T osmostress signaling to the Spc1 MAPK, and therefore these MAPKKK paralogues do not appear to be redundant. Indeed, a previous study found that overexpression of Wis4 cannot complementMolecular Biology of the Celldetected the Wis4 in1 heteromer complex (Figure 2C). The observed Wis4 in1 interaction showed little change before and after osmostress and oxidative stress, suggesting constitutive int
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