Table 3.

Restored normal level of components of ribosome-associated chaperone can eliminate each of [PSI+] variants

Isolate	ssb1/2Δ [PSI+sbs] transformants (Ura+/total transformants)		zuo1Δ [PSI+zos] transformants (Ura+/total transformants)		ssz1Δ [PSI+szs] transformants (Ura+/total transformants)
	Vector	pSSB1	Vector	pZUO1	Vector	pSSZ1
1	49/50	16/50	49/50	25/50	48/50	5/30
2	48/50	18/50	46/50	16/50	47/50	6/30
3	47/50	17/50	48/50	30/50	48/50	5/30
4	47/50	16/30	49/50	27/50	48/50	6/30
5	48/50	14/40	50/50	14/50	48/50	7/30
6	49/50	18/45	48/50	31/50	50/50	15/50
7	26/26	4/30	26/27	7/50	50/50	9/40
8	23/24	14/50	29/29	7/50	46/50	5/50
9	28/29	16/50	32/34	32/50	45/50	7/40
10	27/28	14/50	52/57	14/50	44/50	5/31
11	24/28	9/50	38/44	18/50	36/40	8/30
12	28/30	3/50	32/33	6/50	34/40	11/50
Total	444/465	159/545	499/524	227/600	544/580	81/441
% Ura+	95.48%	29.17%	95.23%	37.8%	93.79%	20.18%

Twelve strains carrying [PSI+sbs], [PSI+zos], or [PSI+szs] were transformed with the CEN plasmid pRS313 or the same plasmid carrying SSB1, ZUO1, or SSZ1, respectively, under their native promoters (pM76 = pSSB1, pM75 = pZUO1, pM78 = pSSZ1). Transformants were selected in the presence of uracil and were replica-plated to a plate lacking uracil to test the stability of [PSI+]. Subclones of Ura⁻ transformants that had lost pM76, pM75, or pM78 were tested for uracil auxotrophy by replica-plating; 86–100% of such subclones in each case showed Ura⁻ phenotype, indicating that the [PSI+] variants had been largely eliminated by pM76, pM75, and pM78.