Lateral Phase Separation of Lipids in Plasma Membranes: Effect of Temperature on the Mobility of Membrane Antigens

Petit, Valérie; Edidin, Michael

doi:10.1126/science.184.4142.1183

Cited by 103 publications

(29 citation statements)

References 13 publications

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“…1 and 2 indicate that there is no phase transition in the lipid bilayer at the temperature range of 5-38'. Similar observations were reported for normal and transformed 3T3 cells (20) and for normal lymphocytes and malignant lymphoma cells (9), whereas phase separation was reported for mouse-human heterokaryons (21 (9). Another difference between the two systems is that the cells used in our study were grown in monolayers in a well-defined medium.…”

Section: Methodssupporting

confidence: 72%

Fluorescence polarization and viscosities of membrane lipids of 3T3 cells.

Fuchs¹,

Parola²,

Robbins³

et al. 1975

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

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Section: Methodssupporting

confidence: 72%

Fluorescence polarization and viscosities of membrane lipids of 3T3 cells.

Fuchs¹,

Parola²,

Robbins³

et al. 1975

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

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“…1) suggests another possible role for membranes. Many membrane-related processes are known to change their rates at break-point temperatures (22)(23)(24)(25) (26); variation of the cel phase-transition temperature with different fatty acid supplements could account for the supplement effects (27). Alternatively, the temperaturecompensation mechanism in cel-, but not in cel+, could be sensitive to some phase transition that would be present in both strains near 22TC.…”

Section: Discussionmentioning

confidence: 99%

Circadian rhythms in Neurospora crassa: a mutation affecting temperature compensation.

Mattern¹,

Forman²,

Brody³

1982

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

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The circadian rhythm of conidiation (spore formation) in Neurospora crassa is known to be temperature compensated, that is, the period is only slightly affected by the incubation temperature. Thus, the Q10 (the relative rate enhancement corresponding to a 10C rise in temperature) of the rhythm of the bd cap strain from 14 to 300C was 1.1, whereas the Q10 of the uncompensated growth rate in the same interval was 2.4. A mutation at the cel locus resulted in loss of the temperature-compensation property in cultures grown below 22TC. The Q10 of the rhythm below 220C was 2.2, and periods of about 40 hr were observed. In contrast, the Q10 of the rhythm above 220C was 1.1, with circadian periods of 18-21 hr. Thus, cel displayed a threshold temperature or "break point" for the temperature compensation of its rhythm. Supplementation of cel strains, which require fatty acids, with unsaturated or short-chain fatty acids raised the threshold temperature to 260C, whereas supplementation with long-chain saturated fatty acids lowered it to 18C. These data suggest a role for fatty acids, as lipid components or as cellular metabolites, in the mechanism of temperature compensation.Circadian rhythms are the most widely studied of the endogenous biological oscillations. Three characteristics are ordinarily used to identify a rhythm as circadian: its period (about 24 hr when free-running); its sensitivity to light (reflecting the ability to adjust its phase to the phase of the environment); and the relative insensitivity of its period to the growth temperature (1). This last characteristic is called temperature compensation (2). Without such a safeguard, daily biological timekeeping would be highly unreliable, running ahead oflocal time in warm situations (summer, noon, thermal springs) and behind in cool ones (winter, midnight, mountain streams). Examples of uncompensated daily rhythms are rare, and are usually confined to tropical species, which live where ambient temperatures are fairly constant (3).Temperature compensation is often quantified in terms ofthe temperature coefficient Q1o, the relative rate enhancement of a process corresponding to a 100C rise in temperature. Ordinary biological growth rates and reactions have Q10s of 2-3 (2). The

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“…It has been pointed out that cellular motility may be a critical factor in cell adhesion (2,17,19,22,28). The change in the physical state of the lipids may also affect the insertion (13) and distribution (3,4,8,20,23) of proteins in the membrane, and the activity of membrane-bound enzymes (31). These molecular events would also be relevant to cell adhesion (12,24,27,30).…”

Section: Discussionmentioning

confidence: 99%

A correlation between membrane fluidity and the critical temperature for cell adhesion.

Ueda¹,

Ito²,

Okada³

et al. 1976

The Journal of Cell Biology

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BHK 21 cells can adhere to a protein-coated plastic dish in the presence of Ca2+ at temperatures above 12 degrees C. However, they cannot adhere below 8 degrees C. The ESR spectrum of cells spin-labeled with a stearic acid label indicated that the membrane fluidity changed characteristically at 10 degrees C, 20 degrees C, and 30 degrees C. The critical temperature for cell adhesion coincided well with one of the characteristic temperatures for the membrane fluidity change. In the case of adhesion in the presence of Mg2+, no such correlation was observed.

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Lateral Phase Separation of Lipids in Plasma Membranes: Effect of Temperature on the Mobility of Membrane Antigens

Cited by 103 publications

References 13 publications

Fluorescence polarization and viscosities of membrane lipids of 3T3 cells.

Fluorescence polarization and viscosities of membrane lipids of 3T3 cells.

Circadian rhythms in Neurospora crassa: a mutation affecting temperature compensation.

A correlation between membrane fluidity and the critical temperature for cell adhesion.

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