Atypical deletions generated by mutated IS102 elements.

The element IS102 potentially codes for two polypeptide chains. We have introduced several mutations in the larger one near the COOH terminus and determined the residual ability of the mutated elements to generate deletions in order to assign a role to this polypeptide chain. We show that in these elements, deletions still occur, although at a reduced level, but that in all cases examined so far the ends of the element are no longer recognized as the fixed endpoint of IS-mediated deletions, even though some other structural features of normal deletions formation are still present.