Answers are grounded in this paper and cite their sources.
In the model proposed by Brenner (1959) and Fincham (1960) to explain intra-cistronic (interallelic) complementation, monomer subunits derived from each of the mutated cistrons in the heterozygote interact in the same cytoplasm to form an active protein. This mechanism is based on the concept that proteins which can complement contain identical subunits and that mutationally altered monomers may sometimes form enzymatically active molecular hybrids. In the individual mutants these altered subunits are unable to produce active enzyme although they might form antigenically related protein (CRM).
No takes yet. Share an insight, caveat, or question.
Schlesinger et al. (1963) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: