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. 2003 Apr;23(8):2733–2748. doi: 10.1128/MCB.23.8.2733-2748.2003

FIG. 6.

FIG. 6.

Defective sister chromatid cohesion observed in both a pol2-12 mutant and a trf5Δ mutant. (A) Flow-cytometric analysis of nocodazole-arrested pol2-12 mutant and an isogenic wild-type strain carrying the GFP signal. (B) Typical cells with attached sisters (one GFP dot per cell body) or separated sisters (two separated dots per cell body). (C) Defective sister chromatid separation was measured as total GFP dots, relative to double GFP dots (dd), for 500 to 700 cells in two separate experiments for each strain. Both pol2-12 and trf5Δ are defective. Replacing POL2 alleviates the defect. Isogenic controls for 12OG2(pADH-POL2) were wild type, SOG3, and 12OG2 (a pol2-12 mutant) (Table 1). These gave similar values of approximately 20% dd, similar to values observed with isogenic strains AFS479 and JCY122 shown here. Strains are designated as follows: AFS479 wild type (WT), JCY122 (pol2-12), JCYT59 (trf5Δ), 12OG2 [pol2-12(pADH-POL2)], JCYPD18 [cdc2-1 (Pol δ)], and JCYDNA2.