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Behavioural Analysis of Congenic Mouse Strains Confirms Stress–Responsive Loci on Chromosomes 1 and 12

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Abstract

The way in which animals respond to stressful environments correlates with anxiety-related behaviour. To begin identifying the genetic factors that influence anxiety, we have studied the stress–responsiveness of inbred mouse strains using a modified form of the open field activity test (OFA), termed the elevated (e) OFA. In particular, two strains show high (DBA/2J) or low (C57BL/6J) stress–responsiveness in the eOFA. Genetic studies of an F2 intercross between these two strains previously identified two regions, on chromosomes (Chr) 1 and 12, linked to anxiety-related behaviour. To confirm that these regions contain loci for stress–responsiveness, we established separate congenic mouse strains for the linked Chr1 and Chr12 regions. Each congenic strain harbours a DBA/2J-derived interval encompassing the linked region on the C57BL/6J genetic background: the congenic intervals are between, but not including ∼48.6 Mb and ∼194.8 Mb on Chr1, and ∼36.2 Mb and the distal end of Chr12. Cohorts of DBA/2J, C57BL/6J and congenic mice were analysed for a series of stress–responsive phenotypes using the eOFA test. Both congenic strains had significantly different stress–responsive phenotypes compared to the low-stress C57BL/6J parental strain, but the DBA/2J-derived Chr12 interval had a greater genetic effect than the DBA/2J-derived Chr1 interval for changing the behavioral phenotype of the parental C57BL/6J mouse strain. These results confirmed the presence of stress–responsive loci on Chr1 and Chr12. New stress-related phenotypes were also identified, which aided in comparing and differentiating DBA/2J, C57BL/6J and congenic mice.

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Correspondence to M. Murphy.

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Edited by Tamara Phillips.

M. C. Jawahar and T. C. Brodnicki contributed equally to this study.

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Jawahar, M.C., Brodnicki, T.C., Quirk, F. et al. Behavioural Analysis of Congenic Mouse Strains Confirms Stress–Responsive Loci on Chromosomes 1 and 12. Behav Genet 38, 407–416 (2008). https://doi.org/10.1007/s10519-008-9206-3

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