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The present study confirms the view that the membrane is a critical target in pressure inactivation but also suggests that there are fundamental differences in the role of the cell membrane in determining the pressure resistance of exponential- and stationary-phase cells. NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. Find NCBI SARS-CoV-2 literature, sequence, and clinical content: https://www.ncbi.nlm.nih.gov/sars-cov-2/. This is consistent with the observations of Mejía et al. Fatty acid composition of exponential-phase cells of E. coli NCTC 8164 grown at different temperatures, Fatty acid composition of stationary-phase cells of E. coli NCTC 8164 grown at different temperatures. ASM journals are the most prominent publications in the field, delivering up-to-date and authoritative coverage of both basic and clinical microbiology. "Phase Transitions in Lipid Bilayers". 5). The extent of fluidity can be determined by the membrane's melting temperature. This results in the formation of patches of long, saturated, gel-phase lipids in the membrane. The position of the peak maximum (Tm) on the temperature axis indicates the temperature at which the excess specific heat absorbed by the system is at a maximum. This weakens inter-lipid Van der Waals interactions, and lowers the Tm of the lipid. In the case of exponential-phase cells, we believe that membrane fluidity is the dominant factor affecting pressure resistance, so resistance increases under all conditions where the membrane is more fluid, i.e., with decreasing growth temperature and with increasing treatment temperature (up to the optimum). Have questions or comments? Quantitative analysis of the results suggests that ATPase is reversibly inactivated when its vicinal lipids undergo a transition to a state of reduced plasticity at low temperatures. The result is a “liquid ordered phase” with solid-like qualities similar to the gel phase without sacrificing the high rate of lateral diffusion attainable in the liquid-disordered phase. Pressure may be envisioned to have an irreversible effect on membrane proteins in one of two ways: either the proteins could be denatured in situ or they might be squeezed out of the membrane as a result of closer packing of membrane phospholipids. If enough other exposed proteins are nearby, this can result in a hydrophobic effect-mediated protein aggregation event, as displayed in, Factors Affecting Lipid Phase Transitions. The relationship between membrane damage and loss of viability following pressure treatment has previously been examined in strains of E. coli O157 that had inherent differences in their resistance to pressure (5, 32). Longer fatty acid chains have higher surface areas than smaller ones, resulting in stronger Van der Waals interactions between long lipid chains. Rev. If enough other exposed proteins are nearby, this can result in a hydrophobic effect-mediated protein aggregation event, as displayed in Figure \(\PageIndex{8}\). Biological membranes are primarily composed of phospholipids—a diverse class of compounds composed of a hydrophilic head group covalently attached to a pair of hydrophobic fatty acids. May, 2012. (4) used microscopy to examine the effect of pressure on vesicles composed of egg yolk phosphatidylcholine. Biophysical Journal. The liquid disordered phase, as its name implies, is a highly fluid state in which individual lipids can move laterally across the surface of the membrane relatively unhindered. (28) found that the pressure resistance of exponential-phase cells of several psychrotrophic bacteria was less when the cells were grown at 30°C than when they were grown at 8°C, whereas the reverse was true of stationary-phase cells; in addition, Ulmer et al. Tg + 3.60 (R2 = 0.97) (for stationary-phase cells), where Tg is the growth temperature. Growth temperature and membrane fatty acid composition. 1989 Feb;21(1):77-91. doi: 10.1007/BF00762213. Scheve, Christine S., Paul A. Gonzales, Noor Momin, and Jeanne C. Stachowiak. (a) Exponential-phase cells were grown at 10°C in TSB and pressure treated at 10°C (♦), 20°C (▴), or 30°C (□). J Bioenerg Biomembr. "L β ′ → L C ′ Phase Transition in Phosphatidylcholine Lipid Bilayers: A Disorder-order Transition in Two Dimensions." 7, pressure resistance in both exponential- and stationary-phase cells increased with increasing temperatures of pressure treatment (between 10 and ca. Cholesterol is not found in E. coli, but other factors might affect membrane responses to pressure. DSC heating profiles for aqueous suspensions of lipids extracted from whole cells of E. coli NCTC 8164 grown in TSB to stationary phase at 20°C (a) and 37°C (b). The growth temperatures were chosen to produce cells with large differences in membrane fatty acid composition, i.e., 10°C for exponential-phase cells and 37°C for stationary-phase cells. It is also possible that despite sonication in buffer, the phospholipids in our preparations were not fully hydrated, which would also have increased their melting temperature. The reason why more-fluid membranes are less susceptible to pressure damage is not immediately obvious. J. Copyright © 2020 American Society for Microbiology | Privacy Policy | Website feedback, Print ISSN: 0099-2240; Online ISSN: 1098-5336, School of Food Biosciences, University of Reading, Whiteknights, Reading RG6 6AP, United Kingdom, Role of Membrane Fluidity in Pressure Resistance of, Sign In to Email Alerts with your Email Address. The effects of membrane lipid fluidity and phase state on enzyme activity were evaluated by careful analysis of Arrhenius plots of the Na+, Mg2+-dependent adenosine triphosphatase (referred to hereafter as ATPase) from Acholeplasma laidlawii B membranes and differential thermal analysis of the membrane lipid phase transitions. J Bacteriol. This transition is driven by the conversion of the bulk membrane lipid phase to the gel state, but it is less cooperative and occurs at lower temperatures than the bulk lipid transition. The decrease in pressure resistance of exponential-phase cells that occurred with increasing growth temperature is in agreement with the observations of Smelt et al. Such gaps can allow cytoplasmic contents to leak out of the cell until they are plugged via lateral diffusion of neighboring lipids. This leads to increasing Tm’s with increasing chain length, as shown in Figure \(\PageIndex{1}\). The inclusion of cholesterol suppressed the initial volume decrease and prevented loss of material during decompression. With regard to temperatures below the optimum, we suggest that treatment temperature affects membrane fluidity and pressure resistance in exponential- and stationary-phase cells in a similar way. It would be of obvious interest to examine whether displacement of proteins was affected by the initial fluidity of the membrane. This leads to increasing Tm’s with increasing chain length, as shown in, Phase separation between lipids surrounding integral membrane proteins can briefly expose the hydrophobic residues of the middle of the protein to water. In stationary-phase cells, an unexpected and more complex picture emerged. High local concentrations of membrane-associated proteins can decrease the Tm of sections of membrane through steric interactions between crowded proteins. For symmetrical peaks, this corresponds to the phase transition temperature at which 50% of the lipids are in the liquid crystalline state. Proc Natl Acad Sci U S A. Journal of Microbiology & Biology Education, Microbiology and Molecular Biology Reviews. Our results are in agreement with this but showed for the first time that the difference in pressure resistance between exponential- and stationary-phase cells varies widely depending on growth temperature. E: 4446-449. Legal. The Tm was directly related to the growth temperature (Fig. Interpretation of the interrelationships among growth temperature, growth phase, and temperature of pressurization.Based on the results presented here and those previously reported by others, we propose the following interpretation of the effect of the interrelationships among growth temperature, growth phase, treatment temperature, and membrane fluidity on microbial pressure resistance.

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