PMID:2681148: Difference between revisions

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<span style = 'font-size: large'> '''Michelsen, U, Bösl, M, Dingermann, T and Kersten, H'''  (1989) The tyrT locus of Escherichia coli exhibits a regulatory function for glycine metabolism.''J. Bacteriol.'' '''171''':5987-94</span>
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!align=left  |Citation
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'''Michelsen, U, Bösl, M, Dingermann, T and Kersten, H'''  (1989) The tyrT locus of Escherichia coli exhibits a regulatory function for glycine metabolism. ''J. Bacteriol.'' '''171''':5987-94
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!align=left  |Abstract
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The tyrT locus in Escherichia coli codes for two gene copies of tRNA(1Tyr). Both genes are organized in one operon, which has a unique structure. The two tRNA genes are separated by a spacer segment highly homologous to a part of a unit which is repeated three times in the distal portion of the locus. This operon also contains coding capacity for a small basic protein. A genomic deletion of this locus was constructed and marked by a kanamycin resistance cassette. Deletion mutants exhibited a characteristic phenotype when cells were shifted from rich medium to minimal medium. The cells entered a transient lag phase, apparently resulting from specific glycine starvation. This phenotype involved stringent response and was therefore not observed in relA derivatives. The genomic deletion was complemented in trans by a plasmid-borne tyrT locus. From deletion mapping, it can be concluded that a product of the tyrT operon is responsible for complementation. However, neither the tRNA(1Tyr) nor the proposed basic protein is the complementation-competent entity.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2681148 PubMed] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC210463 PMC210463]


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|{{TableHeadingColor}} |'''Abstract''' || The tyrT locus in Escherichia coli codes for two gene copies of tRNA(1Tyr). Both genes are organized in one operon, which has a unique structure. The two tRNA genes are separated by a spacer segment highly homologous to a part of a unit which is repeated three times in the distal portion of the locus. This operon also contains coding capacity for a small basic protein. A genomic deletion of this locus was constructed and marked by a kanamycin resistance cassette. Deletion mutants exhibited a characteristic phenotype when cells were shifted from rich medium to minimal medium. The cells entered a transient lag phase, apparently resulting from specific glycine starvation. This phenotype involved stringent response and was therefore not observed in relA derivatives. The genomic deletion was complemented in trans by a plasmid-borne tyrT locus. From deletion mapping, it can be concluded that a product of the tyrT operon is responsible for complementation. However, neither the tRNA(1Tyr) nor the proposed basic protein is the complementation-competent entity.
!align=left  |Keywords
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Amino Acids/metabolism; Blotting, Southern; Chromosome Deletion; Cloning, Molecular; Escherichia coli/genetics; Escherichia coli/growth & development; Escherichia coli/metabolism; Genes, Bacterial; Genes, Regulator; Genetic Complementation Test; Genotype; Glycine/metabolism; Mutation; Nucleic Acid Hybridization; RNA, Transfer, Amino Acid-Specific/genetics; RNA, Transfer, Tyr/genetics; Restriction Mapping
|{{TableHeadingColor}} nowrap |'''Links''' ||  [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2681148 PubMed]
 
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Latest revision as of 04:44, 15 September 2013

Citation

Michelsen, U, Bösl, M, Dingermann, T and Kersten, H (1989) The tyrT locus of Escherichia coli exhibits a regulatory function for glycine metabolism. J. Bacteriol. 171:5987-94

Abstract

The tyrT locus in Escherichia coli codes for two gene copies of tRNA(1Tyr). Both genes are organized in one operon, which has a unique structure. The two tRNA genes are separated by a spacer segment highly homologous to a part of a unit which is repeated three times in the distal portion of the locus. This operon also contains coding capacity for a small basic protein. A genomic deletion of this locus was constructed and marked by a kanamycin resistance cassette. Deletion mutants exhibited a characteristic phenotype when cells were shifted from rich medium to minimal medium. The cells entered a transient lag phase, apparently resulting from specific glycine starvation. This phenotype involved stringent response and was therefore not observed in relA derivatives. The genomic deletion was complemented in trans by a plasmid-borne tyrT locus. From deletion mapping, it can be concluded that a product of the tyrT operon is responsible for complementation. However, neither the tRNA(1Tyr) nor the proposed basic protein is the complementation-competent entity.

Links

PubMed PMC210463

Keywords

Amino Acids/metabolism; Blotting, Southern; Chromosome Deletion; Cloning, Molecular; Escherichia coli/genetics; Escherichia coli/growth & development; Escherichia coli/metabolism; Genes, Bacterial; Genes, Regulator; Genetic Complementation Test; Genotype; Glycine/metabolism; Mutation; Nucleic Acid Hybridization; RNA, Transfer, Amino Acid-Specific/genetics; RNA, Transfer, Tyr/genetics; Restriction Mapping

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