Figure 2

Yap1 but not Cad1 is important for mediating the cell's adaptation to arsenic. (a) Self-organized heat map (dendograms were removed and boxes 1-3 indicate specific clusters) of 6,172 genes selected from the various indicated conditions. AsIII-treated parent wild type strain with normalized data values that are greater or less than those in condition(s) knocked-out Yap1, Cad1, Rpn4, or Arr1 treated with AsIII, by a factor of twofold. All knockouts tested revealed altered profiles compared to the wild type, except for cad1Δ. (b) yap1Δ (condition 2) loses induced expression of stress response genes found in box 1, such as SIR4, ISU2, MSN1, ATR1, CYT2, MDH1, AAD6, AAD4, TRR1, FLR1, GLR1 and GRE2. (c) rpn4Δ (condition 4) loses induced expression of ubiquitinating and proteasomal genes found in box 3 - UBP6, PRE8, PRE4, PRE7 and PRE1. (d) arr1Δ (condition 5) loses repressed expression of sulfur amino-acid metabolism gene SAM3 and glutamate biosynthesis gene CIT2, among others (box 2). arr1Δ also loses induced expression of serine biosynthesis gene SER3, sulfur amino-acid metabolism gene SAM4, cell-cycle regulator ZPR1, spindle-checkpoint subunit MAD2, ribonucleotide reductase RNR1and RNA polymerase I transcription factor RRN9, to name a few (box 3). Red, induced; green, repressed. For a comprehensive list of genes affected in all knockout experiments, see the Additional data files with the online version of this paper.