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. 2015 Jan 15;14(4):630–640. doi: 10.4161/15384101.2014.994904

Figure 3.

Figure 3.

The Gcn2p kinase mediates β-lap toxicity in yeast. (A) Immunodetection of phospho-eIF2α (p-eIF2α) in WT, gcn1Δ, gcn2Δ and gcn20Δ strains treated with β-lap at the indicated times. Even loading of the gels was confirmed by PonceauS staining of membranes after transfer. Quantitation is shown below as a percent of the intensity of the highest signal, arbitrary assigned as 100. (B) Viability of the WT and GCN pathway mutant strains (gcn1Δ, gcn2Δ, gcn3Δ, gcn4Δ, gcn20Δ and GCN2c) treated during one hour with β-lap. (C and D) Immunodetection of phospho-H2A (p-H2A) in asynchronous (C) and G1-arrested (D) cultures of WT, nde2Δ and GCN2c strains treated with β-lap for the indicated times. Even loading of the gels was confirmed by immunodetection of total H2A protein. Quantitation is shown below as a percent of the intensity of the highest signal for WT cells, arbitrary assigned as 100.