Gene Concepts

Causation has multiple distinct meanings in genetics. One reason for this is meaning slippage between two concepts of the gene: Mendelian and molecular. Another reason is that a variety of genetic methods address different kinds of causal relationships. Some genetic studies address causes of traits in individuals, which can only be assessed when single genes follow predictable inheritance patterns that reliably cause a trait. A second sense concerns the causes of trait differences within a population. Whereas some single genes can (...) be said to cause population-level differences, most often these claims concern the effects of many genes. Polygenic traits can be understood using heritability estimates, which estimate the relative influences of genetic and environmental differences to trait differences within a population. Attempts to understand the molecular mechanisms underlying polygenic traits have been developed, although causal inference based on these results remains controversial. Genetic variation has also recently been leveraged as a randomizing factor to identify environmental causes of trait differences. This technique—Mendelian randomization—offers some solutions to traditional epidemiological challenges, although it is limited to the study of environments with known genetic influences. (shrink)

Darwinian evolutionary theory has two key terms, variations and biological selection, which finally lead to survival of the fittest variant. With the rise of molecular genetics, variations were explained as results of error replications out of the genetic master templates. For more than half a century, it has been accepted that new genetic information is mostly derived from random error-based events. But the error replication narrative has problems explaining the sudden emergence of new species, new phenotypic traits, and genome innovations (...) as a sudden single event. Meanwhile, it is recognized that errors cannot explain the evolution of genetic information, genetic novelty, and complexity. Now, empirical evidence establishes the crucial role of non-random genetic content editors, such as viruses, diversity generating retroelements, and other RNA networks, to produce new genetic information, complex regulatory control, inheritance vectors, genetic identity, immunity, new sequence space, evolution of complex organisms, and evolutionary transitions. (shrink)

Review of: Sophia Roosth, Synthetic: How Life Got Made (University of Chicago Press, 2017); and Andrew S. Balmer, Katie Bulpin, and Susan Molyneux-Hodgson, Synthetic Biology: A Sociology of Changing Practices (Palgrave Macmillan, 2016).

Huang and Bargh’s definition of goals is ambiguous between ‘specific goals’ – the end-state of a token action I am about to perform – and ‘unspecific goals’ – the end-state of an action-type (without specifying how this would be achieved). The analogy with selfish genes pushes the authors towards the former interpretation, but the latter would provide a more robust theoretical framework.

This paper examines causal theories of reference with respect to how plausible an account they give of non-physical natural kind terms such as ‘gene’ as well as of the truth of the associated theoretical claims. I first show that reference fixism for ‘gene’ fails. By this, I mean the claim that the reference of ‘gene’ was stable over longer historical periods, for example, since the classical period of transmission genetics. Second, I show that the theory of partial reference does not (...) do justice to some widely held realist intuitions about classical genetics. This result is at loggerheads with the explicit goals usually associated with partial theories of reference, which is to defend a realist semantics for scientific terms. Thirdly, I show that, contrary to received wisdom and perhaps contrary to physics and chemistry, neither reference fixism nor partial reference are necessary in order to hold on to scientific realism about biology. I pinpoint the reasons for this in the nature of biological kinds, which do not even remotely resemble natural kinds (i.e., Lockean real essences) as traditionally conceived. (shrink)

Personalized genomics companies (PG; also called ‘direct-to-consumer genetics’) are businesses marketing genetic testing to consumers over the Internet. While much has been written about these new businesses, little attention has been given to their roles in science communication. This paper provides an analysis of the gene concept presented to customers and the relation between the information given and the science behind PG. Two quite different gene concepts are present in company rhetoric, but only one features in the science. To explain (...) this, we must appreciate the delicate tension between PG, academic science, public expectation, and market forces. (shrink)

Book Review: What Genes Can’t Do By Lenny Moss .

Darwin's ideas on variation, heredity, and development differ significantly from twentieth-century views. First, Darwin held that environmental changes, acting either on the reproductive organs or the body, were necessary to generate variation. Second, heredity was a developmental, not a transmissional, process; variation was a change in the developmental process of change. An analysis of Darwin's elaboration and modification of these two positions from his early notebooks (1836-1844) to the last edition of the /Variation of Animals and Plants Under Domestication/ (1875) (...) complements previous Darwin scholarship on these issues. Included in this analysis is a description of the way Darwin employed the distinction between transmission and development, as well as the conceptual relationship he saw between heredity and variation. This paper is part of a larger project comparing commitments regarding variation during the latter half of the nineteenth century. (shrink)