Stefan Linquist

The media attention and subsequent scientific backlash engendered by the claim, announced by spokespeople for the Encyclopedia of DNA Elements project, that 80% of the human genome has a “biochemical function” highlights the need for a clearer understanding of function concepts in biology. This article provides an overview of two major function concepts that have been developed in the philosophy of science – the “causal role” concept and the “selected effects” concept – and their relevance to ENCODE. Unlike some previous critiques, the ENCODE project is not considered problematic because it employed a causal role definition of function, but because of how this concept was misused. In addition, several unique challenges that arise when dealing with transposable elements, but which were ignored by ENCODE, are highlighted. These include issues surrounding TE-level versus organism-level selection, the origins versus the persistence of elements, and accidental versus functional organism-level benefits. Finally, some key questions are presented that should be addressed in any studies aiming to ascribe functions to major portions of large eukaryotic genomes, the majority of which is made up of transposable elements.

Research on patients with damage to ventromedial frontal cortices suggests a key role for emotions in practical decision making. This field of investigation is often associated with Antonio Damasio’s Somatic Marker Hypothesis—a putative account of the mechanism through which autonomic tags guide decision making in typical individuals. Here we discuss two questionable assumptions—or ‘myths’—surrounding the direction and interpretation of this research. First, it is often assumed that there is a single somatic marker hypothesis. As others have noted, however, Damasio’s ‘hypothesis’ admits of multiple interpretations (Dunn et al. [2006]; Colombetti [2008]). Our analysis builds upon this point by characterizing decision making as a multi-stage process and identifying the various potential roles for somatic markers. The second myth is that the available evidence suggests a role for somatic markers in the core stages of decision making, that is, during the generation, deliberation, or evaluation of candidate options. On the contrary, we suggest that somatic markers most likely have a peripheral role, in the recognition of decision points, or in the motivation of action. This conclusion is based on an examination of the past twenty-five years of research conducted by Damasio and colleagues, focusing in particular on some early experiments that have been largely neglected by the critical literature. 1 Introduction2 What is the Somatic Marker Model?3 Multiple Somatic Marker Hypotheses3.1 Are somatic markers necessary for practical decision making?3.2 Speed, accuracy, or both?3.3 At which of the five stages of decision making are somatic markers engaged?4 Anecdotal Evidence Suggests a Peripheral Role for Somatic Markers4.1 Chronic indecisiveness4.2 Extreme impulsiveness4.3 Enhanced decision making in the lab4.4 Lack of motivation. 5 Early Experiments Suggest that VMF Damage Leaves Core Processes Intact5.1 The evocative images study5.2 Five problem solving tasks6 Recent Experiments Fail to Discriminate among Alternate Versions of SMH7 Conclusion

A promising recent development in molecular biology involves viewing the genome as a miniecosystem, where genetic elements are compared to organisms and the surrounding cellular and genomic structures are regarded as the local environment. Here we critically evaluate the prospects of Ecological Neutral Theory, a popular model in ecology, as it applies at the genomic level. This assessment requires an overview of the controversy surrounding neutral models in community ecology. In particular, we discuss the limitations of using ENT both as an explanation of community dynamics and as a null hypothesis. We then analyze a case study in which ENT has been applied to genomic data. Our central finding is that genetic elements do not conform to the requirements of ENT once its assumptions and limitations are made explicit. We further compare this genome-level application of ENT to two other, more familiar approaches in genomics that rely on neutral mechanisms: Kimura’s Molecular Neutral Theory and Lynch’s Mutational Hazard Model. Interestingly, this comparison reveals that there are two distinct concepts of neutrality associated with these models which we dub ‘fitness-neutrality’ and ‘competitive neutrality’. This distinction helps to clarify the various roles for neutral models in genomics, for example, in explaining the evolution of genome size.