Molecular Changes in Membrane Lipids During Cold Stress

1989 ◽  
pp. 249-257 ◽  
Author(s):  
G. A. Thompson
2021 ◽  
Vol 12 ◽  
Author(s):  
Xunchao Zhao ◽  
Yulei Wei ◽  
Jinjie Zhang ◽  
Li Yang ◽  
Xinyu Liu ◽  
...  

Low temperature is one of the major abiotic stresses that restrict the growth and development of maize seedlings. Membrane lipid metabolism and remodeling are key strategies for plants to cope with temperature stresses. In this study, an integrated lipidomic and transcriptomic analysis was performed to explore the metabolic changes of membrane lipids in the roots of maize seedlings under cold stress (5°C). The results revealed that major extraplastidic phospholipids [phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidic acid (PA), and phosphatidylinositol (PI)] were dominant membrane lipids in maize root tissues, accounting for more than 70% of the total lipids. In the transcriptome data of maize roots under cold stress, a total of 189 lipid-related differentially expressed genes (DEGs) were annotated and classified into various lipid metabolism pathways, and most of the DEGs were enriched in the “Eukaryotic phospholipid synthesis” (12%), “Fatty acid elongation” (12%), and “Phospholipid signaling” (13%) pathways. Under low temperature stress, the molar percentage of the most abundant phospholipid PC decreased around 10%. The significantly up-regulated expression of genes encoding phospholipase [phospholipase D (PLD)] and phosphatase PAP/LPP genes implied that PC turnover was triggered by cold stress mainly via the PLD pathway. Consequently, as the central product of PC turnover, the level of PA increased drastically (63.2%) compared with the control. The gene-metabolite network and co-expression network were constructed with the prominent lipid-related DEGs to illustrate the modular regulation of metabolic changes of membrane lipids. This study will help to explicate membrane lipid remodeling and the molecular regulation mechanism in field crops encountering low temperature stress.


2019 ◽  
Vol 46 (9) ◽  
pp. 830 ◽  
Author(s):  
Meng Li ◽  
Na Sui ◽  
Lin Lin ◽  
Zhen Yang ◽  
Yuanhu Zhang

Maize is an important food crop. Chilling stress can decrease maize production by affecting seed germination and seedling growth, especially in early spring. We analysed chlorophyll fluorescence, membrane lipids, secondary metabolites and the transcriptome of two maize inbred lines (chilling-tolerant M54 and chilling-sensitive 753F) after 0, 4 and 24 h cold stress. M54 showed better ability to protect PSII and accumulate secondary metabolites. From RNA sequencing data, we determined that the majority of cold-affected genes were involved in photosynthesis, secondary metabolism, and signal transduction. Genes important for maintaining photosystem structure and for regulating electron transport were less affected by cold stress in M54 than in 753F. Expression of genes related to secondary metabolism and unsaturated fatty acid synthesis were upregulated more strongly in M54 than in 753F and M54 accumulated more unsaturated fatty acids and secondary metabolites. As a result, M54 achieved relatively high cold tolerance by protecting the photosystems and maintaining the stability of cell membranes.


Author(s):  
Michael Edidin

Cell surface membranes are based on a fluid lipid bilayer and models of the membranes' organization have emphasised the possibilities for lateral motion of membrane lipids and proteins within the bilayer. Two recent trends in cell and membrane biology make us consider ways in which membrane organization works against its inherent fluidity, localizing both lipids and proteins into discrete domains. There is evidence for such domains, even in cells without obvious morphological polarity and organization [Table 1]. Cells that are morphologically polarised, for example epithelial cells, raise the issue of membrane domains in an accute form.The technique of fluorescence photobleaching and recovery, FPR, was developed to measure lateral diffusion of membrane components. It has also proven to be a powerful tool for the analysis of constraints to lateral mobility. FPR resolves several sorts of membrane domains, all on the micrometer scale, in several different cell types.


Author(s):  
Paulina Iwan ◽  
Jan Stepniak ◽  
Malgorzata Karbownik-Lewinska

Abstract. Iodine is essential for thyroid hormone synthesis. Under normal iodine supply, calculated physiological iodine concentration in the thyroid is approx. 9 mM. Either potassium iodide (KI) or potassium iodate (KIO3) are used in iodine prophylaxis. KI is confirmed as absolutely safe. KIO3 possesses chemical properties suggesting its potential toxicity. Melatonin (N-acetyl-5-methoxytryptamine) is an effective antioxidant and free radical scavenger. Study aims: to evaluate potential protective effects of melatonin against oxidative damage to membrane lipids (lipid peroxidation, LPO) induced by KI or KIO3 in porcine thyroid. Homogenates of twenty four (24) thyroids were incubated in presence of either KI or KIO3 without/with melatonin (5 mM). As melatonin was not effective against KI-induced LPO, in the next step only KIO3 was used. Homogenates were incubated in presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25 mM) without/with melatonin or 17ß-estradiol. Five experiments were performed with different concentrations of melatonin (5.0; 2.5; 1.25; 1.0; 0.625 mM) and one with 17ß-estradiol (1.0 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. KIO3 increased LPO with the strongest damaging effect (MDA + 4-HDA level: ≈1.28 nmol/mg protein, p < 0.05) revealed at concentrations of around 15 mM, thus corresponding to physiological iodine concentrations in the thyroid. Melatonin reduced LPO (MDA + 4-HDA levels: from ≈0.97 to ≈0,76 and from ≈0,64 to ≈0,49 nmol/mg protein, p < 0.05) induced by KIO3 at concentrations of 10 mM or 7.5 mM. Conclusion: Melatonin can reduce very strong oxidative damage to membrane lipids caused by KIO3 used in doses resulting in physiological iodine concentrations in the thyroid.


2003 ◽  
Vol 29 (1) ◽  
pp. 9-17 ◽  
Author(s):  
Gregory D. Bossart ◽  
René A. Meisner ◽  
S. A. Rommel ◽  
Shin-Je Ghim ◽  
A. Bennett Jenson

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