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Citation |
Malki K, Tosto MG, Pain O, Sluyter F, Mineur YS, Crusio WE, de Boer S, Sandnabba KN, Kesserwani J, Robinson E, Schalkwyk LC, Asherson P. Am. J. Med. Genet. B Neuropsychiatr. Genet. 2016; 171(3): 427-436. |
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Affiliation |
King's College London, MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, London, United Kingdom. |
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Copyright |
(Copyright © 2016, John Wiley and Sons) |
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DOI |
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PMID |
26888158 |
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Abstract |
Mouse models of aggression have traditionally compared strains, most notably BALB/cJ and C57BL/6. However, these strains were not designed to study aggression despite differences in aggression-related traits and distinct reactivity to stress. This study evaluated expression of genes differentially regulated in a stress (behavioral) mouse model of aggression with those from a recent genetic mouse model aggression. The study used a discovery-replication design using two independent mRNA studies from mouse brain tissue. The discovery study identified strain (BALB/cJ and C57BL/6J) × stress (chronic mild stress or control) interactions. Probe sets differentially regulated in the discovery set were intersected with those uncovered in the replication study, which evaluated differences between high and low aggressive animals from three strains specifically bred to study aggression. Network analysis was conducted on overlapping genes uncovered across both studies. A significant overlap was found with the genetic mouse study sharing 1,916 probe sets with the stress model. Fifty-one probe sets were found to be strongly dysregulated across both studies mapping to 50 known genes. Network analysis revealed two plausible pathways including one centered on the UBC gene hub which encodes ubiquitin, a protein well-known for protein degradation, and another on P38 MAPK. Language: en |