory networks. Dynamical models, properly formulated and validated, provide the tools to probe cause‐and‐effect relationships in complex biological systems, allowing to go beyond the limitations of genetic reductionism to gain an integrative understanding of the causal processes underlying complex phenotypes. (shrink)

This article is concerned with the problem of the relation between the genetic information contained in the DNA and the emergence of visible structure in multicellular animals. The answer is sought in a reappraisal of the data of experimental embryology, considering molecular, cellular and organismal aspects. The presence of specific molecules only confers a tissue identity on the cells when their concentration exceeds the threshold of differentiation. When this condition is not fulfilled the activity of the genes that code for (...) the specific molecules in question only confers on them a histogenetic potency, i.e. the capacity to form the corresponding tissue in further development (or to transdifferentiate to that tissue). The progressive restriction of histogenetic potencies during development reflects the irreversible repression of more and more genes. The establishment of a given tissue identity under the influence of an inducing tissue (or a morphogenetic hormone) is only possible when the cells have acquired the competence to respond. Tissue differentiation proceeds progressively during development thanks to the cytoplasmic memory that cells retain collectively (or sometimes individually) of the items of information successively registered by their ancestors cells. The increasing complexity of visible structure emerging during development results only from the progression of tissue differentiation. This involves continual exchange of information among the cells and leads to (1) cell displacements and rearrangements, particularly during organogenesis and (2) extreme diversification of cell individualities within tissues, particularly during postembryonic growth. A mutation (just as a teratogenic factor) evokes an anomaly that is localized in both space and time because it alters a certain aspect of cell behaviour (particularly cell surface adhesiveness or mitotic activity) at the time when this is involved in the establishment of a particular structural trait. Neither the organization of the adult nor the modalities of development are encoded in the DNA. The automatic concatenation of cell interactions in the embryo and the structural amplification it entails is conditioned by the specific biochemical composition of the cytoplasm of the egg and by the heterogeneous distribution of its inclusions. (shrink)

The convergence of morphogenesis into viable organisms under variable conditions suggests closed‐loop dynamics involving multiscale functional feedback. We develop the idea that morphogenesis is based on synergy between mechanical and bio‐signaling processes, spanning all levels of organization: molecular, cellular, tissue, up to the whole organism. This synergy provides feedback within and between all levels of organization, to close the loop between the dynamics of the morphogenesis process and its robust functional outcome. Hydra offer a powerful platform to explore this direction, (...) thanks to their simple body plan, extraordinary regeneration capabilities, and the accessibility and flexibility of their tissues. Our recent experiments show that structural inheritance of the actomyosin organization directs body‐axis formation during Hydra regeneration. Morphogenesis is then stabilized through dynamic cytoskeletal reorganization induced by the inherited structure. The observed cytoskeletal stability and reorganization capabilities suggest that mechanical feedback integrates with biochemical processes to establish viable patterns and ensure canalization. (shrink)