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. 2003 Apr;2(2):341–350. doi: 10.1128/EC.2.2.341-350.2003

TABLE 2.

Lack of effect of disruption of hH1 on RIP mutations

Type Crossa Relevant genotype % RIP frequency (mean ± SD)b No. of progeny analyzed
1 FGSC 987 × N228 (+) × al-1+/al-1+ 47 ± 9 1,786
2 N1815 × N228 hH1RIP × al-1+/al-1+ 77 ± 6 2,023
3 s-wt × N228 (+) × al-1+/al-1+ 66 ± 6 6,348
4 s-hH1 × N228 hH1RIP × al-1+/al-1+ 57 ± 6 4,045
5 d-hH1 × FGSC 987 hH1RIP; al-1+/al-1+ × (+) 69 ± 14 3,067
6 d-hH1 × N1815 hH1RIP; al-1+/al-1+ × hH1RIP 73 ± 11 2,870
7 d-wt × FGSC 987 al-1+/al-1+ × (+) 73 ± 6 4,823
8 d-wt × N1815 al-1+/al-1+ × hH1RIP 74 ± 7 4,288
a

Strain N228 has an ectopic duplication of the wild-type al-1+ gene, and FGSC 987 is a wild-type (+) strain. A total of 11 wild-type (s-wt) and 7 hH1RIP (s-hH1) progeny were isolated from a cross between N1815 and FGSC 988. Crosses of s-wt and s-hH1 strains with N228 (type 3 and 4 crosses) were designed to test linkage of the hH1RIP allele with increased RIP frequencies observed in crosses of N1815 and N228 (compare type 1 and 2 crosses). Duplications of al-1+ in wild-type (d-wt) or hH1RIP (d-hH1) progeny were obtained by crossing N1815 and N228 and selecting progeny whose al-1+ copies had survived RIP. Eight d-hH1 and seven d-wt strains were crossed with wild-type or hH1RIP strains (type 5 to 8 crosses).

b

Because all crosses included a parent with a single al-1 gene, the RIP frequency was calculated as (number of white colonies/total number of colonies) × 200.