Abstract
From a strain carrying spoIIA69, a mutation giving rise to asporogeny, a revertant was isolated which sporulated at about 10-2 of the wild-type frequency but in which the time-course of sporulation was much protracted. Genetic analysis of this revertant showed that it retained spoIIA69 but had acquired a secondary mutation sas. Sas failed to suppress mutations in spoIID, spoIIE or spoIIG; it also failed to suppress another mutation in the spoIIA locus. Sas is extremely closely linked (recombination frequency .ltoreq. 1%) with the mutation, spoIIA69, that is specifically suppresses. Strains carrying sas alone sporulated at a frequency at least 2 orders of magnitude below that in the spoIIA sas double mutant. Apparently, spoIIA69 and sas lead to compensating amino acid changes in the protein specified by the spoIIA locus.