Abstract
An E. coli K-12 mutant deficient in S-adenosylmethionine (SAM) synthesis, i.e ΔmetK, but expressing a rickettsial SAM transporter, can grow in glucose minimal medium if provided with both SAM and methionine. It uses the externally provided (R)-enantiomer of SAM as methyl donor to produce most but not all of its methionine, by methylation of homocysteine catalysed by homocysteine methyltransferase (MmuM). The ΔmetK cells are also altered in growth and are twice as long as those of the parent strain. When starved of SAM, the mutant makes a small proportion of very long cells suggesting a role of SAM and of methylation in the onset of crosswall formation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Carbon / metabolism*
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Cell Division*
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Culture Media / chemistry
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Escherichia coli K12 / cytology
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Escherichia coli K12 / genetics
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Escherichia coli K12 / metabolism
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Escherichia coli K12 / physiology*
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Escherichia coli Proteins / metabolism*
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Glucose / metabolism
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Homocysteine S-Methyltransferase / metabolism*
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Methionine / biosynthesis*
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Methionine Adenosyltransferase / deficiency*
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S-Adenosylmethionine / metabolism
Substances
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Culture Media
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Escherichia coli Proteins
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Carbon
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S-Adenosylmethionine
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Methionine
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Homocysteine S-Methyltransferase
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mmuM protein, E coli
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MetK protein, E coli
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Methionine Adenosyltransferase
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Glucose