SignificanceInteraction patterns in human communication networks are characterized by intermittency and unpredictable timing (burstiness). Simulated spreading dynamics through such networks are slower than expected. A technology for automated recording of social interactions of individual honeybees, developed by the authors, enables one to study these two phenomena in a nonhuman society. Specifically, by analyzing more than 1.2 million bee social interactions, we demonstrate that burstiness is not a human-specific interaction pattern. We furthermore show that spreading dynamics on bee social networks are faster than expected, confirming earlier theoretical predictions that burstiness and fast spreading can co-occur. We expect that these findings will inform future models of large-scale social organization, spread of disease, and information transmission.

Humans differ from other primates by marked differences in cognitive abilities and a significantly larger brain. These differences correlate with metabolic changes, as evidenced by the relative up-regulation of energy-related genes and metabolites in human brain. While the mechanisms underlying these evolutionary changes have not been elucidated, altered activities of key transcription factors (TFs) could play a pivotal role. To assess this possibility, we analyzed microarray data from five tissues from humans and chimpanzees. We identified 90 TF genes with significantly different expression levels in human and chimpanzee brain among which the rapidly evolving KRAB-zinc finger genes are markedly over-represented. The differentially expressed TFs cluster within a robust regulatory network consisting of two distinct but interlinked modules, one strongly associated with energy metabolism functions, and the other with transcription, vesicular transport, and ubiquitination. Our results suggest that concerted changes in a relatively small number of interacting TFs may coordinate major gene expression differences in human and chimpanzee brain.comparative transcriptomics ͉ KRAB-zinc finger genes ͉ primate evolution ͉ gene regulatory network evolution H umans differ from chimpanzees in a number of important anatomical and physiological respects, most strikingly in our enhanced cognitive abilities and a substantial increase in the relative size of the human brain (1). Although the human brain is relatively energy-efficient per cell compared with brains of other species, this increased capacity imposes a significant metabolic and oxidative burden (2, 3). Several studies have noted the up-regulation of genes and metabolites involved in oxidative metabolism and mitochondrial function in human brains compared with chimpanzee brains (2, 4, 5). These data, together with evidence of positive selection acting on the promoters of genes involved in energy metabolism during human evolution, indicate that increased energy production has been essential to the evolution of the human brain (6). The relative up-regulation of human genes in other functional categories, including neuroprotection and synaptic transport, has also been documented (7). However, the molecular mechanisms underlying these welldocumented species differences have not been elucidated.Although some differences in human-chimpanzee gene expression may be due to cis-regulatory element divergence, transcription factors (TFs) represent another potential source of expression variability. Whereas most cis-element mutations would be expected to have limited, localized effects, alterations in TF sequence and/or expression could alter the expression of hundreds of target genes in a coordinated fashion (8, 9). Because of these predicted consequences, it is often assumed that TFs are evolutionarily stable, and indeed, TFs as a class are structurally well conserved (8). However, two recent studies have identified TF genes as enriched among genes with expression patterns that are ...

Anthropogenic changes create evolutionarily novel environments that present opportunities for emerging diseases, potentially changing the balance between host and pathogen. Honey bees provide essential pollination services, but intensification and globalization of honey bee management has coincided with increased pathogen pressure, primarily due to a parasitic mite/virus complex. Here, we investigated how honey bee individual and group phenotypes are altered by a virus of concern, Israeli acute paralysis virus (IAPV). Using automated and manual behavioral monitoring of IAPV-inoculated individuals, we find evidence for pathogen manipulation of worker behavior by IAPV, and reveal that this effect depends on social context; that is, within versus between colony interactions. Experimental inoculation reduced social contacts between honey bee colony members, suggesting an adaptive host social immune response to diminish transmission. Parallel analyses with double-stranded RNA (dsRNA)-immunostimulated bees revealed these behaviors are part of a generalized social immune defensive response. Conversely, inoculated bees presented to groups of bees from other colonies experienced reduced aggression compared with dsRNA-immunostimulated bees, facilitating entry into susceptible colonies. This reduction was associated with a shift in cuticular hydrocarbons, the chemical signatures used by bees to discriminate colony members from intruders. These responses were specific to IAPV infection, suggestive of pathogen manipulation of the host. Emerging bee pathogens may thus shape host phenotypes to increase transmission, a strategy especially well-suited to the unnaturally high colony densities of modern apiculture. These findings demonstrate how anthropogenic changes could affect arms races between human-managed hosts and their pathogens to potentially affect global food security.