Summary: Transductional mapping, with phage ES18 or ES18., showed that several mutations causing the RfaH phenotype (defective formation of galactose I and also of more distal units of the lipopolysaccharide core) were located between and in the linkage map; the affected locus is designated The mutation of one strain of RfaH phenotype was located elsewhere, at an unidentified locus. Introduction of an F” plasmid containing the segment of the chromosome into several mutants restored the “smooth” (Rfa) phenotype. Several mutations, and that of the phenotypically similar mutant, caused increased sensitivity to bacitracin, polymyxin, novobiocin, nafcillin and oxacillin, as expected if the mutations have no effect on the formation of the part of the lipopolysaccharide core proximal to the galactose units.


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