Desktop version

Home arrow Psychology arrow Metaphysics and the philosophy of science : new essays


WHAT is a gene? the classical gene concept in scientific practice

What is a gene ? Contemporary geneticists employ multiple gene concepts that seem to offer conflicting answers. At one extreme is what I call the classical gene concept, which provides biologists with a blunt conceptual tool that works well in investigative and explanatory contexts in which precision is not available or useful (Waters 1994 and 2007). At the other extreme is what I call the molecular gene concept, which provides biologists with a remarkably precise and yet flexible tool for contexts in which precision is important (Waters 2000). The classical gene concept, as the name suggests, comes from classical genetics, the practice of genetics developed by T. H. Morgan and his collaborators in the late 1910s and 1920s. This practice continued until it was retooled to become contemporary genetics (Waters 2008a). In this section, I describe conceptual practice in classical genetics. In the next section, I consider how a traditional scientific metaphysician, if working in the 1930s, might have answered the question, “What is a gene ?”

It is important to understand that the classical concept of the gene was grounded in experimental practice, not in abstract theorizing. Experimental practice in classical genetics involved strategically constructing breeding regimens that produced distinctive inheritance patterns. These patterns were explained by a central theory, called the transmission theory. This theory was constructed to apply to artificial experimental situations, and the experimental situations were constructed to instantiate the theory (Waters 200 8b). This may appear to involve a problematic circularity or explanatory triviality. But these practices were aimed, not just at explaining transmission patterns, but at investigating a wide variety of biological processes, including hereditary, physiological, developmental, and evolutionary processes (Kohler 1994). When successful, this experimentation enabled biologists to manipulate processes they did not understand and to thereby reveal new information about these processes (Waters 2004).

While it is important to understand geneticists’ theoretical explanations in the broader context of their experimental practice, one cannot understand this practice without analyzing how the theoretical/explanatory reasoning worked within it. Geneticists’ reasoning about genes invoked a conceptual division between the internal genetic makeup of an organism, called its genotype, and its outward character, called its phenotype. They explained patterns of phenotypic transmission produced in their experiments by following the transmission of genotypic differences from one generation to the next, and then attributing the presence of alternative phenotypic traits to the presence of alternative genotypes (i.e., to the presence of alternative forms of genes). These explanations were based on the transmission theory, which included the idea that genes are located in linear fashion on chromosomes, principles about the transmission of genes that were grounded in an understanding of chromosomal mechanics, and the principle that differences in genes cause differences in phenotypes.

Let us consider the concept of the gene standing behind these explanations. As units passed down from generation to generation, genes were conceived as stable entities, capable of being replicated, located at designated positions in chromosomes. By at least the 1920s, most geneticists thought of genes as having physical structure, and it was the physical make-up of genes that was presumed to provide their stability. Practically nothing, however, was known about the internal structure of the gene until quite late in the development of classical genetics. The idea that there is a linear ordering of genes in chromosomes was essential to complex explanations of gene transmission, but this ordering does not imply anything about the structure of the genes themselves. Morgan and others frequently stated that their theory made two assumptions about the internal structure of genes: (1) gene structure is relatively stable, and (2) the structure of each gene is replicated before chromosomal division (e.g., Morgan 1926, 27). Muller (1922) pointed out that classical explanations positing spontaneous mutation made an additional assumption: (3) mutations in the structure of a gene are also replicated.

Just as Darwin’s Origin of Species contained a scarcity of information about the nature of species and their origins, Morgan’s Theory of the Gene had little to say about the structure of genes or their individual contributions to phenotypes. Genes could be speculatively related to the developing form of an organism, but the connection between genotype and phenotype was spelled out concretely only in terms of what I have called the difference principle: gene differences cause phenotypic differences within the genetic and environmental contexts of particular populations (Waters 1994, 2007). Strevens (this volume, chap. 2) describes a similarly simple model of predator/prey population cycles in ecology that also involves difference making. But he analyzes the ecological model in terms of an abstract explanatory principle (“enion probability analysis”) that is ultimately grounded in a metaphysical theory, whereas I analyze models of transmission in terms of a concrete principle grounded in investigative practice. In the case of genetics, at least, it is important to keep in mind that the explanatory principle is easily and very accurately applied in experimental contexts because geneticists deliberately simplified experimental situations by standardizing environmental conditions and removing genetic differences that might interfere with the expression or transmission of genes being used in an experiment.[1]

It is easy to exaggerate the knowledge (or claims) of classical geneticists by focusing on theoretical explanations in an abstract context (rather than in the context of experimental investigation) or by citing geneticists’ speculations. For example, classical geneticists have sometimes been accused by later scientists, philosophers, and historians of believing in a simple one gene/one character conception, a version of preformationism.[2] This misinterpretation might arise because geneticists’ practices involved creating situations in which just one gene is the actual difference maker of a phenotypic difference in a laboratory population (Waters 2007). From a distance, it might appear that geneticists thought their explanations of experimental phenomena represented inheritance generally. But practicing geneticists understood that they were creating simple situations (which was obvious to them because they had to deliberately set up these situations to make their experiments work).

