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The Origins of Theoretical Developmental Genetics: Reinterpreting William Bateson’s Role in the History of Evolutionary Thought

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Natural Selection

Abstract

By considering the traditional history of evolutionary thought, William Bateson has been portrayed as an irrational anti-Darwinist who found in Mendel’s laws the basis of heredity that supported his belief in saltational evolution; in so doing, he delayed the modern synthesis. However, this chapter suggests a very different interpretation. Bateson was one of the first geneticists whose ideas are closely associated with current developmental biology. I demonstrate that Bateson’s studies were focused on how morphological structures arise and are maintained and not just the research of hereditary transmission of characters. From this framework, he attempted to understand how complex structures can emerge from transmission elements (which we know today as genes) during their ontogeny. In other words, he was one of the first scientists who conceived what we know today as the action of genes in controlling development. This view allowed him to criticize the model of gradual evolution, challenging natural selection as a creative force.

Selection is a true phenomenon; but its function is to select, not to create.

—William Bateson (1904)

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Notes

  1. 1.

    For Mayr, typological thinking traced back to Platonic eidos whose fallout swayed Linnaeus’ notion of the fixity of species, and it was established in its evolutionary version with the saltational evolution. In contrast, population thinking, which is related to Darwinism, emphasizes that the unit of evolution is the population and not the individual. However, this dichotomy between “typological thinking and population thinking” is nothing more than a rhetorical resource that Mayr used to justify his participation in the development of the modern synthesis (see Winsor 2003; Chung 2003; Amundson 2005; Witteveen 2015, 2016; Ochoa 2017).

  2. 2.

    Peterson and Müller (2016) argue that many morphological novelties cannot solely be explained by small continuous variations but also by discontinuous variations: “microevolutionary events are insufficient for explaining discontinuous forms of change and phenotypic novelties. The idea that small, continuous, incremental variational change is the sole cause of phenotypic evolution continues to be challenged by qualitatively discontinuous changes that also need to be accounted for by evolutionary theory” (pp. 328–329).

  3. 3.

    We may associate meristic variation with heterometry; some cases of substantive variation would correspond to heterochrony; and homeotic variation with either heterotopy or heterotypy. Currently, Diogo et al. (2017) claim that some developmental anomalies such as loss and addition (meristic variation), proportion (substantive variation), and identity transformation (homeotic variation) of elements play a fairly important role in evolution.

  4. 4.

    Regarding the model of developmental constraints, Pere Alberch (1982) argues that embryologic interactions drastically constrain evolutionary change by producing a discontinuous and directional distribution of forms. Under this model, some forms are impossible (intermediate) and others are likely to appear (discontinuous).

  5. 5.

    Once he became a Mendelian, he adopted the term and included the notion of the transmission of characters by parents to offspring in his explanatory domain; however, he advises careful use of the terms: “the terms ‘Heredity’ and ‘Inheritance’ are founded on a misapplication of metaphor, and in the light of our present knowledge it is becoming clearer that the ideas of ‘transmission’ of a character by parent to offspring, or of there being any ‘contribution’ made by an ancestor to its posterity, must only be admitted under the strictest reserve, and merely as descriptive terms” (Bateson 1902, p. 26).

  6. 6.

    Recent studies have highlighted the importance of defining homology regarding the biological causes that originate and preserve those morphological units that we call homologues (e.g., Müller 2003; Brigandt 2007; Wagner 2007, 2014; Kuratani 2009; Ochoa and Rasskin-Gutman 2015).

  7. 7.

    Müller (2003) stresses that the study of homology in morphology (biological homology concept) focuses on the underlying biological mechanisms rather than on the genealogical terms used by systematists (historical homology concept).

  8. 8.

    Mendel’s laws were not assigned by early Mendelians; rather, they only referred to a single law—namely, the principle of segregation (see Marks 2008).

  9. 9.

    As we will discuss below, Bateson originally thought that the principle of segregation as a modification to the law of ancestral heredity applied to some cases of prepotency, but in later publications, he argued that the principle of segregation comprises all situations.

  10. 10.

    This assumption refutes the traditional narrative account that Bateson had not realized that Mendel’s principles could also be applied to continuity. In fact, Bateson thought that many continuous characters fell within the domain of the principle of segregation and the “blending” characters were due to processes that may also be explained by this scheme; see below.

