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Does intragenomic conflict predict intrapersonal conflict?

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Abstract

Parts of the genome of a single individual can have conflicting interests, depending on which parent they were inherited from. One mechanism by which these conflicts are expressed in some taxa, including mammals, is genomic imprinting, which modulates the level of expression of some genes depending on their parent of origin. Imprinted gene expression is known to affect body size, brain size, and the relative development of various tissues in mammals. A high fraction of imprinted gene expression occurs in the brain. Biologists including Hamilton, Trivers and Haig have proposed that this may explain some intrapersonal conflict in humans. This speculation amounts to an inference from conflict within the genome (which is well-established) to conflict within the brain or mind. This is a provocative proposal, which deserves serious attention. In this paper I assess aspects of Haig’s version of the proposal. I argue, first, that the notion that intragenomic conflict predicts personal inconsistency should be rejected. Second, while it is unlikely that it credibly predicts sub-personal agents representing conflicting genetic interests, it is plausible that it predicts that the division of cognitive labour could be exploited to turn sub-systems into proxies for conflicting interests.

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Notes

  1. The important early paper by Haig and Westoby (1989) did not use the term ‘genomic imprinting’, but referred to ‘parent-specific gene expression’. In a commentary on that paper Haig (2002) discusses some ambiguities in the term ‘genomic imprinting’. The term ‘kinship theory of genomic imprinting’ is due to Trivers and Burt (1999).

  2. I generally won’t repeat ‘autosomal’ or ‘mammal’ but both are implicit throughout. The points made here don’t apply, or apply only with modifications, in the cases of different taxa or genetic systems, or other genes, including mitochondria and sex chromosomes (Burt and Trivers 2006, p. 133ff).

  3. Mono-allelic expression carries costs, including exposure to harmful recessive traits, and the effective absence of a ‘backup’ allele in cases of disadvantageous mutation on the other.

  4. The number of imprinted genes in humans is not yet definitively known, but recent estimates cluster around values between 100 and 1000. Just as regular gene expression can be contingent on factors including cell type and developmental stage, so can imprinted gene expression.

  5. This consistency of effect is accompanied by fairly heterogeneous mechanisms of imprinting. See Burt and Trivers (2006).

  6. For a more recent and detailed analysis of imprinted gene effects on mouse brain development see Gregg et al. (2010).

  7. There are some candidate theories in the human case, for example, Crespi and Badcock’s (2008), which proposes that maternal genetic interests favour ‘mentalising’ cognition while paternal ones favour ‘mechanising’ cognition, and that these capacities asymmetrically depend on different brain tissues. See (“A mechanism for intra-personal conflict?” section) below.

  8. In the PWS case, deletion of the paternally inherited copy of a region of DNA, maternal uniparental disomy for the gene, or mutation that affects the imprinting mechanism responsible for gene silencing produce the same effects. Angelman syndrome is produced by the opposite conditions, i.e. maternal deletion, paternal uniparental disomy, or corresponding mutation of the imprinting mechanism (Cassidy et al. 2000).

  9. That is, of course, adaptive from the perspective of parts of a genome, even if carrying a net cost for the whole.

  10. McNamara and Houston go on to argue that behavioural ecologists have mostly achieved more modest successes relating behaviour to domain-specific currencies such as rate of calorie intake in foraging. The notion of a unidimensional common currency follows fairly directly from the link to fitness. As Maynard-Smith put it: “Paradoxically it has turned out that game theory […] is more readily applied to biology than to the field of economic behavior for which it was originally designed … the theory requires that the value of different outcomes […] might be measured on a single scale. In human applications this measure is provided by ‘utility’—a somewhat artificial and uncomfortable concept: In biology, Darwinian fitness provides a natural and genuinely one-dimensional scale” (Maynard-Smith 1982, quoted in Glimcher 2002, p. 323).

  11. Both prospect theory (when combined with ‘dual-system’ approaches) and hyperbolic discounting have themselves been put to work in explanations of some kinds of behavioural inconsistency, and in models of intrapersonal conflict (e.g. Ainslie 1992). But in neither case is the conflict standardly connected with intragenomic interests. I emphasise again that the issue here isn’t whether there are any explanations of inconsistency or conflicted choice, but whether intragenomic conflict provides one of the explanations.

  12. There could be more than two, without significant effect on the arguments here.

  13. Thaler and Shefrin’s model involving a ‘planner’ and ‘doer’ is explicitly conflictual, even though the basis for understanding the conflict concerns time horizons rather than kinship (Thaler and Shefrin 1981).

  14. I do not mean proxy in the sense of one agent with authority to act for another. That sense of ‘proxy’ implies too many agents. Rather, I mean proxy in the sense in which one value can be used to represent another in a calculation.

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Acknowledgments

A version of this paper was presented at the 2013 conference of the Australasian Association of Philosophy. I am grateful to the audience on that occasion, as well as to David Haig, Daniel Dennett, Don Ross, Mariam Thalos, J.P. Smit, John Collier and Blaize Kaye for feedback on various versions of the text. Two reviewers for this journal also provided very helpful comments and suggestions.

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  1. Philosophy, University of KwaZulu-Natal, Howard College Campus, Durban, 4041, South Africa

    David Spurrett

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Spurrett, D. Does intragenomic conflict predict intrapersonal conflict?. Biol Philos 31, 313–333 (2016). https://doi.org/10.1007/s10539-016-9521-7

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