PMID:6330740: Difference between revisions

From EcoliWiki
Jump to navigation Jump to search
← Older editNewer edit →
/Volumes/r3/t3/ul/working/touchTables/touch_all_tables.php
imported>Wikientrybot
change PMID template to TableEdit version
Line 1: Line 1:
{{RightTOC}}
{{RightTOC}}
<!--box uid=d41d8cd98f00b204e9800998ecf8427e.149297.L522396397008b-->
<!--
******************************************************************************************
*
*  ** PLEASE DON'T EDIT THIS TABLE DIRECTLY.  Use the edit table link under the table. **
*
****************************************************************************************** -->
{|  id="L522396397008b"  class=" tableEdit PMID_info_table" 


<span style = 'font-size: large'> '''Volkert, MR and Nguyen, DC'''  (1984) Induction of specific Escherichia coli genes by sublethal treatments with alkylating agents.''Proc. Natl. Acad. Sci. U.S.A.'' '''81''':4110-4</span>
|-
!align=left  |Citation
||
'''No author listed'''  (1984) Induction of specific Escherichia coli genes by sublethal treatments with alkylating agents. ''Proc. Natl. Acad. Sci. U.S.A.'' '''81''':4110-4
|-
!align=left  |Abstract
||
Fusions of the lac operon to genes induced by treatment with sublethal levels of alkylating agents have been selected from random insertions of the Mu-dl(ApRlac) phage by screening for induction of beta-galactosidase activity in the presence of methyl methanesulfonate. Genetic analysis reveals that these fusions resulted from insertion of Mu-dl(ApRlac) into two regions of the chromosome. One region (aidA) is near his and, based on phenotypic effects, appears to represent insertion into the alkA gene. The other region (aidB) is in the 92.3- to 98-min region, which harbors no previously identified genes involved in repair of alkylation damage. The aidB fusions caused increased resistance to alkylating agents and caused little or no change in the biological effects of adaptation to alkylating agents. Unlike the aidA fusions, aidB fusions showed increased beta-galactosidase activity in untreated cells in a growth phase-dependent fashion. The ada-5 mutation, which blocks expression of the adaptive response, decreased induction of beta-galactosidase activity in both aidA and aidB fusions after alkylation treatments. Thus, both aidA and aidB share with adaptive response a common regulatory mechanism involving the ada gene. The growth phase-dependent control of the aidB fusions, however, is unaffected by ada, suggesting that a second regulatory mechanism exists that controls only aidB.
|-
!align=left  |Links
||
[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6330740 PubMed] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC345378 PMC345378]


{|{{Prettytable}} align = 'center' width= '70%'
|-
|-
|{{TableHeadingColor}} |'''Abstract''' || <protect>Fusions of the lac operon to genes induced by treatment with sublethal levels of alkylating agents have been selected from random insertions of the Mu-dl(ApRlac) phage by screening for induction of beta-galactosidase activity in the presence of methyl methanesulfonate. Genetic analysis reveals that these fusions resulted from insertion of Mu-dl(ApRlac) into two regions of the chromosome. One region (aidA) is near his and, based on phenotypic effects, appears to represent insertion into the alkA gene. The other region (aidB) is in the 92.3- to 98-min region, which harbors no previously identified genes involved in repair of alkylation damage. The aidB fusions caused increased resistance to alkylating agents and caused little or no change in the biological effects of adaptation to alkylating agents. Unlike the aidA fusions, aidB fusions showed increased beta-galactosidase activity in untreated cells in a growth phase-dependent fashion. The ada-5 mutation, which blocks expression of the adaptive response, decreased induction of beta-galactosidase activity in both aidA and aidB fusions after alkylation treatments. Thus, both aidA and aidB share with adaptive response a common regulatory mechanism involving the ada gene. The growth phase-dependent control of the aidB fusions, however, is unaffected by ada, suggesting that a second regulatory mechanism exists that controls only aidB.</protect>
!align=left  |Keywords
|-
||
|{{TableHeadingColor}} nowrap |'''Links''' ||  [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6330740 PubMed]<br/>
Acclimatization; Alkylating Agents/toxicity; DNA Restriction Enzymes; Enzyme Induction; Escherichia coli/drug effects; Escherichia coli/genetics; Escherichia coli/growth & development; Galactosidases/biosynthesis; Genes/drug effects; Genes, Bacterial/drug effects; Kinetics; Mutagens; Mutation; Species Specificity; Transduction, Genetic; beta-Galactosidase/biosynthesis; beta-Galactosidase/genetics
 
|- class="tableEdit_footer"
|<span class="tableEdit_editLink plainlinks">[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.149297.L522396397008b&page=149297&pagename={{FULLPAGENAMEE}}&type=1&template=PMID_info_table edit table]</span> ||
|}
|}
 
<!--box uid=d41d8cd98f00b204e9800998ecf8427e.149297.L522396397008b-->
==Significance {{HelpIcon|Help:Literature}} ==
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}
{{LitSignificance}}

Revision as of 19:32, 1 September 2013

Citation

No author listed (1984) Induction of specific Escherichia coli genes by sublethal treatments with alkylating agents. Proc. Natl. Acad. Sci. U.S.A. 81:4110-4

Abstract

Fusions of the lac operon to genes induced by treatment with sublethal levels of alkylating agents have been selected from random insertions of the Mu-dl(ApRlac) phage by screening for induction of beta-galactosidase activity in the presence of methyl methanesulfonate. Genetic analysis reveals that these fusions resulted from insertion of Mu-dl(ApRlac) into two regions of the chromosome. One region (aidA) is near his and, based on phenotypic effects, appears to represent insertion into the alkA gene. The other region (aidB) is in the 92.3- to 98-min region, which harbors no previously identified genes involved in repair of alkylation damage. The aidB fusions caused increased resistance to alkylating agents and caused little or no change in the biological effects of adaptation to alkylating agents. Unlike the aidA fusions, aidB fusions showed increased beta-galactosidase activity in untreated cells in a growth phase-dependent fashion. The ada-5 mutation, which blocks expression of the adaptive response, decreased induction of beta-galactosidase activity in both aidA and aidB fusions after alkylation treatments. Thus, both aidA and aidB share with adaptive response a common regulatory mechanism involving the ada gene. The growth phase-dependent control of the aidB fusions, however, is unaffected by ada, suggesting that a second regulatory mechanism exists that controls only aidB.

Links

PubMed PMC345378

Keywords

Acclimatization; Alkylating Agents/toxicity; DNA Restriction Enzymes; Enzyme Induction; Escherichia coli/drug effects; Escherichia coli/genetics; Escherichia coli/growth & development; Galactosidases/biosynthesis; Genes/drug effects; Genes, Bacterial/drug effects; Kinetics; Mutagens; Mutation; Species Specificity; Transduction, Genetic; beta-Galactosidase/biosynthesis; beta-Galactosidase/genetics

edit table

Significance

You can help EcoliWiki by summarizing why this paper is useful

Useful Materials and Methods

You can help Ecoliwiki by describing the useful materials (strains, plasmids, antibodies, etc) described in this paper.

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status
edit table


EcoliWiki Links

Add links to pages that link here (e.g. gene, product, method pages)

See also

References

See Help:References for how to manage references in EcoliWiki.

Retrieved from "https://ecoliwiki.org/colipedia/index.php?title=PMID:6330740&oldid=1437243"