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Social hierarchy

ABSTRACT: social hierarchy Raw sequence reads

PROVIDER: PRJNA1108947 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR28974008_1.fastq.gz	Fastqsanger.gz
	SRR28974008_2.fastq.gz	Fastqsanger.gz
	SRR28974009_1.fastq.gz	Fastqsanger.gz
	SRR28974009_2.fastq.gz	Fastqsanger.gz
	SRR28974010_1.fastq.gz	Fastqsanger.gz

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Distinct prefrontal projections oppositely orchestrate social competition and hierarchy

Project description:The medial prefrontal cortex (mPFC) is known as a hub of social hierarchy determination in the brain, Using high throughput single cell transcriptomic analysis and projection-specific genetic manipulation, we discovered that the expression level of Pou3f1 in mPFC-VTA neurons controls social hierarchy.

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Project description:Many animal groups are organized hierarchically, which generates behavioral states that facilitate social interactions. Although generally stable, social status can change, underscoring the plasticity of underlying neural circuits. We examined competition among unfamiliar male mice and uncovered how the molecular and biophysical characteristics of a forebrain-thalamocortical circuit affect hierarchy. We identify the mediodorsal thalamus (MDT) as a hub receiving inputs from orbitofrontal cortex and basal forebrain and projecting to caudal anterior cingulate cortex (cACC) to regulate competitive performance. This circuit becomes potentiated or depressed in high- and low-rank males, respectively, in part through altered expression of the voltage-gated ion channel Trpm3 and synaptic plasticity. In high-rank mice, MDT projections drive inhibition of cACC pyramidal cells, promoting winning, in a pattern strikingly opposite to dorsomedial prefrontal cortex, where winners display increased pyramidal cell activity. Our data suggests a model in which hierarchy modulation relies on coordinated remodeling of multiple forebrain-thalamocortical circuits.

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Project description:Distinct prefrontal projections oppositely orchestrate social competition and hierarchy

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Project description:Appropriately responding to stressful events is important for maintaining health and well-being of an organism. With respect to social stress, the response is not always as straightforward as reacting to physical stressors, e.g. extreme heat, and thus has to be balanced subtly. Particularly, regulatory mechanisms contributing to gaining resilience in the face of mild social stress are not fully deciphered yet. We employed an intrinsic social hierarchy stress paradigm in mice of both sex to identify key factors for coping strategies. While global transcriptomic changes could not be observed in male mice, several genes which were previously reported to be involved in synaptic plasticity, learning and anxiety-like behavior were differentially regulated in female mice. Moreover, changes in N6-methyladenosine-modification of mRNA associated with corticosterone level occurred. Further investigation of proteins involved in m6A modification revealed that no significant changes of amount or activity could be detected for male mice. However, METTL3 and WTAP, subunits of the methyltransferase complex, showed elevated levels in female mice. N6-adenosyl-methylation is the most prominent type of mRNA methylation and plays a crucial role in processes such as metabolism, but also response to physical stress. Our findings underpin its important role by attributing it also to social stress evoked by hierarchy building within same-sex groups.

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Project description:Social experiences are an important predictor of disease susceptibility and survival in humans and other social mammals. Chronic social stress is thought to generate a pro-inflammatory state characterized by elevated antibacterial defenses and reduced investment in antiviral defense. Here, we manipulated long-term social status in female rhesus macaques to show that social subordination alters the gene expression response to ex vivo bacterial and viral challenge. As predicted by current models, bacterial lipopolysaccharide polarizes the immune response such that low status corresponds to higher expression of genes in NF-κB dependent pro-inflammatory pathways and lower expression of genes involved in the antiviral response and type I interferon (IFN) signaling (see Snyder-Mackler et al. Science, 2016 doi:10.1126/science.aah3580 and GSE83304). Here we show that, counter to predictions, low status drives more exaggerated expression of both NF-κB and IFN-associated genes after cells are exposed to the viral mimic Gardiquimod. Status-driven gene expression patterns are not only linked to social status at the time of sampling, but also to social history (i.e., past social status), especially in unstimulated cells. However, for a subset of genes, we observed interaction effects in which females who fell in rank were more strongly affected by current social status than those who climbed the social hierarchy. Together, our results indicate that the effects of social status on immune cell gene expression depend on pathogen exposure, pathogen type, and social history – in support of social experience-mediated biological embedding in adulthood, even in the conventionally memory-less innate immune system.

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