Relationship of growth temperature and thermotropic lipid phase changes in cytoplasmic and outer membranes from Escherichia coli K12

Janoff, Andrew S.; Haug, A.; McGroarty, Estelle J.

doi:10.1016/0005-2736(79)90071-3

Cited by 62 publications

(19 citation statements)

References 38 publications

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“…We believe that this more fluid domain corresponds to the external leaflet of the cell wall, as defined in our model (see Discussion). When spin-labeled fatty acids are added to structures containing domains of different degrees of fluidity-for example, the outer membrane of Gram-negative bacteria (14)-they become inserted nearly exclusively into the most fluid domain, as can be seen from the observation that the fluidity reported by such probes (15,16) is fairly close to that of the fluid phospholipid domain (13,16) and very far away from that of the much less fluid lipopolysaccharide domain (13,16). We have shown, furthermore, that 5-SASL added to intact M. chelonae cells produced ESR spectra of a similar 2T11 value as that added to the isolated cell wall (Fig.…”

Section: Resultsmentioning

confidence: 93%

“…There is, indeed, a precedent for the last interpretation. Thus, 5-SASL inserted into the presumably more fluid phospholipid leaflet of the bacterial outer membrane reports fluidity values (15,16) slightly lower than that inserted into phospholipid bilayer (13,16), possibly because of the immobilizing effect of the less fluid lipopolysaccharide leaflet.…”

Section: Discussionmentioning

confidence: 99%

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Fluidity of the lipid domain of cell wall from Mycobacterium chelonae.

Liu

Rosenberg²,

Nikaido³

1995

Proc. Natl. Acad. Sci. U.S.A.

134

118

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The mycobacterial cell wall contains large amounts of unusual lipids, including mycolic acids that are covalently linked to the underlying arabinogalactanpeptidoglycan complex. Hydrocarbon chains of much of these lipids have been shown to be packed in a direction perpendicular to the plane of the cell surface. In this study we examined the dynamic properties of the organized lipid domains in the cell wall isolated from Mycobacterium chelonae grown at 30°C. Differential scanning calorimetry showed that much of the lipids underwent major thermal transitions between 30°C and 65°C, that is at temperatures above the growth temperature, a result suggesting that a significant portion of the lipids existed in a structure of extremely low fluidity in the growing cells. Spin-labeled fatty acid probes were successfully inserted into the more fluid part of the cell wall. Our model of the cell wall suggests that this domain corresponds to the outermost leaflet, a conclusion reinforced by the observation that labeling of intact cells produced electron spin resonance spectra similar to those of the isolated cell wall. Use of stearate labeled at different positions showed that the fluidity within the outer leaflet increased only slightly as the nitroxide group was placed farther away from the surface. These results are consistent with the model of mycobacterial cell wall containing an asymmetric lipid bilayer, with an internal, less fluid mycolic acid leaflet and an external, more fluid leaflet composed of lipids containing shorter chain fatty acids. The presence of the low-fluidity layer will lower the permeability of the cell wall to lipophilic antibiotics and chemotherapeutic agents and may contribute to the well-known intrinsic resistance of mycobacteria to such compounds.Mycobacterium tuberculosis causes tuberculosis, a disease that kills 3 million people a year mostly in developing countries. In industrialized countries, the appearance of multiple-drugresistant strains of M tuberculosis has made it once again a major public health problem (1). Furthermore, Mycobacterium leprae causes leprosy in >10 million people worldwide, and several Mycobacterium species, including M. avium complex, M. kansasii, M. fortuitum, and M. chelonae, cause opportunistic infections in immunologically compromised patients, such as AIDS patients. The treatment of mycobacterial infection is often difficult because these bacteria are intrinsically resistant to most common antibiotics and chemotherapeutic agents (2). This general resistance is thought to be related to the unusual structure of mycobacterial cell wall, which is located outside the cytoplasmic membrane yet contains large amounts of lipids, many of them with unusual structure. The major fraction of the cell wall is occupied by unusually long-chain fatty acids containing 70-90 carbons, the mycolic acids (3). The peptidoglycan, which contains N-glycolylmuramic acid instead of the usual N-acetylmuramic acid, is linked to arabinogalactan via a phosphodiester bridge. About 10% of the...

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Section: Resultsmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Fluidity of the lipid domain of cell wall from Mycobacterium chelonae.

Liu

Rosenberg²,

Nikaido³

1995

Proc. Natl. Acad. Sci. U.S.A.

