The Bacillus subtilis mutant cal1 carries a non-reverting mutation in ribosomal protein L17 (r-protein L17) that causes both resistance to the antibiotic chalcomycin (Calr) and temperature-sensitive sporulation (Spots). Second-site suppressor (rev) mutations that relieve the Spots phenotype have been isolated from cal1. Three suppressor mutations - rev4, rev10, rev11 - each increase the sporulation frequency of cal1 at the non-permissive temperature from 3% to 95% of the wild-type level. The cal1 rev strains remain resistant to chalcomycin and two-dimensional gel electrophoresis analysis indicates that they contain the same altered r-protein L17 as the original cal1 strain and no additional altered r-proteins. The three rev mutations have been mapped at a single locus between narA and sacA on the B. subtilis chromosome and recombination indexes for the rev mutations indicate that they are tightly linked to one another. Antibiotic resistance Spots mutations that cause temperature-sensitive sporulation have previously been isolated in RNA polymerase, in the 30S and 50S subunits of the ribosome, and in elongation factor G. The rev4, 10, and 11 suppressor mutations are non-specific in their action in that they restore significant levels of sporulation at the non-permissive temperature in all of the Spots strains that we have tested. This result suggests that Spots mutations in components of the B. subtilis transcription and translation systems share a common molecular basis for their sporulation-defective phenotypes.