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Rizzo, R.

Publications and source records attributed to Rizzo, R..

2 recordsLinked to original sources

The spent culture supernatant of Pseudomonas syringae contains azelaic acid

Pseudomonas syringae pv. actinidiae (PSA) is an emerging kiwifruit bacterial pathogen which since 2008 has caused considerable losses. No quorum sensing (QS) signaling molecule has yet been reported from PSA and the aim of this study was to identify possible intercellular signals produced by PSA. A metabolome analysis resulted in the identification of 83 putative compounds, one of them was the nine carbon saturated dicarboxylic acid azelaic acid which for several reasons was decided to further study. Firstly azelaic acid, which is a straight chained nine-carbon (C9) saturated dicarboxylic acid, has been reported in plants as mobile signal that primes systemic defenses. Secondly its structure, which is associated with fatty acid biosynthesis, is similar to other known bacterial QS signals like the Diffusible Signal Facor (DSF). Analytical and structural studies by NMR spectroscopy confirmed that in the PSA spent supernatant azelaic acid was present. Quantification studies further revealed that 20 {micro}g/L of azelaic acid was present and was also found in spent supernatants of several other P. syringae pathovars. An RNAseq transcriptome study however did not reveal whether azelaic acid behaved as a QS molecule. This is the first report of the possible natural biosynthesis of azelaic acid by bacteria.

microbiology

Sphingolipid metabolic flow controls phosphoinositide turnover at thetrans Golgi network

Sphingolipids are membrane lipids, which are globally required for eukaryotic life. Sphingolipid composition varies among endomembranes with pre- and post-Golgi compartments being poor and rich in sphingolipids, respectively. Thanks to this different sphingolipid content, pre- and post-Golgi membranes serve different cellular functions. Nevertheless, how subcellular sphingolipid levels are maintained in spite of trafficking and metabolic fluxes is only partially understood. Here we describe a homeostatic control circuit that controls sphingolipid levels at the trans Golgi network. Specifically, we show that sphingomyelin production at the trans Golgi network triggers a signalling reaction leading to PtdIns(4)P dephosphorylation. Since PtdIns(4)P is required for cholesterol, and sphingolipid transport to the trans Golgi network, PtdIns(4)P consumption leads to the interruption of this transport in response to excessive sphingomyelin production. Based on this evidence we envisage a model where this homeostatic circuit maintains the sphingolipid composition of trans Golgi network and thus of post-Golgi compartments constant, against instant fluctuations in the sphingolipid biosynthetic flow.

cell biology