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Microcin-E492-insensitive Mutants of Escherichia coli K12
Author(s) -
Anthony P. Pugsley,
Francisco J. Moreno,
Vı́ctor de Lorenzo
Publication year - 1986
Publication title -
microbiology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 179
eISSN - 1465-2080
pISSN - 1350-0872
DOI - 10.1099/00221287-132-12-3253
Subject(s) - colicin , escherichia coli , mutant , operon , biology , locus (genetics) , siderophore , gene , bacteriocin , bacterial outer membrane , microbiology and biotechnology , genetics , bacteria
Mutations in three Escherichia coli K12 genes, tonB, exbB and the newly discovered semA, reduce sensitivity to the low Mr polypeptide antibiotic microcin E492. The products of the tonB and exbB genes were previously shown to be involved in the uptake of siderophore-complexed iron and in the action of a number of colicins. Strains mutated at or close to semA (collectively referred to as sem mutations) remained fully sensitive to these colicins, and grew as well as wild-type strains under conditions of iron starvation. Expression of a number of sem-lacZ operon fusions was not affected by iron limitation, and sem mutations did not affect the production of iron-regulated outer membrane proteins which are known or thought to be involved in iron uptake. Hfr conjugation and P1 phage transduction experiments indicated that semA is located close to pabB at 40 min on the E. coli K12 chromosome. This places semA close to the mng locus, wherein mutations result in decreased manganese sensitivity. However, strains carrying the semA mutation exhibited increased manganese sensitivity.

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