TABLE 4.

High-copy PIF1 suppresses the appearance of DNA repair foci in top3Δ cells

		% of cells with a Rad52 focus
Genotype	Vector	G1a	S/G2/M
Wild type	p2μ	0.25b	9.7
	p2μ-PIF1	0.37	10
	p2μ-pif1-KR	1.7	10
top3Δ	p2μ	17	64
	p2μ-PIF1	17	30
	p2μ-pif1-KR	8.1	32

^aWild-type (MATa TOP3 LYS2 BAR1 segregant from W4436) and top3Δ (MATa top3Δ LYS2 BAR1 segregant from W4436) strains with RAD52–YFP integrated at the endogenous locus were transformed with p2μ-PIF1 (clone 1), p2μ-pif1-KR (pWJ1286), or an empty vector (YEp51B) and Rad52 localization was analyzed by fluorescence microscopy. Over 500 cells were viewed for each strain + plasmid background. Cells were categorized for cell-cycle stage as unbudded (G1) or budded (S/G2/M). The cell-cycle distribution for each strain is as follows: Wild type (WT) + p2μ, 63% unbudded and 37% budded; WT + p2μ-PIF1, 56% unbudded and 44% budded; WT + p2μ-pif1-KR, 54% unbudded and 46% budded; top3Δ + p2μ, 34% unbudded and 66% budded; top3Δ + p2μ-PIF1, 51% unbudded and 49% budded; top3Δ + p2μ-pif1-KR, 48% unbudded and 52% budded.

^bEach number represents the percentage of cells in the indicated cell-cycle stage that contain a Rad52–YFP focus.