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. 2016 Jan 8;6:1522. doi: 10.3389/fmicb.2015.01522

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Copyright © 2016 Pérez-Torrado and Querol.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Molecular mechanisms of persistence of Saccharomyces cerevisiae cells after neutrophil engulfment. Opportunistic S. cerevisiae strains redirect the low levels of the nitrogen sources inside the phagosome to increase amino acids (aa’s) biosynthesis. These strains also increase the oxidative stress response by activating the Yap1p transcription factor regulon to counteract the lethal effects of reactive oxygen species (ROS) generated by the macrophage. De novo dNTP biosynthesis is activated to allow DNA repair machinery to counteract ROS-induced mutations.