TABLE 2.

rpl3 alleles obtained from the primary screen

Primary mutant	Mutation	Anisomycin resistancea	Killerb	% −1 PRFc
WT		1+	K+	8.8 ± 0.6
mak8-1	W255C, P257T	4+	K−	14.5 ± 0.4
W255C, A3	W255C	4+	K−	14.2 ± 0.3
P257T	P257T	3+	K−	13.9 ± 0.4
I282T, A9, A19, A30, A41, A43, A49, A52	I282T	2+	K−	13.2 ± 0.3
A1	L387F	2+	K−	11.3 ± 0.8
A2	Y49F, A107T	3+	K+	ND
A4	G225S, Y283C, T344S	3+	K++	ND
A5	S347F, K357M, K384T	3+	Ksl	9.0 ± 0.7
A6	H256Q, I282T, L387F	2+	Ksl	8.9 ± 0.6
A7	S2T, F16I, I278T, I282T, F365Y, K385T	2+	K−	8.1 ± 0.8
A8	V312I, K357E, I282T	2+	K+	ND
A10	I282T, M261I	3+	K+	ND
A11	H198T, I282T	2+	K+	ND
A12	K66E, I282T, R348G, R369S	2+	K+	ND
A13	I282T, Y343N	2+	K+	ND
A14	T81A, I282T, A285V	2+	K+	ND
A15	I282T, E316V	3+	K+	ND
A16, A23	T54A, L99F, I282T	3+	K+	ND
A18	V76I, L171W, I282T	2+	K+	ND
A20	P18S, G141R, I282T, L387F	3+	K+	ND
A22	F67L, I282T	2+	K+	ND
A27	K201E, N212S, A267S, I282T, L387F	2+	Ksl	11.3 ± 0.8
A29	L17S, H259L, I282T	2+	K−	12.1 ± 0.8
A31	L171W, I282T	2+	K+	ND
A36	V90A, W122G, I282T, L338S	2+	K+	ND
A37	I282T, K367M	2+	K++	ND
A38	I282T, T382S	2+	Ksl	17 ± 0.6
A42	E227V, I282T, T382S	3+	Ksl	16.4 ± 0.2
A44	G15C, I282T	2+	K−	11.6 ± 0.8
A45	I282T, L387F	3+	Ksl	7.3 ± 0.2
A48	K120N, I282T	3+	Ksl	7.9 ± 0.4
A50	R196L, I282T, F298I	3+	Ksl	14.6 ± 0.8
A53	H273Q, I282T, K333E	3+	Ksl	ND
A54	I282T, D299G	3+	K−	ND

^aNomenclature used to describe relative resistance to anisomycin refers to Fig. 1, where 1+ is wild type and additional pluses indicate the relative ability of 10-fold dilutions of cells to grow.

^bKiller phenotype of the mutants. K⁺ is wild type, K⁺⁺ represents the superkiller (Ski⁻) phenotype, K^sl indicates slow but eventual killer loss, and K⁻ means complete inability to maintain the phenotype.

^cProgrammed −1 ribosomal frameshifting efficiencies were determined in vivo using dual luciferase reporters (22). Mean and standard errors were calculated as previously described (24). ND, not determined.