Physiological and in vitro measurements showed that the RNA polymerase from streptolydigin-resistant cells was resistant to the drug. It was then desired to map the mutation. Most likely this mutation...

Physiological and in vitro measurements showed that the RNA polymerase from streptolydigin-resistant cells was resistant to the drug. It was then desired to map the mutation. Most likely this mutation would map near the rifamycin resistance mutation. The most straightforward way to show that the two markers were close to each other would have been to start with Stl r Rifs strain and to transduce it to Rif r from Rif r Stl s and determine if it became Stl s . Presumably this would show that the Rif and Stl alleles cotransduce. Why is this reasoning risky?