Gene product 0.4 increases bacteriophage T7 competitiveness by inhibiting host cell division
Bacteriophages take over host resources primarily via the activity of proteins expressed early in infection. One of these proteins, produced by the Escherichia coli phage T7, is gene product (Gp) 0.4. Here, we show that Gp0.4 is a direct inhibitor of the E. coli filamenting temperature-sensitive mut...
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Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2013-11, Vol.110 (48), p.19549-19554 |
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creator | Kiro, Ruth Molshanski-Mor, Shahar Yosef, Ido Milam, Sara L. Erickson, Harold P. Qimron, Udi |
description | Bacteriophages take over host resources primarily via the activity of proteins expressed early in infection. One of these proteins, produced by the Escherichia coli phage T7, is gene product (Gp) 0.4. Here, we show that Gp0.4 is a direct inhibitor of the E. coli filamenting temperature-sensitive mutant Z division protein. A chemically synthesized Gp0.4 binds to purified filamenting temperature-sensitive mutant Z protein and directly inhibits its assembly in vitro. Consequently, expression of Gp0.4 in vivo is lethal to E. coli and results in bacteria that are morphologically elongated. We further show that this inhibition of cell division by Gp0.4 enhances the bacteriophage’s competitive ability. This division inhibition is thus a fascinating example of a strategy in bacteriophages to maximize utilization of their hosts’ cell resources. |
doi_str_mv | 10.1073/pnas.1314096110 |
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One of these proteins, produced by the Escherichia coli phage T7, is gene product (Gp) 0.4. Here, we show that Gp0.4 is a direct inhibitor of the E. coli filamenting temperature-sensitive mutant Z division protein. A chemically synthesized Gp0.4 binds to purified filamenting temperature-sensitive mutant Z protein and directly inhibits its assembly in vitro. Consequently, expression of Gp0.4 in vivo is lethal to E. coli and results in bacteria that are morphologically elongated. We further show that this inhibition of cell division by Gp0.4 enhances the bacteriophage’s competitive ability. This division inhibition is thus a fascinating example of a strategy in bacteriophages to maximize utilization of their hosts’ cell resources.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1314096110</identifier><identifier>PMID: 24218612</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Adaptation, Biological - genetics ; Bacteria ; Bacterial proteins ; Bacterial Proteins - genetics ; Bacteriophage T7 ; Bacteriophage T7 - genetics ; Bacteriophages ; Binding sites ; Biological Sciences ; Blotting, Western ; Cell division ; Cytoskeletal Proteins - antagonists & inhibitors ; Cytoskeletal Proteins - genetics ; Daughter cells ; E coli ; Escherichia coli ; Escherichia coli - cytology ; Escherichia coli - virology ; Gene expression ; Genetic mutation ; Genetics ; Genomes ; Infections ; Morphology ; Phage T7 ; Plasmids ; Plasmids - genetics ; Polymerase chain reaction ; Viral Proteins - genetics ; Viral Proteins - metabolism ; Viral Proteins - pharmacology</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2013-11, Vol.110 (48), p.19549-19554</ispartof><rights>copyright © 1993—2008 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Nov 26, 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-529ba1d15a5b5ea6f5854a6086204441816c9a5ed8294fa980db91960e1c2abd3</citedby><cites>FETCH-LOGICAL-c525t-529ba1d15a5b5ea6f5854a6086204441816c9a5ed8294fa980db91960e1c2abd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/110/48.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/23757296$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/23757296$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,315,728,781,785,804,886,27929,27930,53796,53798,58022,58255</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24218612$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kiro, Ruth</creatorcontrib><creatorcontrib>Molshanski-Mor, Shahar</creatorcontrib><creatorcontrib>Yosef, Ido</creatorcontrib><creatorcontrib>Milam, Sara L.</creatorcontrib><creatorcontrib>Erickson, Harold P.