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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1999-4-22
pubmed:abstractText
The glucose analog 2-deoxyglucose (2dGlc) inhibits the growth and multicellular development of Myxococcus xanthus. Mutants of M. xanthus resistant to 2dGlc, designated hex mutants, arise at a low spontaneous frequency. Expression of the Escherichia coli glk (glucokinase) gene in M. xanthus hex mutants restores 2dGlc sensitivity, suggesting that these mutants arise upon the loss of a soluble hexokinase function that phosphorylates 2dGlc to form the toxic intermediate, 2-deoxyglucose-6-phosphate. Enzyme assays of M. xanthus extracts reveal a soluble hexokinase (ATP:D-hexose-6-phosphotransferase; EC 2.7.1.1) activity but no phosphotransferase system activities. The hex mutants have lower levels of hexokinase activities than the wild type, and the levels of hexokinase activity exhibited by the hex mutants are inversely correlated with the ability of 2dGlc to inhibit their growth and sporulation. Both 2dGlc and N-acetylglucosamine act as inhibitors of glucose turnover by the M. xanthus hexokinase in vitro, consistent with the finding that glucose and N-acetylglucosamine can antagonize the toxic effects of 2dGlc in vivo.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-1097393, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-127561, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-13888810, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-14185314, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-14216425, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-1435260, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-1938885, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-1938915, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-1938958, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-19417, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-2152913, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-2201568, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-2509436, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-2825185, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-2985470, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-3011607, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-3017794, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-3060316, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-3280031, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-340926, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-3843705, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-3918984, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-415048, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-416222, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-42906, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-4302296, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-4868349, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-5788715, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-5929775, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-5929776, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-7592449, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-7716545, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-7716546, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-7783619, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-7815935, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-789368, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-7988874, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-8572884, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-8824635, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-8982095, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-8996101, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-9023215, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-9209041, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-9457865, http://linkedlifedata.com/resource/pubmed/commentcorrection/10094702-9765567
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0021-9193
pubmed:author
pubmed:issnType
Print
pubmed:volume
181
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2225-35
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Mutations that confer resistance to 2-deoxyglucose reduce the specific activity of hexokinase from Myxococcus xanthus.
pubmed:affiliation
Department of Microbiology, Molecular Biology and Biochemistry, University of Idaho, Moscow, Idaho 83844-3052, USA. pay@uidaho.edu
pubmed:publicationType
Journal Article
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