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. 2015 Nov 30;10(11):e0143457. doi: 10.1371/journal.pone.0143457

Fig 2. The αβ-NAC complex and β-NAC under control of their endogenous promoter complement the growth defect of nacΔssbΔ cells.

Fig 2

a) Schematic drawing of the different plasmid-encoded NAC constructs used in this study. Plasmids encoding wild type (wt) and mutant αβ-NAC, either alone or in complex, were cloned in the vector backbone pRS316 reported by [18]. b) Growth analysis of wt and mutant yeast cells expressing different NAC versions from plasmids as indicated. Serial dilutions were spotted on synthetic complete media without uracil (SD-Ura) containing the indicated drugs. When cells were plated on the arginine analogue L-canavanine, arginine was omitted. The cells were incubated for 3 days at 30°C. c) The promoter (P)—and terminator (T)- regions of EGD1 were replaced with the corresponding regions of BTT1 and vice versa and cloned in the vector backbone of pRS316 with or without EGD2. BTT1 under its endogenous promoter and terminator was also cloned into pRS316 together with EGD2. d) Growth analyses were performed as described in b).