a. Mutant1: Reversion could not occur in this mutant. So it may be a deletion. Any cause of mutation could be a radiation.
Mutant2: In this mutant, proflavin cause addition or deletion of bases. Spontaneous reversion may arise during addition or deletion of bases.
Mutant3: 5-BU causes transition mutations. So, we understand that the original mutation is transition. Hydroxyl amine can cause GC- to -AT transition, but cannot revert it. The actual mutation in the mutant 3 should have been GC-to-AT transition.
Mutant4: Transitions or frameshift mutations are caused by chemical agents. Here, there is a spontaneous reversion. Hence, this mutation must be a transversion.
Mutant5: In this mutant, Hydroxyl amine can cause GC- to -AT transition and 5-BU also can result in transition mutations. There is spontaneous reversion. Hence, we can understand that the original mutation must be an AT-to-GC transition.
b. Mutant 1: The original mutation may be due to radiation.
Mutant 2: The possible mutagen may be an intercalating agent. The intercalating agents cause frameshift mutation.
Mutant3: The mutant must be a base analog. The original mutation must be GC-to-AT transition.
Mutant4: The mutagen may be X irradiation or any oxidizing agents.
Mutant 5: the original mutagen could be a base analog.
c. The second –site reversion is connected to the actual mutant at a distance of 20 map units. It can be considered as second gene. Auxotrophs are equal to half of the recombinants. These recombinants are produced by lab methods.