134

118

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“…Further, the interactions between certain sHSPs and specific domains of membranes remodel the status of the MPS (overall phase state, lipid order, permeability, etc.) (21,22,31). There is evidence that in eukaryotes the role of HSP70 depends on its intracellular, membrane-bound, or extracellular location.…”

Section: Discussionmentioning

confidence: 99%

Genetic Modification of theSalmonellaMembrane Physical State Alters the Pattern of Heat Shock Response

et al. 2010

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It is now recognized that membranes are not simple physical barriers but represent a complex and dynamic environment that affects membrane protein structures and their functions. Recent data emphasize the role of membranes in sensing temperature changes, and it has been shown that the physical state of the plasma membrane influences the expression of a variety of genes such as heat shock genes. It has been widely shown that minor alterations in lipid membranes are critically involved in the conversion of signals from the environment to the transcriptional activation of heat shock genes. Previously, we have proposed that the composition, molecular arrangement, and physical state of lipid membranes and their organization have crucial roles in cellular responses during stress caused by physical and chemical factors as well as in pathological states. Here, we show that transformation of Salmonella enterica serovar Typhimurium LT2 (Salmonella Typhimurium) with a heterologous ⌬ 12 -desaturase (or with its trans-membrane regions) causes major changes in the pathogen's membrane dynamic. In addition, this pathogen is strongly impaired in the synthesis of major stress proteins (heat shock proteins) under heat shock. These data support the hypothesis that the perception of temperature in Salmonella is strictly controlled by membrane order and by a specific membrane lipid/protein ratio that ultimately causes transcriptional activation of heat shock genes. These results represent a previously unrecognized mode of sensing temperature variation used by this pathogen at the onset of infection.The heat shock response, one of the most studied cellular homeostatic mechanisms, is involved in the maintenance of cell functionality during stress (25, 60). The heat shock response is also elicited by pathogens at the onset of infection as a result of exposure to environmental stresses such as a heat shock or during macrophage infection (25,55). In addition, the heat shock response is severely altered as a result of several chronic diseases, cancer, apoptosis, and the aging process (3, 27, 45). The resulting protection from different types of stresses is due to the transcriptional activation of heat shock genes (29, 54). Further, moderate heat (or stress) treatment induces transient acquisition of thermotolerance, even in the absence of denatured proteins (40, 51), due to the accumulation of heat shock proteins (HSPs) (35). These proteins are not only essential under a variety of stress conditions, such as heat, drought, salinity, osmotic shock, membrane shearing, ischemia, etc. (11,23,55,67), but are also crucial under physiological conditions for protein folding, translocation, mRNA splicing, nucleic acid and protein syntheses, mitochondrial electron transport, and photosynthesis, for example (4,24,25,39). Members of the group of small HSPs (sHSPs) have also been shown to antagonize heat-induced membrane hyperfluidization and to stabilize the bilayer state under stress conditions (40,54,59).According to the conventional model, during s...

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“…This may be inferred from results obtained on microbial systems (Sinenski, 1974;Martin et al, 1981;Janoff et al, 1979;Dickens and Thompson, 1981), plants (Chapman et al, 1979;Furtado et al, 1979;Vigh et al, 1979Vigh et al, , 1986, Tetrahymena (Umeki et al, 1983), and some poikilothermic animals (Kallapur et al, 1982;Cossins, 1977;Farkas, 1984). Thus we may speculate that the seasonal occurrence or geographical distribution of different species is related to their ability to manipulate cell membranes in order to survive at a given temperature .…”

Section: Introductionmentioning

confidence: 87%

The fatty acid constitution and ordering state of membranes in dominant temperature-sensitive lethal mutation and wild-typeDrosophila melanogaster larvae

1990

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The ordering state and changes in fatty acid composition of microsomal (MS) and mitochondrial (MC) membranes of two dominant temperature-sensitive (DTS) lethal mutations and the wild-type Oregon-R strain larvae of Drosophila melanogaster have been studied at 18 and 29 degrees C and after temperature-shift experiments. The membranes of wild-type larvae have a stable ordering state, with "S" values between 0.6 (18 degrees C) and 0.5 (29 degrees C) in both membranes which remained unchanged in shift experiments, although the ratios of saturated/unsaturated fatty acids were changed as expected. The strongly DTS mutation 1(2) 10DTS forms very rigid membranes at the restrictive temperature (29 degrees C) which cannot be normalized after shift down, while shift up or development at the permissive temperature results in normal ordering state. This mutant is less able to adjust MS and MC fatty acid composition in response to the growth temperature than the wild type. The less temperature-sensitive 1(2)2DTS allele occupies an intermediate state between Oregon-R and 1(2)10DTS in both respects. We assume and the genetical data suggest that the DTS mutant gene product is in competition with the wild-type product, resulting in a membrane structure which is not able to accommodate to the restrictive temperature.

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Relationship of growth temperature and thermotropic lipid phase changes in cytoplasmic and outer membranes from Escherichia coli K12

Cited by 62 publications

References 38 publications

Fluidity of the lipid domain of cell wall from Mycobacterium chelonae.

Fluidity of the lipid domain of cell wall from Mycobacterium chelonae.

Genetic Modification of theSalmonellaMembrane Physical State Alters the Pattern of Heat Shock Response

The fatty acid constitution and ordering state of membranes in dominant temperature-sensitive lethal mutation and wild-typeDrosophila melanogaster larvae

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