Antibiotic resistances of two sets of transductants (along with those of their smooth and sister transductants) were measured. One set was derived from a smooth LT2 parent and the other from a smooth LT7 parent. Results showed that strains with defects at the (R-res-2) level and deeper were more susceptible to bacitracin, novobiocin and polymyxin. Those with defects at the level or deeper were in addition more sensitive to vancomycin, erythromycin, oxacillin and nafcillin. At these levels the presence or absence of galactose I or glucose I from the lipopolysaccharide core made a considerable difference. A heptose-less mutant was the most sensitive of the strains tested to the above named antibiotics. Strains with lesions at several levels of defect showed slight increases in resistances to tetracycline, cephalothin, ampicillin and penicillin.

One would expect strains with mutations to be similar to (R-res-2) strains and those with mutations to be similar to strains if the core defects accounted for the differing antibiotic resistances. They proved to be so except that the and strains in the FIRN line were as resistant to novobiocin as were smooth strains.

The results are interpreted in respect to Nikaido's hypothesis that hydrophilic antibiotics with molecular weights of less than about 650 can gain access to the periplasmic space through protein-lined, water-filled pores and that hydrophobic ones can gain access in deep rough strains when phospholipid patches appear on the surface due to absence of polysaccharides and proteins.


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