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Although gene-environment interactions are known to significantly influence psychopathology-related disease states, only few animal models cover both the genetic background and environmental manipulations. Therefore, we have taken advantage of the bidirectionally inbred high (HAB) and low (LAB) anxiety-related behavior mouse lines to generate HAB × LAB F1 hybrids that intrinsically carry both lines’ genetic characteristics, and subsequently raised them in three different environments—standard, enriched (EE) and chronic mild stress (CMS). Assessing genetic correlates of trait anxiety, we focused on two genes already known to play a role in HAB  vs.  LAB mice, corticotropin releasing hormone receptor type 1 ( Crhr1 ) and high mobility group nucleosomal binding domain 3 ( Hmgn3 ). While EE F1 mice showed decreased anxiety-related and increased explorative behaviors compared to controls, CMS sparked effects in the opposite direction. However, environmental treatments affected the expression of the two genes in distinct ways. Thus, while expression ratios of  Hmgn3  between the HAB- and LAB-specific alleles remained equal, total expression resembled the one observed in HAB  vs . LAB mice, i.e., decreased after EE and increased after CMS treatment. On the other hand, while total expression of  Crhr1  remained unchanged between the groups, the relative expression of HAB- and LAB-specific alleles showed a clear effect following the environmental modifications. Thus, the environmentally driven bidirectional shift of trait anxiety in this F1 model strongly correlated with  Hmgn3  expression, irrespective of allele-specific expression patterns that retained the proportions of basic differential HAB  vs.  LAB expression, making this gene a match for environment-induced modifications. An involvement of  Crhr1  in the bidirectional behavioral shift could, however, rather be due to different effects of the HAB- and LAB-specific alleles described here. Both candidate genes therefore deserve attention in the complex regulation of anxiety-related phenotypes including environment-mediated effects.

Environmental manipulations generate bidirectional shifts in both behavior and gene regulation in a crossbred mouse model of extremes in trait anxiety