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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Semin Cell Dev Biol. 2018 Jun 6;88:21–35. doi: 10.1016/j.semcdb.2018.05.015

Figure 4. Mechanistic examples of buffering and potentiating.

Figure 4

A. Activity of v-Src but not c-Src is dependent on Hsp90 (reprint from Xu and Lindquist, 1993). B. Likewise, malignant transformation with v-Src is also dependent on Hsp90. Upon treatment with the Hsp90 inhibitor geldanamycin, the normal contact inhibition of growth is restored (reprint from Whitesell et al., 1994). C. Graphic illustration of Hsp90 potentiating oncogenic v-Src constitutively active kinase activity. The original observed phenotype is graphed on a phenotypic scale in black. The phenotype dependent on Hsp90 is graphed in purple with a vector designating the phenotypic difference of buffered alleles. D. Ste12 contributes to both mating and invasion. A wild-type STE12 allele results in normal mating efficiency and invasion. A mutant ste12 K150I allele results in decreased mating efficiency only at high temperature or upon inhibition of Hsp90. The same allele results in increased invasion only at high temperature. E. In the RM background, the MEC1 allele is not dependent on Hsp90. In the BY background, the MEC1 allele is dependent on Hsp90; HU-resistance and UV-resistance decreases when Hsp90 in inhibited. F. Hsp90 potentiates BCR-ABL imatinib resistance. G. Hsp90 potentiates fluconazole resistance in several erg3 alleles and other gene deletions.