Deletion of competence-induced genes over-expressed in biofilms caused transformation deficiencies in Streptococcus mutans.
Previous studies identified nine genes with increased expression in Streptococcus mutans biofilms of which six possessed putative ComX promoter sequences and were homologous to competence-induced genes in Streptococcus pneumoniae, Streptococcus gordonii and Bacillus subtilis. As competence increases in biofilms, a study was undertaken into the roles that these biofilm-induced genes might play in transformation. Only five of the nine gene deletions had a significant effect on transformation efficiency. Deletion of the genes for recombinase A, recA, DNA processing protein, dprA and single-stranded DNA-binding protein, ssbA, produced results comparable with those from other bacteria, supporting the contention that these proteins have similar functions in S. mutans competence. The uncharacterized genes SMU.769 and SMU.836 produced results in variance to deletion mutants of putative homologues in S. pneumoniae. Deletion of SMU.769 reduced chromosomal transformation 2.3-fold. SMU.769 belongs to a family of conserved genes induced by the competence-stimulating peptide and which have no established function. In contrast, deletion of SMU.836 reduced transformation of both plasmid and chromosomal DNA to <3%. Homology searches suggested that Smu.836 belongs to a family of competence-induced peptidoglycan hydrolases with a conserved enzyme domain and a species-variable cell-binding domain for which the best characterized member is the choline-binding protein D, CbpD, of S. pneumoniae.
Institute of Dental Research, Westmead Millennium Institute and Westmead Centre for Oral Health, Wentworthville, NSW, Australia.
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Eaton
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Jacques
D001412:Bacillus subtilis / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics*; D018441:Biofilms; D002876:Chromosomes, Bacterial / Q000235:genetics; D017124:Conserved Sequence / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics; D015252:Deoxyribonucleases, Type II Site-Specific / Q000235:genetics; D004926:Escherichia coli / Q000235:genetics; D017353:Gene Deletion; D015964:Gene Expression Regulation, Bacterial / Q000235:genetics; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics; D009154:Mutation / Q000235:genetics; D009238:N-Acetylmuramoyl-L-alanine Amidase / Q000235:genetics; D010957:Plasmids / Q000235:genetics; D053038:Quorum Sensing / Q000235:genetics; D011938:Rec A Recombinases / Q000235:genetics; D012689:Sequence Homology, Nucleic Acid; D013295:Streptococcus mutans / Q000235:genetics* / Q000502:physiology; D013296:Streptococcus pneumoniae / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics*; D014169:Transformation, Bacterial / Q000235:genetics
D001426:Bacterial Proteins; C093539:ComS protein, Bacillus subtilis; C120829:ComX protein, Streptococcus; D004268:DNA-Binding Proteins; C093815:DprA protein, bacteria; D008565:Membrane Proteins; D014157:Transcription Factors; C423628:competence factor, Streptococcus; D011938:Rec A Recombinases; D015252:Deoxyribonucleases, Type II Site-Specific; C024405:GATC-specific type II deoxyribonucleases; D009238:N-Acetylmuramoyl-L-alanine Amidase