TABLE 1.
Gene | Taxet al. (1997) | Our study | % suppresseda |
---|---|---|---|
lin-12b | 109 | 247 | ND |
sup-17 | 5 | 10 | 52 (n = 353)c |
lag-2 | 2 | 0d | 94 (n = 189)c |
sel-6 | 2 | 0 | 90c |
sel-5e | 2 | 13 | 51c |
sel-4 | 1 | 1 | 31c |
sel-8 | 1 | 0 | 25c |
sel-7 | 1 | 6 | 53c |
sel(ar526) | 0 | 1 | 10 (n = 68)f |
lag-1g | 0 | 1 | 73 (n = 19)f |
bre-5(ar560) | 0 | 1 | 4 (n = 193)f |
sel(ar562) | 0 | 1 | 37 (n = 49)f |
sel(ar584) | 0 | 1 | 17 (n = 51)f |
sel(ar522, ar570) | 0 | 2 | 17 (n = 93)f |
sel(ar578) | 0 | 1 | 5 (n = 40)f |
Suppression of the lin-12(n302) egg-laying defect by the most penetrant allele of each sel gene.
Sequence changes associated with new alleles of lin-12:ar563, E492K; ar564, R721Q; and ar575, K1127E.
Suppression of egg laying by the most penetrant allele. Data are from Tax et al. (1997).
lag-2 alleles recovered by Tax et al. (1997) were dominant and would have been eliminated by our triage step.
Sequence changes associated with new alleles of sel-5: ar568, Q551stop; ar571, g → a acceptor splice-site mutation; ar574, R91stop; ar579, 525-bp deletion within the coding region; and ar588, g → a acceptor splice-site mutation.
Animals were also homozygous for unc-36(e251).
lag-1(ar519) encodes the L302F change.