The effect of vitamin E on the structure of membrane lipid assemblies

Bradford, A. L.; Atkinson, Jeffrey; Fuller, Nola; Rand, R. P.

doi:10.1194/jlr.m300146-jlr200

Cited by 87 publications

(64 citation statements)

References 31 publications

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“…This is also consistent with the need for substantially less αT (~1.2 amol/CV) to selectively rescue fusion extent. As αT has~2-fold higher negative curvature (−0.073Å −1 ) [10] than does CHOL and has limited transbilayer mobility [78], and thus remains almost (Fig. 6c).…”

Section: Critical Roles For Chol In Triggered Membrane Fusionmentioning

confidence: 97%

A new approach to the molecular analysis of docking, priming, and regulated membrane fusion

Rogasevskaia

Coorssen

2011

J Chem Biol

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Studies using isolated sea urchin cortical vesicles have proven invaluable in dissecting mechanisms of Ca 2+ -triggered membrane fusion. However, only acute molecular manipulations are possible in vitro. Here, using selective pharmacological manipulations of sea urchin eggs ex vivo, we test the hypothesis that specific lipidic components of the membrane matrix selectively affect defined late stages of exocytosis, particularly the Ca 2+ -triggered steps of fast membrane fusion. Egg treatments with cholesterol-lowering drugs resulted in the inhibition of vesicle fusion. Exogenous cholesterol recovered fusion extent and efficiency in cholesterol-depleted membranes; α-tocopherol, a structurally dissimilar curvature analogue, selectively restored fusion extent. Inhibition of phospholipase C reduced vesicle phosphatidylethanolamine and suppressed both the extent and kinetics of fusion. Although phosphatidylinositol-3-kinase inhibition altered levels of polyphosphoinositide species and reduced all fusion parameters, sequestering polyphosphoinositides selectively inhibited fusion kinetics. Thus, cholesterol and phosphatidylethanolamine play direct roles in the fusion pathway, contributing negative curvature. Cholesterol also organizes the physiological fusion site, defining fusion efficiency. A selective influence of phosphatidylethanolamine on fusion kinetics sheds light on the local microdomain structure at the site of docking/fusion. Polyphosphoinositides have modulatory upstream roles in priming: alterations in specific polyphosphoinositides likely represent the terminal priming steps defining fully docked, release-ready vesicles. Thus, this pharmacological approach has the potential to be a robust high-throughput platform to identify molecular components of the physiological fusion machine critical to docking, priming, and triggered fusion.

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Section: Critical Roles For Chol In Triggered Membrane Fusionmentioning

confidence: 97%

A new approach to the molecular analysis of docking, priming, and regulated membrane fusion

Rogasevskaia

Coorssen

2011

J Chem Biol

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“…Two other membrane components of high intrinsic negative curvature, ␣-tocopherol (␣-toc) and dioleoylphosphatidylethanolamine (DOPE) Epand et al, 1996;Leikin et al, 1996;Chen and Rand, 1997;Bradford et al, 2003), were tested for their ability to substitute for cholesterol in selectively rescuing fusion ability. Incorporation of ␣-toc or DOPE into cholesterol-depleted CVs produced a selective recovery of fusion extent, without rescuing either Ca 2+ sensitivity or kinetics (Fig.…”

Section: Squares) Addition Of Exogenousmentioning

confidence: 99%

Cholesterol facilitates the native mechanism of Ca2+-triggered membrane fusion

Churchward

Rogasevskaia

Höfgen

et al. 2005

Journal of Cell Science

174

312

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The process of regulated exocytosis is defined by the Ca2+-triggered fusion of two apposed membranes, enabling the release of vesicular contents. This fusion step involves a number of energetically complex steps and requires both protein and lipid membrane components. The role of cholesterol has been investigated using isolated release-ready native cortical secretory vesicles to analyze the Ca2+-triggered fusion step of exocytosis. Cholesterol is a major component of vesicle membranes and we show here that selective removal from membranes, selective sequestering within membranes, or enzymatic modification causes a significant inhibition of the extent, Ca2+ sensitivity and kinetics of fusion. Depending upon the amount incorporated, addition of exogenous cholesterol to cholesterol-depleted membranes consistently recovers the extent, but not the Ca2+ sensitivity or kinetics of fusion. Membrane components of comparable negative curvature selectively recover the ability to fuse, but are unable to recover the kinetics and Ca2+ sensitivity of vesicle fusion. This indicates at least two specific positive roles for cholesterol in the process of membrane fusion: as a local membrane organizer contributing to the efficiency of fusion, and, by virtue of its intrinsic negative curvature, as a specific molecule working in concert with protein factors to facilitate the minimal molecular machinery for fast Ca2+-triggered fusion.

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“…Structurally, all four tocopherols (a-, b-, g-, and d-tocopherols) consist of a chromanol head group attached to a phytyl tail and differ only in the number and positions of methyl groups on the chromanol ring ( Figure 1). Tocopherols are amphipathic molecules, and in vitro studies using artificial membranes have shown that tocopherols form complexes with specific lipid constituents and physically stabilize membranes (Wassall et al, 1986;Stillwell et al, 1996;Wang and Quinn, 2000;Bradford et al, 2003). Tocopherols can efficiently quench singlet oxygen, scavenge various radicals, particularly lipid peroxy radicals, and thereby terminate lipid peroxidation chain reactions (Liebler and Burr, 1992;Bramley et al, 2000;Schneider, 2005).…”

Section: Introductionmentioning

confidence: 99%

Tocopherols Play a Crucial Role in Low-Temperature Adaptation and Phloem Loading in Arabidopsis

et al. 2006

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To test whether tocopherols (vitamin E) are essential in the protection against oxidative stress in plants, a series of Arabidopsis thaliana vitamin E (vte) biosynthetic mutants that accumulate different types and levels of tocopherols and pathway intermediates were analyzed under abiotic stress. Surprisingly subtle differences were observed between the tocopheroldeficient vte2 mutant and the wild type during high-light, salinity, and drought stresses. However, vte2, and to a lesser extent vte1, exhibited dramatic phenotypes under low temperature (i.e., increased anthocyanin levels and reduced growth and seed production). That these changes were independent of light level and occurred in the absence of photoinhibition or lipid peroxidation suggests that the mechanisms involved are independent of tocopherol functions in photoprotection. Compared with the wild type, vte1 and vte2 had reduced rates of photoassimilate export as early as 6 h into low-temperature treatment, increased soluble sugar levels by 60 h, and increased starch and reduced photosynthetic electron transport rate by 14 d. The rapid reduction in photoassimilate export in vte2 coincides with callose deposition exclusively in phloem parenchyma transfer cell walls adjacent to the companion cell/sieve element complex. Together, these results indicate that tocopherols have a more limited role in photoprotection than previously assumed but play crucial roles in low-temperature adaptation and phloem loading.

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The effect of vitamin E on the structure of membrane lipid assemblies

Cited by 87 publications

References 31 publications

A new approach to the molecular analysis of docking, priming, and regulated membrane fusion

A new approach to the molecular analysis of docking, priming, and regulated membrane fusion

Cholesterol facilitates the native mechanism of Ca2+-triggered membrane fusion

Tocopherols Play a Crucial Role in Low-Temperature Adaptation and Phloem Loading in Arabidopsis

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