</creatorcontrib><creatorcontrib>Qimron, Udi</creatorcontrib><title>Gene product 0.4 increases bacteriophage T7 competitiveness by inhibiting host cell division</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Bacteriophages take over host resources primarily via the activity of proteins expressed early in infection. One of these proteins, produced by the Escherichia coli phage T7, is gene product (Gp) 0.4. Here, we show that Gp0.4 is a direct inhibitor of the E. coli filamenting temperature-sensitive mutant Z division protein. A chemically synthesized Gp0.4 binds to purified filamenting temperature-sensitive mutant Z protein and directly inhibits its assembly in vitro. Consequently, expression of Gp0.4 in vivo is lethal to E. coli and results in bacteria that are morphologically elongated. We further show that this inhibition of cell division by Gp0.4 enhances the bacteriophage’s competitive ability. This division inhibition is thus a fascinating example of a strategy in bacteriophages to maximize utilization of their hosts’ cell resources.</description><subject>Adaptation, Biological - genetics</subject><subject>Bacteria</subject><subject>Bacterial proteins</subject><subject>Bacterial Proteins - genetics</subject><subject>Bacteriophage T7</subject><subject>Bacteriophage T7 - genetics</subject><subject>Bacteriophages</subject><subject>Binding sites</subject><subject>Biological Sciences</subject><subject>Blotting, Western</subject><subject>Cell division</subject><subject>Cytoskeletal Proteins - antagonists & inhibitors</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Daughter cells</subject><subject>E coli</subject><subject>Escherichia coli</subject><subject>Escherichia coli - cytology</subject><subject>Escherichia coli - virology</subject><subject>Gene expression</subject><subject>Genetic mutation</subject><subject>Genetics</subject><subject>Genomes</subject><subject>Infections</subject><subject>Morphology</subject><subject>Phage T7</subject><subject>Plasmids</subject><subject>Plasmids - genetics</subject><subject>Polymerase chain reaction</subject><subject>Viral Proteins - genetics</subject><subject>Viral Proteins - metabolism</subject><subject>Viral Proteins - pharmacology</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUFv1DAQhSMEotvCmRNgiQuXbGcc27EvlVBFC1IlDrQ3JMtxnF2vduNgJyv13-Noly1w4mTJ872nN_OK4g3CEqGuLofepCVWyEAJRHhWLBAUloIpeF4sAGhdSkbZWXGe0gYAFJfwsjijjKIUSBfFj1vXOzLE0E52JLBkxPc2OpNcIo2xo4s-DGuzcuS-JjbsBjf60e-zKGXgMdNr3-SffkXWIY3Euu2WtH7vkw_9q-JFZ7bJvT6-F8XDzef76y_l3bfbr9ef7krLKR9LTlVjsEVueMOdER2XnBkBUlBgjKFEYZXhrpVUsc4oCW2jUAlwaKlp2uqiuDr4DlOzc611_RjNVg_R70x81MF4_fek92u9CntdScZRYTb4eDSI4efk0qh3Ps2rmN6FKWlkiuYwNaX_gQpa1cBxRj_8g27CFPt8iZkSWFWCyUxdHigbQ0rRdafcCHouWc8l66eSs-Ldn-ue-N-tZoAcgVl5sst-TGpUnKmMvD0gmzSG-GRR1bymSuT5-8O8M0GbVfRJP3yngAIg52CSV78A82-_jw</recordid><startdate>20131126</startdate><enddate>20131126</enddate><creator>Kiro, Ruth</creator><creator>Molshanski-Mor, Shahar</creator><creator>Yosef, Ido</creator><creator>Milam, Sara L.</creator><creator>Erickson, Harold P.</creator><creator>Qimron, Udi</creator><general>National Academy of Sciences</general><general>NATIONAL ACADEMY OF SCIENCES</general><general>National Acad Sciences</general><scope>FBQ</scope><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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20131126</creationdate><title>Gene product 0.4 increases bacteriophage T7 competitiveness by inhibiting host cell division</title><author>Kiro, Ruth ; 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subjects | Adaptation, Biological - genetics Bacteria Bacterial proteins Bacterial Proteins - genetics Bacteriophage T7 Bacteriophage T7 - genetics Bacteriophages Binding sites Biological Sciences Blotting, Western Cell division Cytoskeletal Proteins - antagonists & inhibitors Cytoskeletal Proteins - genetics Daughter cells E coli Escherichia coli Escherichia coli - cytology Escherichia coli - virology Gene expression Genetic mutation Genetics Genomes Infections Morphology Phage T7 Plasmids Plasmids - genetics Polymerase chain reaction Viral Proteins - genetics Viral Proteins - metabolism Viral Proteins - pharmacology |
title | Gene product 0.4 increases bacteriophage T7 competitiveness by inhibiting host cell division |
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