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. 2007 Jun 15;6(8):1363–1372. doi: 10.1128/EC.00165-07

FIG. 2.

FIG. 2.

The tpk2(Ts) growth defect is suppressed by alterations of the amino-terminal sequence of Cdc37. (A) Suppression of the tpk2(Ts) growth defect by the CDC37-101 mutation. Strains were streaked onto minimal medium and incubated for several days. Wild-type (WT) [SGY559(pRS316)], tpk2-63(Ts) CDC37+ [SGY446(pYZ1)], tpk2-63(Ts) CDC37-101 [SGY446(pGS224)], tpk2-62(Ts) CDC37+ [SGY562 (pYZ1)], and tpk2-62(Ts) CDC37-101 [SGY562(pGS224)] strains were used. (B) Suppression of the tpk2(Ts) growth defect in the absence of Bcy1. Strain SGY398 (tpk2-63 bcy1Δ) was transformed with a low-copy-number vector or the same vector containing wild-type (CDC37+) or mutant (CDC37-101) alleles of CDC37 and incubated on minimal medium for several days at 23°C and 34°C. (C) The dominant CDC37 mutations fall within the amino terminus of Cdc37. The individual mutations are indicated by lines within the putative protein kinase interaction domain (filled box) of Cdc37.