Abstract
According to the proponents of Developmental Systems Theory and the Causal Parity Thesis, the privileging of the genome as “first among equals” with respect to the development of phenotypic traits is more a reflection of our own heuristic prejudice than of ontology—the underlying causal structures responsible for that specified development no more single out the genome as primary than they do other broadly “environmental” factors. Parting with the methodology of the popular responses to the Thesis, this paper offers a novel criterion for ‘causal primacy’, one that is grounded in the ontology of the unique causal role of dispositional properties. This paper argues that, if the genome is conceptualised as realising dispositional properties that are “directed toward” phenotypic traits, the parity of ‘causal roles’ between genetic and extra-genetic factors is no longer apparent, and further, that the causal primacy of the genome is both plausible and defensible.
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Notes
Griffiths and Knight (1998: 254).
The general agreement by most metaphysicians that all dispositional properties, as a matter of principle, are capable of being “interrupted” after receiving their stimulus and before they come to their manifestation—a consequence of the so-called “problem of masks”—is, I think, plausibly construed as the assumption that every dispositional property’s manifestation lies causally downstream from its stimulus conditions.
I say “primarily with respect to its manifestation state” because it is typically the products of genes that we are most interested in when we are doing the business of biological classification.
“Reliably and repeatedly” is meant to express that the causal link from ‘stimulus’ to ‘manifestation’ is not one of necessity, but neither is it one of contingency—for it furnishes reliable inductive inferences for the bearers of those properties. See Mumford and Anjum (2011: Chapter 8).
See Armstrong (2004) for the canonical formulation.
See Mumford and Anjum (2011) for a thorough rejection of dispositional properties as truthmakers for subjunctive conditionals.
Keeping in mind that these counterfactuals are meant to express “reliable and repeatable” connections, and are, as mentioned above, sensitive to context, etc.
Lewontin (1982: 21–22).
Powell et al. (2010).
Gibson (1970).
In fact, I think that even the seemingly most mundane of dispositions exhibit this level of complexity. Take the philosophers’ favourite “simple” disposition—‘fragility’: the realisation base of ‘fragility’ is undoubtedly (at least) a multi-faceted, complex chemical structure, and its manifestation—‘shattering’—is no “simple” event, but must be comprised of the aligning of various micro-events that represent decreasing degrees of structural integrity.
Of course, transcription factors alone do not comprise the full ‘stimulus’ of these dispositional properties, as many other intra-cellular causal factors are required for the initiation of the process of transcription—a fact not ignored in the following discussion of the causal parity thesis. They have been singled-out here only because their central importance in the regulation of transcription, and thus, the genome’s pattern of expression.
Oyama (2000: S340).
Schaffner (1998: 234).
Sterelny and Griffiths (1999: 101).
Typically the “correlation” between the two states/entities/systems is cashed out in terms of reduction of uncertainty, or the decrease of epistemic entropy, in the sense that knowing the value of the second variable allows one to know the value of the first (or vice versa).
Gray (1992: 179).
Gannett (1999: 356; my emphasis).
Stegmann (2005).
Stegmann’s (2012a) ‘external ordering’ is a possible example of this.
Although most philosophers would undoubtedly classify some of the following ‘stimulus’ factors as “background conditions”, I ignore that distinction here, given the preceding discussion of causal parity, showing that any causal factor can be “held constant” while manipulations on the others are correlated with changes in the effect. For other arguments against the distinction between ‘causes’ and ‘conditions’ with respect to dispositional properties, see Mumford and Anjum (2011), and Hauska (2009).
I thank the editor for bringing this important question to my attention.
If the fact that a causal factor couldn’t play its purported causal role outside its specific, proper context disqualified it from playing that role, which causal factor (especially in the biological realm) could be said to perform any causal role whatsoever?
Hollenhorst et al. (2009).
It’s worth noting that although the following argument addresses only the central case of informational parity with respect to the environment and the genome, I think it can be applied, mutatis mutandis, to any other non-genetic causal factor one proposes to play the role of causal responsibility.
Cf. §3.
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Austin, C.J. The dispositional genome: primus inter pares . Biol Philos 30, 227–246 (2015). https://doi.org/10.1007/s10539-014-9454-y
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DOI: https://doi.org/10.1007/s10539-014-9454-y