Supplementary Materials

The PDF file includes:

  • Fig. S1. The hog1-3C mutant shows wild-type resistance to osmotic stress.
  • Fig. S2. Analysis of the proteomic data.
  • Fig. S3. Induction of Arr2 and Arr3 after treatment with sodium arsenite.
  • Fig. S4. Arsenic-induced expression of ARR2 and ARR3 is entirely or nearly entirely dependent on Yap8.
  • Fig. S5. Quantification of data from Fig. 3.
  • Fig. S6. Quantification of data from Fig. 4C.
  • Fig. S7. Osmotic stress–induced phosphorylation of Sko1 is unaffected in the hog1-3C mutant.
  • Fig. S8. Arsenite-induced expression of ARR2 and ARR3 is reduced in the absence of Yap8 phosphorylation.
  • Fig. S9. Enhanced induction of the Rpn4 proteotoxic stress response in the yap8Δ mutant.
  • Fig. S10. Confirmation that the hog1-T174A/Y176F mutant is deficient in osmotic stress–induced phosphorylation.
  • Fig. S11. Quantification of data from Fig. 5.
  • Fig. S12. Arsenite sensitivity of hog1 mutants persists in the mtq2Δ background.
  • Fig. S13. Phylogenetic relationship between yeast Hog1 and a subset of human MAPKs.
  • Table S1. Yeast strains.
  • Table S2. Plasmids.
  • Legend for table S3

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Other Supplementary Material for this manuscript includes the following:

  • Table S3 (Microsoft Excel format). Proteomic data.