Phosphosite-specific regulation of the oxidative-stress response of P. brasiliensis: A Shotgun Phosphoproteomic Analysis
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ABSTRACT: Paracoccidioides brasiliensis, a thermally dimorphic fungus, is the causative agent of paracoccidioidomycosis, a systemic mycosis that is widespread in Latin America. P. brasiliensis infection occurs when conidia or mycelial fragments are inhaled by the host, which causes these cells to transition to the yeast form. The development of disease requires conidia inside host alveoli to differentiate into yeast cells in a temperature-dependent manner. This fungus is a facultative intracellular pathogen able to survive and replicate inside non-activated macrophages. Therefore, the survival of P. brasiliensis inside the host depends on the ability to adapt to oxidative stress induced by immune cells, especially alveolar macrophages. For several years, reactive oxygen species (ROS) were only associated with pathological processes. Currently, a plethora of roles for ROS in cell signaling have emerged. We have previously reported that low ROS concentrations cause cell proliferation in the human pathogenic fungus P. brasiliensis. In the present report, we investigated the influence of phosphorylation events in that process. Using a mass spectrometry-based approach, we mapped 440 phosphorylation sites in 230 P. brasiliensis proteins and showed that phosphorylation at different sites determines fungal responses to oxidative stress. Furthermore, we described, for the first time, the presence of a two-component signal transduction system in P. brasiliensis. These findings will help us to understand the phosphorylation events involved in the oxidative stress response.
INSTRUMENT(S): LTQ Orbitrap Velos
ORGANISM(S): Paracoccidioides Brasiliensis (strain Pb18)
SUBMITTER: Alexandre Keiji Tashima
LAB HEAD: Alexandre Keiji Tashima
PROVIDER: PXD001181 | Pride | 2022-03-03
REPOSITORIES: Pride
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