Postgenomics function monism

Abstract

The ENCODE project has made important new estimates of human genome functionality, now revising the percentage considered functional to more than 80%, which is in stark contrast to the received view, which estimated that less than 10% of the conserved parts of the human genome are functional. ENCODE's unorthodox use of the notion of biological function has stirred the so-called ENCODE controversy, involving conflicting views about the correct notion of function in postgenomics. The debate hinges on the traditional philosophical contrast between the causal role (CR) and selected effects (SE) approaches. In this paper, we examine the ENCODE controversy in terms of the distinction between function monism and pluralism. We propose to apply a weak etiological account to genomic function ascriptions. In this approach, we can ascribe a function to a genomic structure of an organism if and only if performing the function persists in causally contributing to the organism's and its ancestors' fitness. In comparison to the strong etiological (i.e., the selected effects) approach, the present account does not require there to be selection for the structure in question. This is a monistic approach that enables us to avoid the main difficulties of CR, as well as SE's overdependence on natural selection, while still preserving an evolutionary-constrained notion of biological functions. Our proposal is much more moderate in accommodating the estimates of the functionality of the human genome than both ENCODE's proposal itself and the views of the critics relying on a version of the SE account of functions.

Keywords: Causal role accounts; ENCODE; Function monism; Function pluralism; Human genome; Junk DNA; Postgenomics; Selected effect accounts; Weak functional etiology.