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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Curr Genet. 2018 Oct 30;65(2):417–421. doi: 10.1007/s00294-018-0898-5

Fig 1.

Fig 1.

A. The High Osmolarity Glycerol (HOG) pathway. In response to hyper-osmotic shock, two pathway branches are activated at the cell surface by plasma membrane osmosensors, and converge upon Pbs2, the MEK of the HOG pathway. B. Mechanism of Hog1 activation by arsenite. Arsenite (As[III]) is converted to methylarsenite (MAs[III]) by the dimeric methyl transferase Mtq2:Trm122. MAs inhibits Ptp2 and Ptp3, the tyrosine-specific protein phosphatases that maintain Hog1 in a low-activity state. This shifts the equilibrium to phosphorylated (active) Hog1 and relies on basal phosphorylation of Hog1 by MEK Pbs2.