Fan-shaped ejections of regularly arranged murosomes involved in penicillin-induced death of staphylococci

Abstract

Electron microscopic research into the murosomes of staphylococci has shown that the number of murosomes involved in penicillin-induced death varies depending on the experimental conditions employed. With 0.1 ,ug of penicillin G per ml, only 1 of a total of about 20 murosomes, the "killing murosome," completely perforated the pressure-stabilized peripheral cell wall during a three-step process. This strictly localized event was mainly attributed to a mechanical effect being comparable to the process of aneurysm formation. Wall perforation was also considered to mark the very moment of penicillin-induced death ("nonlytic killing event"), while bacteriolysis started only postmortem. By varying the osmolarity of the growth medium, the number of murosomes involved in penicillin-induced killing increased considerably, which resulted in the ejection of a fan-shaped row of murosomes at the second division plane. These data are compatible with the finding that, in untreated or chloramphenicol-treated staphylococci, the activation of the murosomes resulted in (i) the formation of regularly arranged "blebs" on the cell surface, containing traces of disintegrated wall material, and (ii) the subsequent liberation of the murosomes lying underneath, leaving behind their former sites in the peripheral wall as a row of regularly arranged "pores" in every division plane. The number, distribution, and positioning of these blebs corresponded with those of the pores and the original murosomes. The significance of wall autolysins liberated from the first division plane for penicillin-induced wall perforation at the second division plane is discussed.

Molecular Control of Bacterial Death and Lysis

“…Consistent with this is the observation that staphylococcal murein hydrolases specifically localize to the septa of a dividing cell (11,279). The activation of murein hydrolase activity and disruption of the cell wall in the presence of penicillin were also localized to the division planes in S. aureus (82,83), suggesting that murein hydrolase activity in this pathogen is not homogeneously distributed.…”

Mode of action of the lantibiotic mersacidin: inhibition of peptidoglycan biosynthesis via a novel mechanism?

“…In contrast to mersacidin, ␤-lactam antibiotics also induce morphological aberrations in staphylococci that are most obvious in the septal area (7). Comparison of the ultrastructures of mersacidin-and tunicamycin-treated cells as well as determination of the phosphate contents of purified cell walls showed that teichoic acid biosynthesis cannot be the primary target for mersacidin.…”

“…Similarities appeared after the incubation with vancomycin, but neither penicillin nor tunicamycin caused a reduction in the cell wall diameter. Unlike mersacidin, tunicamycin triggered the formation of an electron-lucent cell wall, and penicillin-treated cells possessed characteristically thickened septa, as reported by Giesbrecht et al (7). Since comparison with tunicamycin by electron microscopy pointed to peptidoglycan biosynthesis rather than teichoic acid biosynthesis as the primary target for mersacidin, the phosphate contents of purified cell walls of S. simulans 22 were determined as a measure of teichoic acid content.…”

Localized perforation of the cell wall by a major autolysin: atl gene products and the onset of penicillin-induced lysis of Staphylococcus aureus

“…Whether the mode of activation or deregulation of atl gene products at localized sites in PCG-treated cells is similar to that in normal cells remains to be studied. Giesbrecht and coworkers suggested that there are about 20 sites at the periphery of the division plane where murosomes erupt (3,4). During PCG-induced lysis, one or two eruptions of murosomes at nascent cross wall may cause initial perforation of the cell wall (4).…”