A high-copy plasmid, pGA217, which carries a deletion (lacking the carboxy-terminal 20 amino acids) of the structural gene for ribosomal protein L10 (rplJ) is lethal to the cell in the absence of the gene (rplL) for r-proteins L7/L12, but only if the upstream operon for r-proteins L11 (rplK) and L1 (rplA) is present on the same plasmid. Measurements of beta-galactosidase activity of a hybrid protein expressed by a rplL-lacZ fusion indicated that the L10 fragment peptide which lacks the carboxy-terminal 20 amino acids is capable of exerting feedback regulation. Double transformation experiments with two compatible plasmids showed that the detrimental effect of the rplJ deletion on pGA217 can be reversed by the addition of a second plasmid which carries a functional gene for L7/L12. These two pieces of evidence suggest that the lethal effect of pGA217 is due to its property of feeding back on L7/L12 production from the chromosomal rplK gene. The upstream rplKA operon was inferred to have a cis-acting, stimulating effect on rplJ expression from the following evidence: (1) donor plasmids carrying the genes for L11 and/or L1 fail to exert a trans-acting effect, (2) deletion mutants which removed portions of rplK and/or rplA, but maintained the rplKA promoter, rplKp, still retained a severe growth-inhibiting effect. We suggest that these results can be explained by assuming that there is transcription from the rplKA promoter through rplJ and perhaps beyond.