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. 1999 May;10(5):1325–1335. doi: 10.1091/mbc.10.5.1325

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Copyright © 1999, The American Society for Cell Biology

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Activation of either the Cdc42p/Ste20p/MAPK pathway or the PKA is sufficient to induce invasive growth in strains lacking RAS2. (A) Invasive growth of yeast strain YHUM120 (ras2) containing pRS426 (vector), pRS316-RAS2 (RAS2), YCp50-RAS2^Val19 (RAS2^V19), pRS426-STE20 (2 μm STE20), B2616 (STE11-4), pRS426-STE12 (2 μm STE12), pRS202-TEC1 (2 μm TEC1), pRS316-GAL-CDC42^Val12 (GAL-CDC42^V12), pRS316-GAL-CDC42^Leu61 (GAL-CDC42^L61), pYGEX-STE20 (GAL-STE20), B2065 (GAL-STE12), pGAL-TEC1 (GAL-TEC1), YEplac195-TPK1 (2 μm TPK1), pRS426-TPK2 (2 μm TPK2), pRS426-TPK3 (2 μm TPK3), or a bcy1 disruption mutation (bcy1), respectively. Strains were grown on solid SC-Ura medium containing either 2% glucose (upper and lower panels) or a mixture of 3% raffinose and 0.1% galactose (middle panel). After incubation for 4 d, plates were photographed before (Total growth) or after (Invasive growth) washing cells from the agar surface. (B) FRE(Ty1)::lacZ expression levels. β-Galactosidase activity was measured on strains described in A. Units are nanomoles per minute per milligram. Bars depict means of three independent measurements. White bars indicate RAS2-independent expression of FG(Ty1)::lacZ.