Multiple factors and processes involved in host cell killing by bacteriophage Mu: Characterization and mapping
The regions of bacteriophage Mu involved in host cell killing were determined by infection of a λ-immune host with 12 λpMu-transducing phages carrying different amounts of Mu DNA beginning at the left end. Infecting λpMu phages containing 5.0 (±0.2) kb or less of the left end of Mu DNA did not kill...
Gespeichert in:
Veröffentlicht in: | Virology (New York, N.Y.) N.Y.), 1984-07, Vol.136 (1), p.168-185 |
---|---|
Hauptverfasser: | , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 185 |
---|---|
container_issue | 1 |
container_start_page | 168 |
container_title | Virology (New York, N.Y.) |
container_volume | 136 |
creator | Waggoner, Barbara T. Marrs, Carl F. Howe, Martha M. Pato, Martin L. |
description | The regions of bacteriophage Mu involved in host cell killing were determined by infection of a λ-immune host with 12 λpMu-transducing phages carrying different amounts of Mu DNA beginning at the left end. Infecting λpMu phages containing 5.0 (±0.2) kb or less of the left end of Mu DNA did not kill the λ-immune host, whereas λpMu containing 5.1 kb did kill, thus locating the right end of the
kil gene between approximately 5.0 and 5.1 kb. For the Kil
+ phages the extent of killing increased as the multiplicity of infection (m.o.i.) increased. In addition, killing was also affected by the presence of at least two other regions of Mu DNA: one, located between 5.1 and 5.8 kb, decreased the extent of killing; the other, located between 6.3 and 7.9 kb, greatly increased host cell killing. Killing was also assayed after λpMu infection of a λ-immune host carrying a mini-Mu deleted for most of the
B gene and the middle region of Mu DNA. Complementation of mini-Mu replication by infecting B
+ λpMu phages resulted in killing of the λ-immune, mini-Mu-containing host, regardless of the presence or absence of the Mu
kil gene. The extent of host cell killing increased as the m.o.i. of the infecting λpMu increased, and was further enhanced by both the presence of the
kil gene and the region located between 6.3 and 7.9 kb. These distinct processes of
kil-mediated killing in the absence of replication and non-
kil-mediated killing in the presence of replication were also observed after induction of replication-deficient and
kil mutant prophages, respectively. |
doi_str_mv | 10.1016/0042-6822(84)90257-5 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_81148106</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>0042682284902575</els_id><sourcerecordid>81148106</sourcerecordid><originalsourceid>FETCH-LOGICAL-c388t-e97b7e3dcc1b20dac40a08477edfbafc1e7e6e97416cb53164302c15e0815d043</originalsourceid><addsrcrecordid>eNqFUcFO3DAQtSoQbGn_ACSfED2EjmPHcThUqlYtVAJxoWfLsSesaTZO7WQl-Pp62RVHevLY897zzHuEnDK4ZMDkVwBRFlKV5YUSXxooq7qoPpAFg0YWwAU7IIs3yDH5mNIT5HtdwxE5kiUXsmkWZLib-8mPPdLO2CnERM3g6BiDxZQwUT9sQr9Blwu6CmmiFvue_vF974dH2j7TNtMw-jCuzCPSu_mKLlcm7h5fzOTD8Kq4NuOYGZ_IYWf6hJ_35wn5_fPHw_KmuL2__rX8fltYrtRUYFO3NXJnLWtLcMYKMKDy7Oi61nSWYY0ygwSTtq04k4JDaVmFoFjlQPATcr7TzZv8nTFNeu3TdnQzYJiTVowJxUD-F8h4U_JGNhkodkAbQ0oROz1GvzbxWTPQ2zz01my9NVsroV_z0FWmne3153aN7o20DyD3v-36mN3YeIw6WY-DRecj2km74N__4B9Bwps2</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>13923969</pqid></control><display><type>article</type><title>Multiple factors and processes involved in host cell killing by bacteriophage Mu: Characterization and mapping</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Waggoner, Barbara T. ; Marrs, Carl F. ; Howe, Martha M. ; Pato, Martin L.</creator><creatorcontrib>Waggoner, Barbara T. ; Marrs, Carl F. ; Howe, Martha M. ; Pato, Martin L.</creatorcontrib><description>The regions of bacteriophage Mu involved in host cell killing were determined by infection of a λ-immune host with 12 λpMu-transducing phages carrying different amounts of Mu DNA beginning at the left end. Infecting λpMu phages containing 5.0 (±0.2) kb or less of the left end of Mu DNA did not kill the λ-immune host, whereas λpMu containing 5.1 kb did kill, thus locating the right end of the
kil gene between approximately 5.0 and 5.1 kb. For the Kil
+ phages the extent of killing increased as the multiplicity of infection (m.o.i.) increased. In addition, killing was also affected by the presence of at least two other regions of Mu DNA: one, located between 5.1 and 5.8 kb, decreased the extent of killing; the other, located between 6.3 and 7.9 kb, greatly increased host cell killing. Killing was also assayed after λpMu infection of a λ-immune host carrying a mini-Mu deleted for most of the
B gene and the middle region of Mu DNA. Complementation of mini-Mu replication by infecting B
+ λpMu phages resulted in killing of the λ-immune, mini-Mu-containing host, regardless of the presence or absence of the Mu
