Table 2.

Phenotypes of ada mutants

Double mutantaPhenotypee
ada1Δ swi1Δ b, dDead
ada1Δ snf5Δ2 c Dead
ada1Δ srb5Δ c Dead
ada1Δ gal11Δ b, dDead
ada2Δ swi1Δ Alive, sick
ada2Δ snf2Δ d Alive, sick
ada2Δ srb5Δ Alive, slow growing
ada2Δ srb2Δ Alive, slow growing
ada2Δ gal11Δ Alive
ada3Δ swi1Δ d Alive, sick
ada3Δ snf2Δ Alive, sick
ada3Δ srb5Δ Alive, slow growing
ada3Δ srb2Δ Alive, slow growing
ada3Δ gal11Δ d Alive
ada3Δ sin4Δ Alive
  • a In each cross, genetic markers allowed us to unambiguously identify all relevant markers in every tetrad. The parents for the crosses in the order listed are as follows: FY602 × FY1254, FY1658 × FY1557, FY1557 × L937, FY602 × FY1657, FY1548 × FY1254, FY602 × FY1656, FY1548 × L937, FY1548 × FY1359, FY1554 × FY1657, FY602 × FY1254, FY1542 × FY1656, FY1542 × L937, FY1542 × FY1359, FY602 × FY1657, and FY1253 × FY1545.

  • b Viability was scored by the ability of the double mutant to lose a URA3-marked wild-typeSWI1 (BD1) or GAL11 (FB565) plasmid as determined by growth on 5-FOA medium (alive, growth on 5-FOA; dead, no growth on 5-FOA).

  • c Viability was determined by failure to recover any double mutants after dissecting 20 tetrads.

  • d For all crosses in which FY602 is listed as the MAT a parent, the double mutant was constructed by first creating a diploid between FY602 and the correspondingMATα parent. This diploid was then transformed with a PCR fragment containing the relevant ADA ORF completely disrupted by the HIS3 gene. Those single purified His+ diploid transformants that displayed correctADA knockout integration (as described in Materials and Methods) were used in tetrad analysis.

  • e Sick, extremely small colonies after 2 to 3 days of growth at 30°C. Slow growing, colonies were moderately smaller than those of wild-type strains after 2 to 3 days of growth at 30°C.