Catálogo de publicaciones - revistas

<jats:title>Abstract</jats:title><jats:p>Repeated interactions provide an evolutionary explanation for one-shot human cooperation that is counterintuitive but orthodox<jats:sup>1–3</jats:sup>. Intergroup competition<jats:sup>4–7</jats:sup> provides an explanation that is intuitive but heterodox. Here, using models and a behavioural experiment, we show that neither mechanism reliably supports cooperation. Ambiguous reciprocity, a class of strategies that is generally ignored in models of reciprocal altruism, undermines cooperation under repeated interactions. This finding challenges repeated interactions as an evolutionary explanation for cooperation in general, which further challenges the claim that repeated interactions in the past can explain one-shot cooperation in the present. Intergroup competitions also do not reliably support cooperation because groups quickly become extremely similar, which limits scope for group selection. Moreover, even if groups vary, group competitions may generate little group selection for multiple reasons. Cooperative groups, for example, may tend to compete against each other<jats:sup>8</jats:sup>. Whereas repeated interactions and group competitions do not support cooperation by themselves, combining them triggers powerful synergies because group competitions constrain the corrosive effect of ambiguous reciprocity. Evolved strategies often consist of cooperative reciprocity with ingroup partners and uncooperative reciprocity with outgroup partners. Results from a behavioural experiment in Papua New Guinea fit exactly this pattern. They thus suggest neither an evolutionary history of repeated interactions without group competition nor a history of group competition without repeated interactions. Instead, our results suggest social motives that evolved under the joint influence of both mechanisms.</jats:p>

<jats:title>Abstract</jats:title><jats:p>Although <jats:italic>KDM5C</jats:italic> is one of the most frequently mutated genes in X-linked intellectual disability<jats:sup>1</jats:sup>, the exact mechanisms that lead to cognitive impairment remain unknown. Here we use human patient-derived induced pluripotent stem cells and <jats:italic>Kdm5c</jats:italic> knockout mice to conduct cellular, transcriptomic, chromatin and behavioural studies. KDM5C is identified as a safeguard to ensure that neurodevelopment occurs at an appropriate timescale, the disruption of which leads to intellectual disability. Specifically, there is a developmental window during which KDM5C directly controls WNT output to regulate the timely transition of primary to intermediate progenitor cells and consequently neurogenesis. Treatment with WNT signalling modulators at specific times reveal that only a transient alteration of the canonical WNT signalling pathway is sufficient to rescue the transcriptomic and chromatin landscapes in patient-derived cells and to induce these changes in wild-type cells. Notably, WNT inhibition during this developmental period also rescues behavioural changes of <jats:italic>Kdm5c</jats:italic> knockout mice. Conversely, a single injection of WNT3A into the brains of wild-type embryonic mice cause anxiety and memory alterations. Our work identifies KDM5C as a crucial sentinel for neurodevelopment and sheds new light on <jats:italic>KDM5C</jats:italic> mutation-associated intellectual disability. The results also increase our general understanding of memory and anxiety formation, with the identification of WNT functioning in a transient nature to affect long-lasting cognitive function.</jats:p>