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. 2020 Jan 8;11:127. doi: 10.1038/s41467-019-13890-z

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© The Author(s) 2020

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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Fig. 4 — a KN99 deletion strains from the C. neoformans deletion collection show that deletion of UXS1 confers resistance to 5FC and 5FU. The RBB18-2 strain carrying a fur1 mutation is resistant to 5FC and 5FU although more weakly to 5FU. The R265-3 strain carrying a fur1 mutation is completely resistant to both drugs. b Spot dilution assay on YNB, YNB plus 5FC, and YNB plus 5FU demonstrating overexpression of UXS1 driven by the actin promoter does not confer increased sensitivity to 5FC or 5FU. c Spot dilution assays on YNB, YNB plus 5FC, and YNB plus 5FU demonstrating that mutants deficient in UDP-xylose transport (uxt1Δ, uxt2Δ, uxt1Δ uxt2Δ) and xylose transferase mutants (cxt1Δ, cxt2Δ, cxt1Δ cxt2Δ) show no change in 5FC and 5FU sensitivity. d Spot dilution assay on YPD, YPD plus 5FC, and YPD plus 5FU showing that ugd1 mutants are viable on rich YPD media but retain sensitivity to 5FC and 5FU. In addition, ugd1 uxs1 double mutants retain sensitivity to 5FC and 5FU like a ugd1 single mutant rather than gain resistance like the uxs1 single mutant.