page 625 suggest that the plasmid accomplishes this by recruiting a cellular factor used for chromosomal separation.
The authors first noticed that mutations that disturb chromosome segregation similarly affect plasmid segregation, so they examined whether proteins involved in sister chromatid pairing also function during plasmid partitioning. They found that a cohesin subunit, Mcd1, was recruited by plasmid proteins Rep1p and Rep2p to a plasmid sequence, STB. STB does not resemble chromosomal cohesin-binding sequences, and cohesin abnormally expressed during G1 was found on STB but not chromosomes. Thus, the plasmid has independently evolved the ability to recruit cohesin.
A noncleavable form of cohesin blocked segregation of the plasmids, suggesting that cohesin is used to ensure even partitioning of the plasmids. However, it is also possible that the effect is due to association of the plasmids with missegregating chromosomes, as the Rep proteins were seen in association with chromosomes. Mutations that perturb the ability of plasmids, but not chromosomes, to recruit cohesin should clarify these possibilities. ▪