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. 1998 May;9(5):1065–1080. doi: 10.1091/mbc.9.5.1065

Table 2.

Suppression of the mating and meiosis deficiency in the ste9 strains by the cig2 mutation

Relevant genotype Frequency (%)
ZA AA V
Δste9 Δcig2 6.1 ± 0.8 10.6 ± 1.0 83.4 ± 1.8
ste9-B36 cig2-S18 17.1 ± 1.2 11.4 ± 0.6 71.6 ± 1.7
ste9-59 Δcig2 48.9 ± 3.7 0.8 ± 0.1 50.4 ± 3.7
ste9* <0.2 <0.2 >99.6

All strains are homothallic mating type (h90). Each strain was cultured on MEA for 2 d at 28°C. Data are the average of four to six independent countings and expressed as mean ± SE. At least 500 cells were examined in each counting. ZA, Zygotes and zygotic asci; AA, aberrant azygotic asci derived from haploid cells; V, vegetative cells. Construction and characterization of Δste9 allele is described in the text. ste9-B36 is a nonsense allele isolated by Leupold and Sipiczki (1991). ste9-59 is a novel allele encoding partially active protein (our unpublished result, see text). ste9* represents all three ste9 alleles described above. The cig2-S18 mutation was identified as an extragenic suppressor of the sterility of ste9-B36 strain. This cig2 mutation inactivates the protein because it cannot complement the deleted cig2 allele (Kitamura, unpublished).