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From Biological Determination to Entangled Causation

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Abstract

Biologists and philosophers often use the language of determination in order to describe the nature of developmental phenomena. Accounts in terms of determination have often been reductionist. One common idea is that DNA is supposed to play a special explanatory role in developmental explanations, namely, that DNA is a developmental determinant. In this article we try to make sense of determination claims in developmental biology. Adopting a manipulationist approach, we shall first argue that the notion of developmental determinant is causal. We suggest that two different theses concerning developmental determination can be articulated: determination of occurrence and structural determination. We shall argue that, while the first thesis is problematic, the second, opportunely qualified, is feasible. Finally, we shall argue that an analysis of biological causation in terms of determination cannot account for entangled dynamics. Characterising causal entanglement as a particular kind of interactive causation whereby difference-making causes ascribable to different levels of biological organisation influence a particular ontogenetic outcome, we shall, via two illustrative examples, diagnose some potential limits of a reductionist, molecular and intra-level understanding of biological causation.

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Notes

  1. We prefer the expression “phenotypic outcome” to “gene product” because the latter betrays a DNA-centric causal bias.

  2. Here the point is simply that synchronic constitutive analysis accounts for the difference in spatial organisation of the two biosystems independently of the nature of the relationship between its constituent entities. This is sufficient to vindicate a principled constitution-causality distinction. At the same time, the direction of the arrow implies causation and a relationship of diachronic ‘influencing’ between the entities. It is for this reason that constitutive analysis is intrinsically limited when dealing with biological processes.

  3. Halder et al.’s (1995) genetic experiments with Drosophila in which the expression of gene Ey is argued to be “necessary and sufficient to induce ectopic eyes” (Halder et al. 1995, p. 1791) even in wings and antennae seems to contravene our argument. However, note that the claim that Ey determines eye morphogenesis should be qualified. First of all, this gene is not the only one regulating this morphogenetic process because “…we estimate that more than 2500 genes are involved in eye morphogenesis” (Halder et al. 1995, p. 1791). Nonetheless, some interesting determination claims remain compatible with the evidence, namely that either Ey causes one or a series of switch points or even that the entire developmental trajectory is entirely regulated by genomic resources (i.e., that all its switch-points are caused by genomic inputs, e.g. Ey and thousands of other genes). This latter hypothesis is a form of genetic determinism because an adult phenotype would be fully determined by genomic inputs. At the end of this section we show that even such hypotheses are suspicious.

  4. This applies to the Ey case as well (see note 3). Gene expression processes do not happen in a vacuum but in a developmental context that is rich in extra-genomic developmental resources such as molecular agents and environmental inputs. To emphasise Ey’s and the 2.500 other genes’s causal contribution to the process of eye morphogenesis in Drosophila is to dismiss as causally irrelevant these extra-genomic resources of the developmental context.

  5. The concept of determination of occurrence seen in Sect. 4 (i.e., that a developmental factor is a necessary and sufficient condition for the occurrence of a specific developmental outcome at a specific switch point) and the concept of structural determination (i.e., that a developmental factor is a highly specific cause that fully accounts for the structural features of a developmental outcome) to be articulated in this section are different. The reason is that a difference-making cause could be a structural determinant without being an occurrence determinant.

  6. It should be added that these naturally produced molecular conformations should not be caused by DNA differences. For instance, they might be phenotypic mutations (Bürger et al. 2006).

  7. Evolutionary studies concerning the nature of extant bacterial polymerases might indeed substantiate this argument if natural “manipulations” were discovered. We thank Staffan Müller–Wille for this suggestion.

  8. It should be noted that Noble himself speaks explicitly of downward causation (2006).

  9. It should also be noted that Lesne and Victor (2006) indifferently use expressions like “emergent property”, “regulation” and “constraint”. Whether the notion of constraint used by Lesne and Victor bears a close relationship with that articulated by Umerez and Mossio (2013) is beyond the scope of the paper.

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Acknowledgements

D.V. acknowledges the financial support of the Fundação para a Ciência e a Tecnologia (FCT Grant No. SFRH/BPD/99879/2014, BIODECON R&D Project. Grant PTDC/IVC-HFC/1817/2014) and of the Fondo Nacional de Desarrollo Científico y Tecnológico de Chile (Grant No. 1171017 FONDECYT REGULAR). We thank Lorenzo Baravalle, Maurizio Esposito, Gil Santos and the reviewers for feedback.

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Authors and Affiliations

  1. Centro de Filosofia das Ciências, Departamento de História e Filosofia das Ciências, Faculdade de Ciências, Universidade de Lisboa, 1749-016, Lisbon, Portugal

    Davide Vecchi

  2. Departamento de Filosofía, Facultad de Humanidades, Universidad de Santiago de Chile, Avenida Libertador Bernardo O’Higgins #3677, Santiago, Chile

    Davide Vecchi

  3. Laboratoire ERRAPHIS, PhSciVi, Université Toulouse Jean Jaurès, Maison de la Recherche 5 allée Antonio-Machado, 31058, Toulouse Cedex 9, France

    Paul-Antoine Miquel & Isaac Hernández

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  1. Davide Vecchi
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Correspondence to Davide Vecchi.

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Vecchi, D., Miquel, PA. & Hernández, I. From Biological Determination to Entangled Causation. Acta Biotheor 67, 19–46 (2019). https://doi.org/10.1007/s10441-018-9339-6

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