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Barki, N.

Publications and source records attributed to Barki, N..

2 recordsLinked to original sources

Phosphorylation bar-coding of Free Fatty Acid receptor 2 is generated in a tissue-specific manner

Free Fatty Acid receptor 2 (FFA2) is activated by short-chain fatty acids and expressed widely, including in white adipocytes and various immune and enteroendocrine cells. Using both wild type human FFA2 and a Designer Receptor Exclusively Activated by Designer Drugs (DREADD) variant we explored the activation and phosphorylation profile of the receptor, both in heterologous cell lines and in tissues from transgenic knock-in mouse lines expressing either human FFA2 or the FFA2-DREADD. FFA2 phospho-site specific antisera targeting either pSer296/pSer297 or pThr306/pThr310 provided sensitive biomarkers of both constitutive and agonist-mediated phosphorylation as well as an effective means to visualise agonist-activated receptors in situ. In white adipose tissue phosphorylation of residues Ser296/Ser297 was enhanced upon agonist activation whilst Thr306/Thr310 did not become phosphorylated. By contrast, in immune cells from Peyers patches Thr306/Thr310 become phosphorylated in a strictly agonist-dependent fashion whilst in enteroendocrine cells of the colon both Ser296/Ser297 and Thr306/Thr310 were poorly phosphorylated. The concept of phosphorylation bar-coding has centred to date on the potential for different agonists to promote distinct receptor phosphorylation patterns. Here we demonstrate that this occurs for the same agonist-receptor pairing in different patho-physiologically relevant target tissues. This may underpin why a single G protein-coupled receptor can generate different functional outcomes in a tissue-specific manner. Significance StatementThe concept that agonist-occupancy of a G protein-coupled receptor can result in distinct patterns of phosphorylation of residues on the intracellular elements of the receptor in different tissues is referred to bar-coding. This has been challenging to demonstrate conclusively in native tissues. We now show this to be the case by using tissues from transgenic knock-in mouse lines expressing either wild type or a DREADD variant of human Free Fatty Acid Receptor 2 and a pair of phospho-site specific antisera. Clear differences in the pattern of phosphorylation of the receptor induced by the same ligand were observed in white adipose tissue and immune cells derived from Peyers patches. These outcomes provide direct evidence in tissues, at endogenous expression levels, of a well promoted hypothesis.

cell biology↗

Chemogenetic analysis of how receptors for short chain fatty acids regulate the gut-brain axis

The gut-brain axis allows bi-directional communication between the enteric and central nervous systems. Short chain fatty acids (SCFAs) generated by the gut microbiota are important regulators of this interface. However, defining mechanisms by which SCFAs do so has been challenging because, amongst various roles, they co-activate both of a pair of closely related and poorly characterized G protein-coupled receptors, FFA2 and FFA3. Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) can provide an important approach in defining receptor-specific functions. By screening a library of carboxylate-containing small molecules we identified 4-methoxy-3-methyl-benzoic acid (MOMBA) as a specific agonist of a DREADD variant of FFA2 which is not activated by SCFAs. Using mice engineered to replace FFA2 with this FFA2-DREADD, whilst retaining FFA3 expression, combinations of MOMBA and the now FFA3 receptor selective SCFAs defined key, but distinct, roles of FFA2 and FFA3 in each of gut transit time, secretion of entero-endocrine hormones, and communication from the gut to each of autonomic and somatic sensory ganglion cells and the spinal cord. These studies map mechanisms and signalling pathways by which each of FFA2 and FFA3 act to link the gut and the brain and provide both animal models and novel tool compounds to further explore this interface.

pharmacology and toxicology↗