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. 2011 Apr 1;39(14):6148–6160. doi: 10.1093/nar/gkr178

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© The Author(s) 2011. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 1. — Genetic interactions of EKC mutants. (A) Synthetic lethality of pcc1-4 and tif5-K55E cells. Double pcc1-4/tif5-K55E mutant is inviable when a URA3 marked plasmid expression the wt PCC1 gene is cured by selection on 5-FOA plates (rightmost panel). (B) Dissection of kae1-18/KAE1, thr4Δ/THR4 and kae1-18/KAE1, thr1Δ/THR4 diploids reveals the inviability of kae1-18/thr1Δ and kae1-18/thr4Δ spores. Both lethal phenotypes can be saved by expression of wild-type KAE1 gene (shown for the kae1-18/thr1Δ mutant in the rightmost set of panels). (C) Synthetic slow growth phenotype of double kae1-18/pus1Δ and kae1-18/hom2Δ strains. Growth was for 2 days at the indicated temperature.