title: Effect of inhibition of deoxyribonucleic acid and protein synthesis on the direction of cell wall growth in Streptococcus faecalis.
abstract: Selective inhibition of protein synthesis in Streptococcus faecalis (ATCC 9790) was accompanied by a rapid and severe inhibition of cell division and a reduction of enlargement of cellular surface area. Continued synthesis of cell wall polymers resulted in rapid thickening of the wall to an extent not seen in exponential-phase populations. Thus, the normal direction of wall growth was changed from a preferential feeding out of new wall surface to that of thickening existing cell surfaces. However, the overall manner in which the wall thickened, from nascent septa toward polar regions, was the same in both exponential-phase and inhibited populations. In contrast, selective inhibition of deoxyribonucleic acid (DNA) synthesis using mitomycin C was accompanied by an increase in cellular surface area and by division of about 80% of the cells in random populations. Little or no wall thickening was observed until the synthesis of macromolecules other than DNA was impaired and further cell division ceased. Concomitant inhibition of both DNA and protein synthesis inhibited cell division but permitted an increase in average cell volume. In such doubly inhibited cells, walls thickened less than in cells inhibited for protein synthesis only. On the basis of the results obtained, a model for cell surface enlargement and cell division is presented. The model proposes that: (i) each wall enlargement site is influenced by an individual chromosome replication cycle; (ii) during chromosome replication peripheral surface enlargement would be favored over thickening (or septation); (iii) a signal associated with chromosome termination would favor thickening (and septation) at the expense of surface enlargement; and (iv) a factor or signal related to protein synthesis would be required for one or more of the near terminal stages of cell division or cell separation, or both.
mesh_terms: D001374:Azacitidine / Q000494:pharmacology; D001426:Bacterial Proteins / Q000096:biosynthesis*; D002250:Carbon Radioisotopes; D002455:Cell Division; D002473:Cell Wall / Q000378:metabolism*; D002701:Chloramphenicol / Q000494:pharmacology; D002876:Chromosomes, Bacterial; D004269:DNA, Bacterial / Q000096:biosynthesis*; D003609:Dactinomycin / Q000494:pharmacology; D013293:Enterococcus faecalis / Q000166:cytology* / Q000254:growth & development / Q000378:metabolism; D008854:Microscopy, Electron; D008937:Mitomycins / Q000494:pharmacology; D008954:Models, Biological; D010457:Peptidoglycan / Q000096:biosynthesis; D011135:Polysaccharides, Bacterial / Q000096:biosynthesis; D012329:RNA, Bacterial / Q000096:biosynthesis; D012293:Rifampin / Q000494:pharmacology; D014316:Tritium
chemical_list: D001426:Bacterial Proteins; D002250:Carbon Radioisotopes; D004269:DNA, Bacterial; D008937:Mitomycins; D010457:Peptidoglycan; D011135:Polysaccharides, Bacterial; D012329:RNA, Bacterial; D014316:Tritium; D003609:Dactinomycin; D002701:Chloramphenicol; D001374:Azacitidine; D012293:Rifampin