C1qc Knockout mouse models

Encoding the C chain of C1q, mouse C1qc is the ortholog of human C1QC and completes the obligate ABC subunit whose globular head contributes to the recognition surface for IgG Fc, C-reactive protein, calreticulin, and apoptotic cell ligands, while its collagen-like domain participates in the interlocking stalk that transmits binding energy to the C1r2C1s2 protease tetramer. Human C1QC mutations cause hereditary C1q deficiency with severe early-onset systemic lupus erythematosus and recurrent encapsulated bacterial infection, a phenotype mapping directly onto complement-dependent handling of nucleosomal debris. Deletion in mouse removes assembled C1q rather than a single chain, so the null is a clean loss-of-function model, and because the three chains cannot compensate for one another, no compound genetics is needed. Point knockins of patient missense alleles are the right choice for studying assembly and secretion defects, while conditional nulls address whether locally synthesized C1q from microglia or tissue macrophages drives a given pathology.

C1qc null animals are straightforward to genotype and phenotype when survival is acceptable. They remain a standard background for pharmacology, biomarker, and rescue studies.