kil gene. The extent of host cell killing increased as the m.o.i. of the infecting λpMu increased, and was further enhanced by both the presence of the
kil gene and the region located between 6.3 and 7.9 kb. These distinct processes of
kil-mediated killing in the absence of replication and non-
kil-mediated killing in the presence of replication were also observed after induction of replication-deficient and
kil mutant prophages, respectively.</description><identifier>ISSN: 0042-6822</identifier><identifier>EISSN: 1096-0341</identifier><identifier>DOI: 10.1016/0042-6822(84)90257-5</identifier><identifier>PMID: 6234699</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Bacteriophage lambda - genetics ; Bacteriophage mu - genetics ; Bacteriophage mu - physiology ; DNA Replication ; DNA, Viral - genetics ; Escherichia coli - physiology ; Genes, Viral ; Kinetics ; Lysogeny ; Mutation ; phage Mu ; Recombination, Genetic ; Viral Plaque Assay ; Virus Replication</subject><ispartof>Virology (New York, N.Y.), 1984-07, Vol.136 (1), p.168-185</ispartof><rights>1984</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c388t-e97b7e3dcc1b20dac40a08477edfbafc1e7e6e97416cb53164302c15e0815d043</citedby><cites>FETCH-LOGICAL-c388t-e97b7e3dcc1b20dac40a08477edfbafc1e7e6e97416cb53164302c15e0815d043</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0042-6822(84)90257-5$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6234699$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Waggoner, Barbara T.</creatorcontrib><creatorcontrib>Marrs, Carl F.</creatorcontrib><creatorcontrib>Howe, Martha M.</creatorcontrib><creatorcontrib>Pato, Martin L.</creatorcontrib><title>Multiple factors and processes involved in host cell killing by bacteriophage Mu: Characterization and mapping</title><title>Virology (New York, N.Y.)</title><addtitle>Virology</addtitle><description>The regions of bacteriophage Mu involved in host cell killing were determined by infection of a λ-immune host with 12 λpMu-transducing phages carrying different amounts of Mu DNA beginning at the left end. Infecting λpMu phages containing 5.0 (±0.2) kb or less of the left end of Mu DNA did not kill the λ-immune host, whereas λpMu containing 5.1 kb did kill, thus locating the right end of the
kil gene between approximately 5.0 and 5.1 kb. For the Kil
+ phages the extent of killing increased as the multiplicity of infection (m.o.i.) increased. In addition, killing was also affected by the presence of at least two other regions of Mu DNA: one, located between 5.1 and 5.8 kb, decreased the extent of killing; the other, located between 6.3 and 7.9 kb, greatly increased host cell killing. Killing was also assayed after λpMu infection of a λ-immune host carrying a mini-Mu deleted for most of the
B gene and the middle region of Mu DNA. Complementation of mini-Mu replication by infecting B
+ λpMu phages resulted in killing of the λ-immune, mini-Mu-containing host, regardless of the presence or absence of the Mu
kil gene. The extent of host cell killing increased as the m.o.i. of the infecting λpMu increased, and was further enhanced by both the presence of the
kil gene and the region located between 6.3 and 7.9 kb. These distinct processes of
kil-mediated killing in the absence of replication and non-
kil-mediated killing in the presence of replication were also observed after induction of replication-deficient and
kil mutant prophages, respectively.</description><subject>Bacteriophage lambda - genetics</subject><subject>Bacteriophage mu - genetics</subject><subject>Bacteriophage mu - physiology</subject><subject>DNA Replication</subject><subject>DNA, Viral - genetics</subject><subject>Escherichia coli - physiology</subject><subject>Genes, Viral</subject><subject>Kinetics</subject><subject>Lysogeny</subject><subject>Mutation</subject><subject>phage Mu</subject><subject>Recombination, Genetic</subject><subject>Viral Plaque Assay</subject><subject>Virus Replication</subject><issn>0042-6822</issn><issn>1096-0341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUcFO3DAQtSoQbGn_ACSfED2EjmPHcThUqlYtVAJxoWfLsSesaTZO7WQl-Pp62RVHevLY897zzHuEnDK4ZMDkVwBRFlKV5YUSXxooq7qoPpAFg0YWwAU7IIs3yDH5mNIT5HtdwxE5kiUXsmkWZLib-8mPPdLO2CnERM3g6BiDxZQwUT9sQr9Blwu6CmmiFvue_vF974dH2j7TNtMw-jCuzCPSu_mKLlcm7h5fzOTD8Kq4NuOYGZ_IYWf6hJ_35wn5_fPHw_KmuL2__rX8fltYrtRUYFO3NXJnLWtLcMYKMKDy7Oi61nSWYY0ygwSTtq04k4JDaVmFoFjlQPATcr7TzZv8nTFNeu3TdnQzYJiTVowJxUD-F8h4U_JGNhkodkAbQ0oROz1GvzbxWTPQ2zz01my9NVsroV_z0FWmne3153aN7o20DyD3v-36mN3YeIw6WY-DRecj2km74N__4B9Bwps2</recordid><startdate>19840715</startdate><enddate>19840715</enddate><creator>Waggoner, Barbara T.</creator><creator>Marrs, Carl F.</creator><creator>Howe, Martha M.</creator><creator>Pato, Martin L.