Journal of Biochemistry and Cell Biology
Open Access

Lipid signalling, broadly defined, refers to any biological signalling event involving a lipid messenger that binds a protein target, such as a receptor, kinase or phosphatase, which in turn mediate the goods of these lipids on specific cellular responses. Lipid signalling is thought to be qualitatively different from other classical signalling paradigms (such as monoamine neurotransmission) because lipids can freely diffuse through membranes (see osmosis). One consequence of this is that lipid couriers cannot be stored in vesicles prior to release and so are frequently biosynthesized “on demand “at their intended point of action. As similar, numerous lipid signalling molecules cannot circulate freely in solution but, rather, live bound to special carrier proteins in serum. Lipids aren't just used as a passive element of membranes, or as a source of stored energy.

They're involved in the process of signal transduction at the cell membrane, a process by which the interior components of the cell respond to a signal external to the cell [1], allowing the cell to respond to their original terrain. Usually a chemical signal on the outside of the cell is the" primary messenger “that causes the cell to respond. Usually the chemical transmitter of information doesn't get into the cell. Rather it binds to face receptors on the cell membrane face [2]. Somehow, the cells sense that a ligand is bound to the outside. Enzymes, generally in the membrane or at the intracellular surface of the lipid bilayer are activated. Numerous of these enzymes stick lipids in the membrane. The adhered fragments of the lipid molecules serve as intracellular signals or" secondary messengers”, which can bind to intracellular enzymes to spark intracellular processes.

Recently, fatty acid amides have been shown to be potent mediators of neurological processes [3]. In one interesting experiment, sheep were sleep deprived. Reasoning that the brain might release a biochemical signal into cerebrospinal fluid to induce sleep, scientists at Scripps removed some of this fluid and isolated a substance that wasn't plant in rested sheep [4]. On analysis, the structure was shown to be an amide of oleic acid. Oleylethanolamide has been shown to bind to the peroxisome-proliferator-actuated receptor-a (PPAR-a) which resides in the nucleus [5]. This ligand, by affecting gene transcription, appears to regulate body weight and the feeling of fullness after eating (satiety) as it leads to reduced eating.

More lately, membrane lipids have been shown to alter integral membrane receptor signalling either through direct or circular stoichiometric relations. Investigations within the last five years have identified important places of lipids in the regulation of membrane protein receptors during cell signalling. These functions have been uncovered due to recent developments in crystal structure resolution and identification of lipid binding sites in the context of 3D structures. These technical advances have paved the way to a better understanding as to how the composition of the PM offers both a tremendous level of versatility and plasticity in cell signalling. This short review highlights work done, chiefly within the last two years that have significantly expanded our view of the contribution of membrane lipids in cell signalling.

Lipid signalling, broadly defined, refers to any biological signalling event involving a lipid messenger that binds a protein target, such as a receptor, kinase or phosphatase, which in turn mediate the effects of these lipids on specific cellular responses [6,7]. Lipid signalling is thought to be qualitatively different from other classical signalling paradigms (such as monoamine neurotransmission) because lipids can freely diffuse through membranes (see osmosis) [8]. One consequence of this is that lipid messengers cannot be stored in vesicles prior to release and so are often biosynthesized "on demand" at their intended site of action. As such, many lipid signalling molecules cannot circulate freely in solution but, rather, exist bound to special carrier proteins in serum.

Every cell produces thousands of lipid species, but studying the function of individual lipids in living cells is almost impossible with existing methodologies. Addressing this experimental bottleneck, we developed a strategy to quantify dissociation constants for lipid– protein interactions and Trans membrane flip-flop rates of native lipids in live-cell experime10nts. Using a combination of plasma membranespecific photochemical probes and mathematical modelling [9-10], we demonstrate that, for diacylglycerols as a model lipid class, the inherent lipid structural diversity caused by variations in acyl chain composition determines lipid protein affinities and Trans bilayer kinetics. In fact, subtle chemical differences change these values by orders of magnitude. Our approach represents a generally applicable method for elucidating the biological function of single lipid species on subcellular scales.

Acknowledgement

I would like to thank my Professor for his support and encouragement.

Conflict of Interest

The authors declare that they are no conflict of interest.

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