Effects of CGA-N12 on the membrane structure of Candida tropicalis cells

The antimicrobial peptide CGA-N12 (NH2-ALQGAKERAHQQ-COOH) is an active peptide derived from chromogranin A (CGA) and consists of the 65th to 76th amino acids of the N-terminus. The results of our previous studies showed that CGA-N12 exerts anti-Candida activity by inducing apoptosis without destroying the integrity of cell membranes. In this study, the effect of CGA-N12 on the cell membrane structure of Candida tropicalis was investigated. CGA-N12 resulted in the dissipation of the membrane potential, the increase in membrane fluidity, and the outflow of potassium ions in C. tropicalis without significantly changing the ergosterol level. Fluorescence quenching was applied to evaluate the membrane channel characteristics induced by CGA-N12 through detection of the following: membrane permeability of hydrated Cl− (ϕ ≈ 0.66 nm) using the membrane-impermeable halogen anion-selective fluorescent dye lucigenin, passage of the membrane-impermeable dye carboxyfluorescein (CF) (ϕ ≈ 1 nm) through the membrane, and membrane permeation of H3O+ based on the membrane non-permeable pH-sensitive fluorescent dye 8-hydroxypyrene-1,3,6-trisulfonic acid, trisodium salt (HPTS). In conclusion, CGA-N12 can induce the formation of non-selective ion channels <1 nm in diameter in the membranes of C. tropicalis, resulting in the leakage of potassium ions, chloride ions, and protons, among others, leading to dissipation of the membrane potential. As a result, the fluidity of membranes is increased without destroying the synthesis of ergosterol is not affected.

Molybdenum induces alterations in the glycerolipidome that confer drought tolerance in wheat

Molybdenum (Mo), which is an essential microelement for plant growth, plays important roles in multiple metabolic and physiological processes, including responses to drought and cold stress in wheat. Lipids also have crucial roles in plant adaptions to abiotic stresses. The aim of this study was to use glycerolipidomic and transcriptomic analyses to determine the changes in lipids induced by Mo that are associated with Mo-enhanced drought tolerance in wheat. Mo treatments increased the transcript levels of genes involved in fatty acid and glycerolipid biosynthesis and desaturation, but suppressed the expression of genes involved in oxylipin production. Wheat plants supplemented with Mo displayed higher contents of monogalactosyldiacyglycerol (MGDG), digalactosyldoacylglycerol (DGDG), phosphatidylglycerol (PG), phosphatidylethanolamine (PE), and phosphatidylcholine (PC) with increased levels of unsaturation. The levels of MGDG, DGDG, PG, and PC increased under PEG-simulated drought (PSD), and the magnitude of the responses varied in the presence and absence of Mo. Mo increased the accumulation of the most abundant glycerolipid species of C36:6, C34:4, and C34:3 by increasing the expression of genes related to desaturation under PSD, and this contributed to maintaining the fluidity of membranes. In addition, Mo attenuated the decreases in the ratios of DGDG/MGDG and PC/PE that were observed under PSD. These changes in lipids in Mo-treated wheat would contribute to maintaining the integrity of membranes and to protecting the photosynthetic apparatus, thus acting together to enhance drought tolerance.

Chemoenzymatic Synthesis of Enantiomeric, Bicyclic δ-Halo-γ-lactones with a Cyclohexane Ring, Their Biological Activity and Interaction with Biological Membranes

Starting from 1-acetyl-1-cyclohexene, three enantiomeric pairs (ee ≥ 99%) of bicyclic δ-halo-γ-lactones with cyclohexane ring were obtained in five-step synthesis. The key stereochemical steps were lipase-catalyzed kinetic resolution of racemic 1-(cyclohex-1-en-1-yl) ethanol followed by transfer of chirality to ethyl 2-(2-ethylidenecyclohexyl) acetate in the Johnson–Claisen rearrangement. Synthesized halolactones exhibited antiproliferative activity towards canine B-cell leukemia cells (GL-1) and canine B-cell chronic leukemia cells (CLB70) and the most potent (IC50 18.43 ± 1.46 μg/mL against GL-1, IC50 11.40 ± 0.40 μg/mL against CLB70) comparable with the control etoposide, was (1R,6R,1′S)-1-(1′-chloroethyl)-9-oxabicyclo[4.3.0]nonan-8-one (8b). All halolactones did not have a toxic effect on erythrocytes and did not change the fluidity of membranes in the hydrophobic region of the lipid bilayer. Only weak changes in the hydrophilic area were observed, like the degree of lipid packing and associated hydration. The racemic halolactones were also tested for their antimicrobial properties and found to exhibit selectivity towards bacteria, in particular, towards Proteus mirabilis ATCC 35659.

A neuronal thermostat controls membrane fluidity in C. elegans

SummaryAn organisms’ ability to adapt to heat can be key to its survival. Cells adapt to temperature shifts by adjusting lipid desaturation levels and the fluidity of membranes in a process that is thought to be controlled cell autonomously. We have discovered that subtle, step-wise increments in ambient temperature can lead to the conserved heat shock response being activated in head neurons of C. elegans. This response is exactly opposite to the expression of the lipid desaturase FAT-7 in the worm’s gut. We find that the over-expression of the master regulator of this response, Hsf-1, in head neurons, causes extensive fat remodeling to occur across tissues. These changes include a decrease in FAT-7 expression and a shift in the levels of unsaturated fatty acids in the plasma membrane. These shifts are in line with membrane fluidity requirements to survive in warmer temperatures. We have identified that the cGMP receptor, TAX-2/TAX-4, as well as TGF-β/BMP signaling, as key players in the transmission of neuronal stress to peripheral tissues. This is the first study to suggest that a thermostat-based mechanism can centrally coordinate membrane fluidity in response to warm temperatures across tissues in multicellular animals.

Erythrocyte Membrane Fluidity in Diabetics: Fluorescence Study

Erythrocyte membrane fluidity is changed in diabetic subjects with long-term complications. As membrane fluidity indicator, the mean steady-state fluorescence anisotropy was measured in 1,6-diphenylhexa-1,3,5-triene labelled erythrocyte membranes prepared from six control healthy donors and six poorly controlled diabetic subjects. Fluorescence anisotropy values of membranes prepared from erythrocytes of diabetic subjects were significantly higher than in control subjects. This indicates a decreased fluidity of membranes prepared from diabetic subjects. The decreased fluidity of diabetic membranes was raised by glycation inhibitors - penicillamine, captopril, and lipoic acid.