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J Bacteriol. 1968 August; 96(2): 462-471
Copyright © 1968 American Society for Microbiology. All Rights Reserved.

Analysis of Melibiose Mutants Deficient in -Galactosidase and Thiomethylgalactoside Permease II in Escherichia coli K-12

^a Laboratory of Molecular Biology, National Institute of Neurological Diseases and Blindness, Bethesda, Maryland 20014

ABSTRACT

Three types of mutants (mel^–) unable to metabolize the -D-galactoside, melibiose, were derived from Escherichia coli K-12. One type lacked -galactosidase; another lacked a specific transport system, termed thiomethylgalactoside (TMG) permease II; and the third lacked both of these functions. The mutational sites were genetically mapped by recombination frequency with different markers and by determination of chromosomal transfer in interrupted-mating experiments. All three mel^– mutant types mapped in a cluster near to the metA marker on the E. coli chromosome and were cotransducible. Induction studies revealed that the three -D-galactosides, melibiose, melibiitol, and galactinol, induced -galactosidase and TMG permease II coordinately; D-galactose also induced them but only in a galactokinaseless mutant. These data suggest that -galactosidase and TMG permease II may be components of a common operon.

¹ Present address: Institut für Mikrobiologie, Universität Erlangen-Nürnberg, 852 Erlangen, Friedrichstrasse 33, Germany.

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