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>19840715</creationdate><title>Multiple factors and processes involved in host cell killing by bacteriophage Mu: Characterization and mapping</title><author>Waggoner, Barbara T. ; Marrs, Carl F. ; Howe, Martha M. ; Pato, Martin L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-e97b7e3dcc1b20dac40a08477edfbafc1e7e6e97416cb53164302c15e0815d043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Bacteriophage lambda - genetics</topic><topic>Bacteriophage mu - genetics</topic><topic>Bacteriophage mu - physiology</topic><topic>DNA Replication</topic><topic>DNA, Viral - genetics</topic><topic>Escherichia coli - physiology</topic><topic>Genes, Viral</topic><topic>Kinetics</topic><topic>Lysogeny</topic><topic>Mutation</topic><topic>phage Mu</topic><topic>Recombination, Genetic</topic><topic>Viral Plaque Assay</topic><topic>Virus Replication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Waggoner, Barbara T.</creatorcontrib><creatorcontrib>Marrs, Carl F.</creatorcontrib><creatorcontrib>Howe, Martha M.</creatorcontrib><creatorcontrib>Pato, Martin L.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Virology (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Waggoner, Barbara T.</au><au>Marrs, Carl F.</au><au>Howe, Martha M.</au><au>Pato, Martin L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Multiple factors and processes involved in host cell killing by bacteriophage Mu: Characterization and mapping</atitle><jtitle>Virology (New York, N.Y.)</jtitle><addtitle>Virology</addtitle><date>1984-07-15</date><risdate>1984</risdate><volume>136</volume><issue>1</issue><spage>168</spage><epage>185</epage><pages>168-185</pages><issn>0042-6822</issn><eissn>1096-0341</eissn><abstract>The regions of bacteriophage Mu involved in host cell killing were determined by infection of a λ-immune host with 12 λpMu-transducing phages carrying different amounts of Mu DNA beginning at the left end. Infecting λpMu phages containing 5.0 (±0.2) kb or less of the left end of Mu DNA did not kill the λ-immune host, whereas λpMu containing 5.1 kb did kill, thus locating the right end of the
kil gene between approximately 5.0 and 5.1 kb. For the Kil
+ phages the extent of killing increased as the multiplicity of infection (m.o.i.) increased. In addition, killing was also affected by the presence of at least two other regions of Mu DNA: one, located between 5.1 and 5.8 kb, decreased the extent of killing; the other, located between 6.3 and 7.9 kb, greatly increased host cell killing. Killing was also assayed after λpMu infection of a λ-immune host carrying a mini-Mu deleted for most of the
B gene and the middle region of Mu DNA. Complementation of mini-Mu replication by infecting B
+ λpMu phages resulted in killing of the λ-immune, mini-Mu-containing host, regardless of the presence or absence of the Mu
kil gene. The extent of host cell killing increased as the m.o.i. of the infecting λpMu increased, and was further enhanced by both the presence of the
kil gene and the region located between 6.3 and 7.9 kb. These distinct processes of
kil-mediated killing in the absence of replication and non-
kil-mediated killing in the presence of replication were also observed after induction of replication-deficient and
kil mutant prophages, respectively.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>6234699</pmid><doi>10.1016/0042-6822(84)90257-5</doi><tpages>18</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0042-6822 |
ispartof | Virology (New York, N.Y.), 1984-07, Vol.136 (1), p.168-185 |
issn | 0042-6822 1096-0341 |
language | eng |
recordid | cdi_proquest_miscellaneous_81148106 |
source | MEDLINE; Elsevier ScienceDirect Journals Complete; EZB-FREE-00999 freely available EZB journals |
subjects | Bacteriophage lambda - genetics Bacteriophage mu - genetics Bacteriophage mu - physiology DNA Replication DNA, Viral - genetics Escherichia coli - physiology Genes, Viral Kinetics Lysogeny Mutation phage Mu Recombination, Genetic Viral Plaque Assay Virus Replication |
title | Multiple factors and processes involved in host cell killing by bacteriophage Mu: Characterization and mapping |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T07%3A40%3A49IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Multiple%20factors%20and%20processes%20involved%20in%20host%20cell%20killing%20by%20bacteriophage%20Mu:%20Characterization%20and%20mapping&rft.jtitle=Virology%20(New%20York,%20N.Y.)&rft.au=Waggoner,%20Barbara%20T.&rft.date=1984-07-15&rft.volume=136&rft.issue=1&rft.spage=168&rft.epage=185&rft.pages=168-185&rft.issn=0042-6822&rft.eissn=1096-0341&rft_id=info:doi/10.1016/0042-6822(84)90257-5&rft_dat=%3Cproquest_cross%3E81148106%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=13923969&rft_id=info:pmid/6234699&rft_els_id=0042682284902575&rfr_iscdi=true |