Reversion studies were done by exposing m- mutants to three mutagens: 5-bromouracil (BU) (causes AT->GC or GC->AT transitions), hydroxylamine (HA) (causes GC->AT transitions), and an acridine dye (small insertions or deletions). The resulting frequencies of wild-type revertants were compared with the spontaneous frequencies in the table below:
Revertants per 108 nuclei
Mutant Spontaneous BU HA Acridine a2 1.5 28.1 1.1 1.9 a4 1.2 1.8 1.9 40 a6 80 670 912 75 a8 5.0 5.0 5.1 5.1
Assume reversion takes place in the same gene originally mutated. What was the nature of the mutational event that gave rise to the mutants in the first place (i.e., the m+ -> m- event)? Be as specific as possible (e.g. if a transition then was it AT->GC or GC->AT or canât be determined which direction) based on the data presented, and ignore the possibility of transposable element mutations.
a2__________________________
a4__________________________
a6__________________________
a8__________________________
Reversion studies were done by exposing m- mutants to three mutagens: 5-bromouracil (BU) (causes AT->GC or GC->AT transitions), hydroxylamine (HA) (causes GC->AT transitions), and an acridine dye (small insertions or deletions). The resulting frequencies of wild-type revertants were compared with the spontaneous frequencies in the table below:
Revertants per 108 nuclei
| Mutant | Spontaneous | BU | HA | Acridine |
| a2 | 1.5 | 28.1 | 1.1 | 1.9 |
| a4 | 1.2 | 1.8 | 1.9 | 40 |
| a6 | 80 | 670 | 912 | 75 |
| a8 | 5.0 | 5.0 | 5.1 | 5.1 |
Assume reversion takes place in the same gene originally mutated. What was the nature of the mutational event that gave rise to the mutants in the first place (i.e., the m+ -> m- event)? Be as specific as possible (e.g. if a transition then was it AT->GC or GC->AT or canât be determined which direction) based on the data presented, and ignore the possibility of transposable element mutations.
a2__________________________
a4__________________________
a6__________________________
a8__________________________
