Large Surface Blebs on Escherichia coli Heated to Inactivating Temperatures

Scheie, Paul; Ehrenspeck, Susan

doi:10.1128/jb.114.2.814-818.1973

Cited by 20 publications

(10 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…No substantial death was detected 15 s after heating, in spite of the formation of visible blebs on 11% of the total cells. This seems to show that the bleb formation itself is not the direct cause of thermal death, in contrast to the proposal of Scheie and Ehrenspeck (35). Although Hitchener and Egan (13) also suggested that outer membrane damage does not contribute to the thermal death of E. coli, further studies are required to elucidate the relation of the outer membrane damage to bacterial death due to heat.…”

Section: Fig 5 Sucrose Gradient Centrifugation Of Mem-contrasting

confidence: 56%

“…According to de Petris (6), who studied the ultrastructure of Escherichia coli envelopes, electron micrographs of heated E. coli B cells at extremely high temperatures (75 to 100°C) indicated the formation of large blebs of the outer membrane. Scheie and Ehrenspeck (35) observed blebs with E. coli B/r and B,_1 under more mild heat stress (49 to 55°C) by using phase contrast microscopy and suggested that the bleb formation was closely related to the thermal death of cells, although they provided no direct evidence of damage to the outer membrane.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Heat-induced blebbing and vesiculation of the outer membrane of Escherichia coli

Katsui¹,

Tsuchido²,

Hiramatsu³

et al. 1982

J Bacteriol

139

View full text Add to dashboard Cite

Thermal damage to the outer membrane of Escherichia coli W3110 was studied. When E. coli cells were heated at 55°C in 50 mM Tris-hydrochloride buffer at pH 8.0, surface blebs were formed on the cell envelope, mainly at the septa of dividing cells. Membrane lipids were released from the cells during the heating period, and part of the released lipids formed vesicle-like structures from the membrane. This vesicle fraction had a lipopolysaccharide to phospholipid ratio similar to that of the outer membrane of intact cells, whereas it had a lower content of protein than the isolated outer membrane. After heating bacterial cells at 55°C for 30 min, the resulting leakage from the cells of a periplasmic enzyme, alkaline phosphatase, amounted to 52% of the total activity, whereas no release of a cytoplasmic enzyme, glucose-6-phosphate dehydrogenase, was detected. The results obtained suggest that surface blebs formed by heat treatment almost completely consist of the outer membrane and that the blebs may be gradually released from the cell surface into the heating menstruum to partially form vesicles.

show abstract

Section: Fig 5 Sucrose Gradient Centrifugation Of Mem-contrasting

confidence: 56%

mentioning

confidence: 99%

Heat-induced blebbing and vesiculation of the outer membrane of Escherichia coli

Katsui¹,

Tsuchido²,

Hiramatsu³

et al. 1982

J Bacteriol

139

View full text Add to dashboard Cite

show abstract

“…Heat can damage protein, lipids, and nucleic acids and destabilize membranes (8,10). However, heat induces primarily blebbing and vesiculation of the outer membrane, leading to bacterial cell inactivation, and consequently increases its permeability to hydrophobic compounds (22,26). Heating-induced membrane destabilization sequentially initiates indirect DNA damage as a consequence of increased nuclease activity in bacteria and is often the critical injury, resulting in death of the cell (7,8,11,23).…”

Section: Discussionmentioning

confidence: 99%

Mechanism by which gamma irradiation increases the sensitivity of Salmonella typhimurium ATCC 14028 to heat

Kim

Thayer

1996

Appl Environ Microbiol

View full text Add to dashboard Cite

Effects of irradiation and heating on survival of Salmonella typhimurium ATCC 14028 were examined by measuring DNA damage and the integrity of the cytoplasmic membrane. S. typhimurium cells fell into two distinct groups following heating: (i) heat-sensitive cells, which were rapidly inactivated at 65؇C and (ii) heat-resistant cells, which were only slowly inactivated at 65؇C. Radiation sensitivity of S. typhimurium was greater in the presence of air than in the presence of N 2 gas (radiation doses required to inactivate 90% of the cells, 0.394 ؎ 0.029 in air and 0.561 ؎ 0.035 in N 2). Recovery of the covalently closed circular form of plasmid pBR322 from S. typhimurium transformants (Amp r Tet r) was decreased by irradiation but not by heating. Heating prior to irradiation significantly decreased the recovery of plasmid DNA without affecting survival of S. typhimurium. Transformability of the recovered plasmid pBR322 was affected by neither irradiation nor heating, and mutation of antibiotic resistance genes was not detected in S. typhimurium. Heating, but not irradiation, caused destabilization of the cytoplasmic membrane, allowing penetration of hydrophobic dye. These results suggest that lethality of heating followed by irradiation for S. typhimurium was additive, reflecting irradiation-induced DNA damage and heat-induced membrane destabilization. When irradiation preceded heating in the absence of air, more cells were inactivated than was expected, because of heat-inactivating radiation-damaged DNA.

show abstract

“…It has been suggested that heat principally affects the DNA by inducing the action of exo-and endonucleases resulting in multi-strand breaks in the DNA [204,205]. In E. coli, the effect of heat has been suggested to result in the denaturation of the cell wall leaving the peptidoglycan layer weakened at one or two points after which the plasma membrane ruptures [206]. Some association of proteins with the nucleoids also occurs as a result of mild heat treatment [207].…”

Section: Microbial Deathmentioning

confidence: 99%