Reduction in Genetics

Since the ENCODE project published its final results in a series of articles in 2012, there is no consensus on what its implications are. ENCODE’s central and most controversial claim was that there is essentially no junk DNA: most sections of the human genome believed to be «junk» are functional. This claim was met with many reservations. If researchers disagree about whether there is junk DNA, they have first to agree on a concept of function and how function, given a (...) particular definition, can be discovered. The ENCODE debate centered on a notion of function that assumes a strong dichotomy between evolutionary and non-evolutionary function and causes, prevalent in the Modern Evolutionary Synthesis. In contrast to how the debate is typically portrayed, both sides share a commitment to this distinction. This distinction is, however, much debated in alternative approaches to evolutionary theory, such as the EES. We show that because the ENCODE debate is grounded in a particular notion of function, it is unclear how it connects to broader debates about what is the correct evolutionary frame- work. Furthermore, we show how arguments brought forward in the controversy, particularly arguments from mathematical population genetics, are deeply embedded in their particular disciplinary contexts, and reflect substantive assumptions about the evolution of genomes. With this article, we aim to provide an anatomy of the ENCODE debate that offers a new perspective on the notions of function both sides employed, as well as to situate the ENCODE debate within wider debates regarding the forces operating in evolution. (shrink)

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)

Dies ist eine ausgezeichnete Überprüfung der Gen-/Umgebungsinteraktionen auf das Verhalten und ist, obwohl sie etwas veraltet ist, eine einfache und lohnende Lektüre. Sie beginnen mit Zwillingsstudien, die den überwältigenden Einfluss der Genetik auf das Verhalten zeigen. Sie stellen die immer bekannter werdenden Studien von Judith Harris fest, die die Fakten erweitern und zusammenfassen, dass die gemeinsame häusliche Umgebung fast keinen Einfluss auf das Verhalten hat und dass adoptierte Kinder so anders wachsen als ihre Stiefbrüder und -schwestern wie zufällig ausgewählte Menschen. (...) Ein grundlegender Punkt, den sie (und fast alle, die über Verhaltensgenetik diskutieren) nicht zur Kenntnis nehmen, ist, dass die Hunderte (Tausende je nach Standpunkt) menschlicher Verhaltensuniversalen, einschließlich aller Grundlagen unserer Persönlichkeiten, zu 100% von unseren Genen bestimmt werden, ohne Variation in normalen Werten. Jeder sieht einen Baum als Baum und nicht als Stein, sucht und isst Nahrung, wird wütend und eifersüchtig usw. Worüber sie hier also meistens sprechen, ist, wie viel Umwelt (Kultur) das Ausmaß beeinflussen kann, in dem verschiedene Merkmale gezeigt werden, und nicht ihr Aussehen. Schließlich diskutieren sie die Eugenik in der üblichen politisch korrekten Weise, ohne festzustellen, dass wir und alle Organismen die Produkte der Eugenik der Natur sind und dass Versuche, die natürliche Selektion mit Medizin, Landwirtschaft und Zivilisation als Ganzes zu besiegen, für jede Gesellschaft, die dies weiterhin tut,katastrophalsind. Bis zu 50 % aller Empfängnisse oder etwa 100 Millionen pro Jahr enden in einer frühen spontanen Abtreibung, fast alle ohne Dassmund die Mutter. Diese natürliche Keulung defekter Gene treibt die Evolution an, hält uns relativ genetisch gesund und macht die Gesellschaft möglich. Dysgenös ist ausreichend, um die Zivilisation zu zerstören, aber Überbevölkerung wirdd o eszuerst. Wer aus der modernen zweisystems-Sichteinen umfassenden, aktuellen Rahmen für menschliches Verhalten wünscht, kann mein Buch "The Logical Structure of Philosophy, Psychology, Mindand Language in Ludwig Wittgenstein and John Searle' 2nd ed (2019) konsultieren. Diejenigen,die sich für mehr meiner Schriften interessieren, können 'Talking Monkeys--Philosophie, Psychologie, Wissenschaft, Religion und Politik auf einem verdammten Planeten --Artikel und Rezensionen 2006-2017' 3rd ed (2019) und andere sehen. (shrink)

Schaffner’s model of theory reduction has played an important role in philosophy of science and philosophy of biology. Here, the model is found to be problematic because of an internal tension. Indeed, standard antireductionist external criticisms concerning reduction functions and laws in biology do not provide a full picture of the limits of Schaffner’s model. However, despite the internal tension, his model usefully highlights the importance of regulative ideals associated with the search for derivational, and embedding, deductive relations among mathematical (...) structures in theoretical biology. A reconstructed Schaffnerian model could therefore shed light on mathematical theory development in the biological sciences and on the epistemology of mathematical practices more generally. *Received November 2006; revised March 2009. †To contact the author, please write to: Philosophy Department, University of California, Santa Cruz, 1156 High St., Santa Cruz, CA 95064; e‐mail: [email protected]. (shrink)

Although epistasis is at the center of the Fisher-Wright debate, biologists not involved in the controversy are often unaware that there are actually two different formal definitions of epistasis. We compare concepts of genetic independence in the two theoretical traditions of evolutionary genetics, population genetics and quantitative genetics, and show how independence of gene action (represented by the multiplicative model of population genetics) can be different from the absence of gene interaction (represented by the linear additive model of quantitative genetics). (...) The two formulations converge with weak selection but not with strong selection or, for multiple loci, when the aggregated interaction terms are not negligible. As a result of the different formulations of gene interaction, the presence or absence of linkage disequilibrium,/D/, does not necessarily indicate the presence or absence of fitness epistasis. Indeed, linkage disequilibrium is generated in ‘additive’ models in quantitative genetics whenever two (or more) loci experience simultaneous selection. As a research strategy, it is often practical, for theoretical or experimental reasons, to minimize gene interaction by assuming independence of gene action in regard to fitness, or by assuming linear additive effects of multiple loci on a phenotype. However, minimizing the role of epistasis in theoretical investigations hinders our understanding of the origins of diversity and the evolution of complex phenotypes. (shrink)