| pubmed-article:7925310 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7925310 | lifeskim:mentions | umls-concept:C0282114 | lld:lifeskim |
| pubmed-article:7925310 | lifeskim:mentions | umls-concept:C0521009 | lld:lifeskim |
| pubmed-article:7925310 | lifeskim:mentions | umls-concept:C0007623 | lld:lifeskim |
| pubmed-article:7925310 | lifeskim:mentions | umls-concept:C1383501 | lld:lifeskim |
| pubmed-article:7925310 | lifeskim:mentions | umls-concept:C0597979 | lld:lifeskim |
| pubmed-article:7925310 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:7925310 | lifeskim:mentions | umls-concept:C1999230 | lld:lifeskim |
| pubmed-article:7925310 | pubmed:issue | 19 | lld:pubmed |
| pubmed-article:7925310 | pubmed:dateCreated | 1994-11-4 | lld:pubmed |
| pubmed-article:7925310 | pubmed:abstractText | A mechanism for bacteria to monitor the status of their vital cell wall peptidoglycan is suggested by the convergence of two phenomena: peptidoglycan recycling and beta-lactamase induction. ampG and ampD, genes essential for beta-lactamase regulation, are here shown to be required for recycling as well. Cells lacking either AmpG or AmpD lose up to 40% of their peptidoglycan per generation, whereas Escherichia coli normally suffers minimal losses and instead recycles 40 or 50% of the tripeptide, L-alanyl-D-glutamyl-meso-diaminopimelic acid, from its peptidoglycan each generation. The ampG mutant releases peptidoglycan-derived material into the medium. In contrast, the ampD mutant accumulates a novel cell wall muropeptide, 1,6-anhydro N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid (anhMurNAc-tripeptide), in its cytoplasm. This work suggests that AmpG is the permease for a large muropeptide and AmpD is a novel cytosolic N-acetylmuramyl-L-alanine amidase that cleaves anhMurNAc-tripeptide to release tripeptide, which is then recycled. These results also suggest that the phenomenon of beta-lactamase induction is regulated by the level of muropeptide(s) in the cytoplasm, since an ampD mutation that results in beta-lactamase expression even in the absence of a beta-lactamase inducer coincides with accumulation of anhMurNAc-tripeptide. The transcriptional regulator AmpR is presumably converted into an activator for beta-lactamase production by sensing the higher level of muropeptide(s). This may be an example of a general mechanism for signaling the progress of external events such as cell wall maturation, cell division or cell wall damage. | lld:pubmed |
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| pubmed-article:7925310 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7925310 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7925310 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7925310 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:7925310 | pubmed:issn | 0261-4189 | lld:pubmed |
| pubmed-article:7925310 | pubmed:author | pubmed-author:NormarkSS | lld:pubmed |
| pubmed-article:7925310 | pubmed:author | pubmed-author:JacobsCC | lld:pubmed |
| pubmed-article:7925310 | pubmed:author | pubmed-author:ParkJ TJT | lld:pubmed |
| pubmed-article:7925310 | pubmed:author | pubmed-author:HuangL JLJ | lld:pubmed |
| pubmed-article:7925310 | pubmed:author | pubmed-author:BartowskyEE | lld:pubmed |
| pubmed-article:7925310 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7925310 | pubmed:day | 3 | lld:pubmed |
| pubmed-article:7925310 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:7925310 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7925310 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7925310 | pubmed:pagination | 4684-94 | lld:pubmed |
| pubmed-article:7925310 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:7925310 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7925310 | pubmed:articleTitle | Bacterial cell wall recycling provides cytosolic muropeptides as effectors for beta-lactamase induction. | lld:pubmed |
| pubmed-article:7925310 | pubmed:affiliation | Department of Molecular Biology and Microbiology, Tufts University, Boston, MA 02111. | lld:pubmed |
| pubmed-article:7925310 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7925310 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7925310 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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