No abstract

Context-dependent female mate choices significantly contribute to lower SSD, suggesting female mate choice is likely to have played an influential role in human self-domestication. Future research on this theme will benefit by including more of the expected symptoms of human self-domestication and examining other potential drivers of this process.

Altered neural crest cell (NCC) behaviour is an increasingly cited explanation for the domestication syndrome in animals. However, recent authors have questioned this explanation, while others cast doubt on whether domestication syndrome even exists. Here, we review published literature concerning this syndrome and the NCC hypothesis, together with recent critiques of both. We synthesize these contributions and propose a novel interpretation, arguing shared trait changes under ancient domestication resulted primarily from shared disruption of wild reproductive regimes. We detail four primary selective pathways for ‘reproductive disruption' under domestication and contrast these succinct and demonstrable mechanisms with cryptic genetic associations posited by the NCC hypothesis. In support of our perspective, we illustrate numerous important ways in which NCCs contribute to vertebrate reproductive phenotypes, and argue it is not surprising that features derived from these cells would be coincidentally altered under major selective regime changes, as occur in domestication. We then illustrate several pertinent examples of Darwin's ‘unconscious selection' in action, and compare applied selection and phenotypic responses in each case. Lastly, we explore the ramifications of reproductive disruption for wider evolutionary discourse, including links to wild ‘self-domestication' and ‘island effect’, and discuss outstanding questions.

This manuscript represents a redrafting of an earlier paper posted at BioRxiv following two rounds of review at Evolution and Human Behaviour. This redrafting will require further changes and review before being resubmitted elsewhere.

Objectives:Pre-historic decline in human craniofacial masculinity has been proposed as evidence of selection for elevated sociability and a process of 'human self-domestication' thought to have promoted complex capacities including language, culture, and cumulative technological development. This follows experimental observation of similar changes in non-human animals under selection for reduced aggression. Two distinct domestication hypotheses posit developmental explanations, involving hypoplasia of embryonic neural crest cells (NCCs), and declining androgen influence, respectively. Here, I assess the operation and potential interactions between these two mechanisms and consider their role in enhanced human adaptation to a cooperative sociocultural niche. Methods: I provide a review and synthesis of related literature with a focus on physiological mechanisms effecting domesticated reductions in masculinity and sexual dimorphism.Further, I examine pre-historic modes of socio-sexual selection likely to drive human selfdomestication via reduced aggression and masculinity. Results:I find pluripotent NCCs provide progenitors for a wide range of vertebrate masculine features, acting as regular targets for sexually driven evolutionary change; suggesting domesticated hypoplasia of NCC-derived tissues would be sufficient to explain declines in masculine traits and features. However, lineage specific androgen receptor variability likely moderates these NCC-based effects. Conclusions:These findings extend theorised mechanisms driving noted physiological, morphological, and behavioural changes thought to indicate enhanced sociability and human and selfdomestication. Multiple current explanations for human sociability are consistent with physiological domestication under socio-sexual selection favouring dampened masculine physiology and behaviour as adaptations to an enhanced sociocultural niche. The analysis highlights multiple avenues for further investigation.Masculinity and the mechanisms of human self-domestication-Ben Gleeson 3