Pantothenate biosynthesis is critical for chronic infection by the neurotropic parasite Toxoplasma gondii

Mass Spec data incl. LC-MS and GC-MS data to study Coenzyme A and pantothenate synthesis and uptake in Toxoplasma gondii

Raw MS Data is of the Study 'Pantothenate biosynthesis is critical for chronic infection by the neurotropic parasite Toxoplasma gondii' by Matteo Lunghi, Joachim Kloehn, Aarti Krishnan, Emmanuel Varesio, Oscar Vadas and Dominique Soldati-Favre

Raw original MS files are included as well as files converted to mzml or mzxml. Files are split into LC-MS and GC-MS datasets and further into folders for each dataset and to what figure panel they belong

Abstract
Coenzyme A (CoA) is an essential molecule acting in metabolism, post-translational modification, and regulation of gene expression. While all organisms synthesize CoA, many, including humans, are unable to produce its precursor, pantothenate. Intriguingly, like most plants, fungi and bacteria, parasites of the coccidian subgroup of Apicomplexa, including the human and animal pathogen Toxoplasma gondii, possess all the enzymes required for de novo synthesis of pantothenate. Here, the importance of CoA and pantothenate biosynthesis for the acute and chronic stages of T. gondii infection was dissected through genetic, biochemical and metabolomic approaches, revealing that CoA synthesis is essential for T. gondii tachyzoites, due to the parasite’s inability to salvage CoA or intermediates of the pathway. In contrast, de novo pantothenate synthesis was only partially active in T. gondii tachyzoites, making the parasite reliant on Pan uptake. However, Pan synthesis proved to be crucial for the establishment of chronic infection, offering a promising target for intervention against the persistent stage of T. gondii.

Files are linked to datasets (Research Manuscript Figures) through the names of the subfolders. Sample prep and instrumentation as in the research manuscript. +/- in the files indicates presence of metabolites or presence of inducer for protein or gene downregulation (auxin, IAA or aTc as indicated for each experiment in the research manuscript).