Gli2 Conditional Knockout mouse models

Gli2, the mouse ortholog of human GLI2, encodes the principal transcriptional activator of Hedgehog signaling, a zinc finger protein bearing an amino-terminal repressor domain, a Sufu-binding region, and carboxy-terminal transactivation sequences; unlike Gli3, it is only inefficiently processed into a repressor form, and its activity is set by PKA-primed GSK3 and CK1 phosphorylation, Spop-directed degradation, and Kif7-dependent trafficking within the primary cilium. Homozygous nulls die perinatally with cleft palate, skeletal and vertebral defects, and lung and foregut abnormalities, so tissue-restricted floxed alleles are the practical route for postnatal or organ-specific questions. A conditional null asks whether a lineage requires activator output, an amino-terminally truncated constitutively active knockin asks whether GLI2 output alone drives proliferation or tumor initiation, and degron-resistant variants isolate turnover from transcription. Gli1 and Gli3 partially buffer loss, arguing for compound alleles, and a well-characterized Cre with confirmed recombination efficiency matters as much as the flox itself.

Conditional deletion of Gli2 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 Gli2 floxed stock yields usable cohorts.