  11. 11.

    Bateson first used the word “genetics” in 1905 in a letter to the zoologist Adam Sedgwick (see Bateson 1928, p. 34).

  12. 12.

    Nowadays, many studies show that the regulation of some genes causes variation in the color. For example, the variation in the melanocortin 1 receptor (MC1R) gene, which participates in the production of melanin in plumage, provides some color differences between birds (see, e.g., Doucet et al. 2004; Hoque et al. 2013).

  13. 13.

    Many authors have currently stressed the importance of gene regulation to control the change in developmental timing (see Richardson 1995; Smith 2003; Arthur 2011).

  14. 14.

    Various authors quoted a letter from Bateson sent to his sister Anna on September 14, 1891: “Did I tell you anything about my new VIBRATORY THEORY of REPETITION of PARTS in Animals and Plants? I have been turning it over again lately and feel sure there is something in it. It is the best idea I ever had or am likely to have— Do you see what I mean?— Divisions between segments, petals, etc. are internodal lines like those in sand figures made by sound, i.e. lines of maximum vibratory strain, while the mid-segmental lines and the petals, etc. are the nodal lines, or places of minimum movement. Hence all the patterns and recurrence of patterns in animals and plants—hence the perfection of symmetry—hence bilaterally symmetrical variation, and the completeness of repetition whether of a part repeated in a radial or linear series etc. etc. I am, as you see, in a great fluster… P.S. Of course, Heredity becomes quite a simple phenomenon in light of this” (Bateson 1928, pp. 42–43; his italics). Here it is interesting to note that Bateson spoke of these processes as a “vibratory theory of repetition of parts” and not as a theory of heredity. In other letters, he refers to this as the “undulatory hypothesis,” but finally in Problems of Genetics (1913), he argued that it was a hypothetical model of mechanisms to be discovered that may be analogous to the physical mechanisms acting upon the production of non-biological patterns; see below.

  15. 15.

    Interestingly, Caballero et al. (2012) suggest a model that explains the color patterns seen in animals through physical and mechanical processes as well as cellular interactions and not only by the participation of genes alone. Likewise, Newman (2017) argues that some structural arrangements such as tissue layers, segments, appendages “can be readily generated by physical organizing forces acting on tissue masses, with minimal programming by the genome.”

  16. 16.

    Similarly, during the late twentieth century, conceptions such as “exaptation” and “spandrel” attempted to exclude the teleonomic aspect of biology (Gould and Lewontin 1979; Gould and Vrba 1982; Gould 2002). Diogo (2017) recently incorporated into his evolutionary framework the assumption that the structures making up an organism do not have an optimal match with their environment.

  17. 17.

    This phenomenon would fall into the domain of what we know today as phenotypic plasticity.

  18. 18.

    However, Stoltzfus and Cable (2014) point out that de Vries’s fluctuations also included partially hereditary variations.

  19. 19.

    On this interpretation of Johannsen’s experiments, see Roll-Hansen (2009, 2014) and Ochoa (2017, pp. 64–74).

  20. 20.

    In similar lines, Linde-Medina (2011) argues that the role of natural selection as a creative force is challenged when we consider how characters develop. She concludes that selection is the cause of the prevalence of the characters, but when development is considered, the explanation behind the character’s existence lies in how they are generated. Granovitch (2021, p. 409) also claims that the role of natural selection “consists in decreasing the morphogenetic potential of a species. Viewed from this angle, selectogenesis should be considered as a conservative force.”

  21. 21.

    As an analogy with a soccer game, Pere Alberch said that natural selection can determine which team wins, but developmental biology determines which teams play.

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Acknowledgments

Thanks especially to Aaron Thompson and Omar Ochoa-Olmos for their invaluable support. I thank Sarah Debbie Wilson Barrera and Philip Daniels for the English editing. Many thanks to Richard Delisle for the invitation to contribute to this volume and for his suggestions and corrections that improve this work. I also want to thank the reviewers for their suggestions.

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Ochoa, C. (2021). The Origins of Theoretical Developmental Genetics: Reinterpreting William Bateson’s Role in the History of Evolutionary Thought. In: Delisle, R.G. (eds) Natural Selection. Evolutionary Biology – New Perspectives on Its Development, vol 3. Springer, Cham. https://doi.org/10.1007/978-3-030-65536-5_6

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