C1qa Conditional Knockout mouse models

C1qa encodes the A chain of C1q, ortholog of human C1QA, contributing one of the three collagen-like stalks and globular gC1q heads that assemble with C1QB and C1QC into the hexameric bouquet recognizing IgG and IgM Fc, pentraxins, and exposed phosphatidylserine on apoptotic cells and synapses. Head engagement induces a conformational change in the collagenous arms that activates the associated C1r2C1s2 tetramer, cleaving C4 and C2 to build the classical pathway C3 convertase, while C1q deposited on synapses licenses CR3-dependent microglial pruning and drives complement-mediated synapse loss in neurodegeneration models. Critically, the three chains are not redundant: loss of C1qa destabilizes the entire molecule, producing functional C1q deficiency with impaired apoptotic clearance and lupus-like autoimmunity. Conditional deletion distinguishes microglial from hepatic and macrophage sources, and humanization is worth the effort only when an anti-C1q antibody or classical pathway inhibitor with human-restricted binding is the endpoint.

Conditional deletion of C1qa 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 C1qa floxed stock yields usable cohorts.