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. 2018 Apr 30;8:6763. doi: 10.1038/s41598-018-25154-9

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Scheme showing how the various deletion mutants affect GSH synthesis (Δyap1) and GSSG reduction, either directly (Δglr1), or by blocking the production of NADPH reducing equivalents (Δzwf1, Δgnd1), or by supressing the NADPH-dependent reduction of protein disulfides (Δtrx2, indirectly Δzwf1, Δgnd1). Dotted lines show the metabolic lesions caused by the deletion mutants.