Maintenance of MAPK signaling specificity: Origins of cross-talk between the HOG pathway and the mating pheromone and filamentous growth pathways..
Patrick J. Westfall, Jeremy Thorner
Biochemistry and Molecular Bio, UC Berkeley, 528 Barker Hall, Berkeley, CA, 94720, USA
Survival of all organisms depends on their ability to sense and react appropriately to changing environmental conditions. When external osmolarity is high, S. cerevisiae utilizes a conserved mitogen-activated protein kinase signaling cascade (the High Osmolarity Glycerol or HOG pathway) to evoke appropriate cellular responses. Prior work has shown that, when either Pbs2 (the MAPKK) or Hog1 (the MAPK) is absent, Ste11 (the MAPKKK for one branch of the HOG pathway) inappropriately activates the mating pheromone response and filamentous growth pathways. This phenomenon is called cross-talk. To rule out that cross-talk is due to chronic absence of Hog1, an analog-sensitive allele (hog1-as) of HOG1 was constructed. Inhibition of hog1-as during osmotic stress leads to expression of reporter genes for both the mating and invasive growth pathways. Thus, continuous Hog1 activity is needed to maintain pathway specificity and prevent cross-talk. Since cross-talk requires the osmosensor, Sho1, it is possible that Hog1 prevents cross-talk at the level of Sho1 itself. Preliminary results using Sho1 point mutants support the idea that Hog1-dependent modification of Sho1 may be involved in preventing cross-talk. Furthermore, chimeric constructs and N-terminal deletions of Sho1 that allow tethering of the cytosolic tail of Sho1 to the membrane are sufficient to confer resistance to hyperosmotic challenge, but do not support cross-activation of the mating pheromone response pathway.
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