Changes in gene expression profiling in the prefrontal cortex from mice lacking glutaminase 1 in CamKIIa-positive neurons

Autism spectrum disorder (ASD) is a heterogeneous group of disorders with shared diagnostic phenotypes, such as reduced interest in social interaction and communication, and increased stereotyped or restricted interests and behaviors. Little is known about the involvement of alterations of glutaminase 1 (Gls1, an enzyme that catalyzes the hydrolysis of glutamine into glutamate) in the pathogenesis of ASD. To investigate the role of Gls1 in forebrain neurons , we generated conditional mouse mutants with loss of Gls1 in forebrain CamKIIα-Cre positive neurons by crossing Gls1flox/flox mice with CamKIIαcre mice. Conditional mouse mutants with loss of Gls1 in forebrain CamKIIα-Cre positive neurons were generated by crossing Gls1flox/flox mice with CamKIIαcre mice. Mosaic homozygous Gls1 mutant (CamKIIαCre;Gls1flox/flox) mice were not viable. Only mosaic heterozygous Gls1 mice (CamKIIαCre;Gls1+/flox mice, referred to as Gls1_CamKIIαCre mice) and their littermate CamKIIαCre;Gls1+/+ mice (referred to as control mice) were used in this study. The prefrontal cortex from 3 Gls1_CamkIIaCre mice and 3 control mice were isolated for RNA seq and for comparative gene expression profiling analysis.