The relation between genotype and phenotype is not “one gene/one character" and classical geneticists knew this. As they clearly stated, one gene can affect a variety of characters, and a single character can be influenced by a number of different genes (genes at different loci). Geneticists knew, for example, that eye color in Drosophila is affected by mutations at many different loci; by 1915, Morgan’s group had already identified mutations at twenty-five separate loci that affected eye color (Morgan et al. 1915, 208). They knew that these mutations generally affect several different characteristics. The white eye allele (located on the X chromosome), for example, was associated not just with white eyes, but with a colorless sheath of the testes, sluggish behavior, and perhaps a shortened life span as well. Experimental practice included protocols for selecting just one such phenotypic difference for experimental purposes. A one gene/one character conception of the gene makes sense only from a decontextualized, abstract perspective.

An examination of Morgan’s sophisticated reflections on genotype/phenotype relations reinforces this interpretation. In Theory of the Gene (1926), Morgan reported that embryology reveals that every organ of the body is the “culmination of a long series of processes" and he presumed that genes act on the steps along the way (1926, 306). If each step in the development of an organ is affected by many genes, he reasoned, then there could not be any single gene for the organ. Likewise, if one gene affects steps in the development of multiple organs, then there could not be any single organ associated with a gene: hence, the many-many relations. Morgan elaborated,

Suppose, for instance, to take perhaps an extreme case, all the genes are instrumental in producing each organ of the body. This may only mean that they all produce chemical substances essential for the normal course of development. If now one gene is changed so that it produces some substance different from that which it produced before, the end-result may be affected, and if the change affects one organ predominantly it may appear that one gene alone has produced this effect. In a strictly causal sense this is true, but the effect is produced only in conjunction with all the other genes. (1926, 306)

Classical geneticists could only speculate about the immediate impact of genes (here, Morgan speculated that they produce chemical substances). This passage and Morgan’s discussion of developmental processes suggest that the immediate impact of a gene is separated from characteristics such as eye color by a series of developmental processes that are also influenced by a number of other genes. This means that it would be impossible to specify a gene’s contribution to phenotype in terms of characteristics such as eye color.

An abstract analysis of the transmission theory might make it appear that classical geneticists had a lot to say about genes, heredity, and development. But an examination of their theoretical knowledge in the broader context of experimental practice reveals that they did not have a lot to say about these matters. The real value of their science involved what they could manipulate and investigate, not what they could explain (and not even what their theory could in principle explain [see Waters 2004]).

My aim in this section is to make two points. First, the structure of the world that geneticists were manipulating and investigating was not directly reflected in the structure of their concepts and theories. Second, one gets a better sense of the complexity of the reality that geneticists were engaging when one analyzes their investigative and manipulative practices in light of their concrete, local aims (instead of analyzing their theoretical explanations abstractly—as if all we need to consider is their aim to explain inheritance patterns or their alleged aim to explain all development in terms of genes). Scientific metaphysicians interested in complex reality should focus on scientific knowledge (including theoretical knowledge) in the context of scientific practices (broadly speaking), not in an abstract context in which theories can be viewed separately from material practices designed to advance investigative and manipulative goals.

  • [1] I worry that Strevens’s simple model cannot be applied to actual population cycles in an accurate way and thathis analysis is too far removed from actual investigative practices in ecology to be useful. Stanford’s critiqueseems to apply (Stanford, this volume, chap. 6).
  • [2] Examples of such exaggeration are too numerous to cite, but I take Moss (2003) and Keller’s (2000) accounts ofclassical genetics as representative of how historians and philosophers exaggerate the claims of classical genetics(claims of which they are very critical). Keller (pers. comm.) makes the compelling argument that geneticists’speculations reveal biases that had significant impact on their research.
Found a mistake? Please highlight the word and press Shift + Enter  
< Prev   CONTENTS   Next >

Related topics