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Involvement of gnt S in the control of GntI, the main system for gluconate metabolism in Escherichia coli
Author(s) -
Istúriz Tomás,
DíazBenjumea Rocio,
Rodriguez Neides,
Porco Antonietta
Publication year - 2001
Publication title -
journal of basic microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.58
H-Index - 54
eISSN - 1521-4028
pISSN - 0233-111X
DOI - 10.1002/1521-4028(200105)41:2<75::aid-jobm75>3.0.co;2-t
Subject(s) - mutant , operon , gene , phenotype , mutation , regulator , escherichia coli , metabolism , regulator gene , suppressor mutation , phosphorylation , biochemistry , chemistry , biology , gene expression
The initial steps of gluconate metabolism in E. coli , transport and phosphorylation, occur through duplicate activities. These activities have been included in two systems designated as GntI (main) and GntII (subsidiary), encoded by differently regulated operons located at the 76.4–77 and 95.3–96.9 regions on the map respectively. Despite recent molecular advances related to genetics and physiology of these systems, there is no information about the coordination of their expression when E. coli grows on gluconate. Under these conditions, the subsidiary gluconokinase ( gnt V gene, min 96.8) as well as the GntI activities are expressed in inducible form. Therefore it was of interest to find out if GntS, the positive regulator of gnt V has a similar effect on GntI activities expression. Our results agree with this hypothesis. GntS, in addition to its regulatory action on the gnt V gene, seems to assist, direct or indirectly, the expression of the GntI activities. A gnt S E. coli mutant does not grow on gluconate but spontaneously pseudoreverts to a gluconate growing phenotype at high rate per cell generation when cultivated in rich media with or without gluconate or mineral medium containing any other suitable carbon source. In the pseudorevertants, the thermosensitive gluconokinase remains repressed while the GntI activities are inducibly expressed. At present, the location and nature of the gnt S suppressor mutation are not known. Phage P1Kc mediated transductions have ruled out that it alters the gnt T gene. This is the first report on GntI activities alteration due to a lesion located out of the bio H‐ asd region.