Regulation of competence for genetic transformation in Streptococcus pneumoniae involves the comAB locus and a small extracellular
protein, the competence factor (CF). The
comA or comB mutations block both spontaneous competence induction and elaboration of CF, yet permit induction of competence by added CF and subsequent transformation at normal levels. Sequence and genetic studies showed that the com locus comprised the
comA and comB genes, encoding 77- and 50-kDa
proteins, respectively, and demonstrated that they were closely flanked by genes and
DNA not required for competence regulation. In-frame deletion of
comA demonstrated that the translation product of this gene is required for normal competence regulation; deletion-replacement mutations showed that no com gene lay in the 0.2-kb gap between comB and purC or within 2.5 kb upstream from
comA. Strong sequence similarities (51-59% identities) showed that
ComA and the
proteins, PdcD and LcnC, which act in the secretion of
pediocin A-1 and
lactococcin A, respectively, form a subfamily within the large
ABC-transporter protein family. ComB was found to be homologous to a single known
protein, LcnD, required for secretion of the
peptide antibiotic lactococcin A. Thus, the comAB locus displays homology to two
lactococcin A secretion genes, but is devoid of additional linked com genes. The results suggest that the mechanism for CF production is similar to that for the small
peptide bacteriocins,
lactococcin A and
pediocin A-1, but that its genetic organization is unusual in being split into at least two separate operons.