Ontology highlight
ABSTRACT:
PROVIDER: PRJNA967220 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24496400_1.fastq.gz | Fastqsanger.gz | |||
| SRR24496400_2.fastq.gz | Fastqsanger.gz | |||
| SRR24496500_1.fastq.gz | Fastqsanger.gz | |||
| SRR24496500_2.fastq.gz | Fastqsanger.gz | |||
| SRR24496600_1.fastq.gz | Fastqsanger.gz |
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Project description:Social network position is a major predictor of ant behaviour, microbiota composition, and brain gene expression
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2018-05-23 | GSE114702 | GEO
Project description:Genes not only control traits of their carrier organism (known as Direct Genetic Effects or DGEs) but also shape their carrier's physical environment and the phenotypes of their carrier's social partners (known as Indirect Genetic Effects or IGEs). Theoretical research has shown that the effects that genes exert on social partners can have profound consequences, potentially altering heritability and the direction of trait evolution. Complementary empirical research has shown that in various contexts (particularly in animal agriculture) IGEs can explain a large proportion of variation in specific traits. However, little is known about the general prevalence of IGEs. We conducted a reciprocal cross-fostering experiment with two genetic lineages of the clonal raider ant Ooceraea biroi to quantify the relative contribution of DGEs and IGEs to variation in brain gene expression (which underlies behavioral variation). We find that thousands of genes are differentially expressed by DGEs but not a single gene is differentially expressed by IGEs. This is surprising given the highly social context of ant colonies and given that individual behavior varies according to the genotypic composition of the social environment in O. biroi. Overall, these findings indicate that we have a lot to learn about how the magnitude of IGEs varies across species and contexts.
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Project description:Copy number variations (CNVs) of the human 16p11.2 locus are associated with several developmental/neurocognitive syndromes. Particularly, deletion and duplication of this genetic interval are found in patients with autism spectrum disorders, intellectual disability and other psychiatric traits. The high gene density associated with the region and the strong phenotypic variability of incomplete penetrance, make the study of the 16p11.2 syndromes extremely complex. To systematically study the effect of 16p11.2 CNVs and identify candidate genes and molecular mechanisms involved in the pathophysiology, mouse models were generated previously and showed learning and memory, and to some extent social deficits. To go further in understanding the social deficits caused by 16p11.2 syndromes, we engineered deletion and duplication of the homologous region to the human 16p11.2 genetic interval in two rat outbred strains, Sprague Dawley (SD) and Long Evans (LE). The 16p11.2 rat models displayed convergent defects in social behaviour and only a few cognitive defects. Interestingly major pathways affecting MAPK3 and CUL3 were found altered in the rat 16p11.2 models with additional changes in males compared to females. Altogether, the consequences of the 16p11.2 genetic region dosage on social behaviour are now found in three different species: humans, mice and rats. In addition, the rat models pointed to sexual dimorphism, with lower severity of phenotypes in rat females compared to male mutants. This phenomenon is also observed in humans. We are convinced that the two rat models will be key to further investigating social behaviour and understanding the brain mechanisms and specific brain regions that are key to controlling social behaviour.
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