Dlg1 Conditional Knockout mouse models

Dlg1, ortholog of human DLG1, encodes SAP97, a membrane-associated guanylate kinase built from three PDZ domains, an SH3 module and a catalytically inactive guanylate kinase domain, whose alternatively spliced N-terminal L27 or palmitoylated variants determine whether it acts in epithelial polarity with Scribble and Lgl or in neuronal receptor trafficking. In neurons it escorts GluA1 through the secretory pathway and binds Kv1.4 and the cardiac sodium channel Nav1.5, linking it to both synaptic delivery and excitability, while in epithelia it enforces basolateral identity and is a target of viral oncoproteins. Constitutive nulls die perinatally with cleft palate, urogenital and kidney defects, so a conditional null is mandatory for adult neural work; pair Camk2a-Cre for forebrain synapses or a cardiomyocyte driver for conduction endpoints. Dlg2, Dlg3 and Dlg4 share domain architecture and partially substitute at the postsynaptic density, so compound alleles and direct receptor surface measurements are advisable.

Conditional deletion of Dlg1 limits the genetic change to the lineage you choose. That helps in oncology, immunology, and metabolic work where systemic loss would muddy the read. After you confirm Cre specificity, crossing to Dlg1 floxed stock yields usable cohorts.