Chlamydia trachomatis homotypic inclusion fusion is promoted by host microtubule trafficking
The developmental cycle of the obligate intracellular pathogen Chlamydia is dependant on the formation of a unique intracellular niche termed the chlamydial inclusion. The inclusion is a membrane bound vacuole derived from host cytoplasmic membrane and is modified significantly by the insertion of c...
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description | The developmental cycle of the obligate intracellular pathogen Chlamydia is dependant on the formation of a unique intracellular niche termed the chlamydial inclusion. The inclusion is a membrane bound vacuole derived from host cytoplasmic membrane and is modified significantly by the insertion of chlamydial proteins. A unique property of the inclusion is its propensity for homotypic fusion. The vast majority of cells infected with multiple chlamydial elementary bodies (EBs) contain only a single mature inclusion. The chlamydial protein IncA is required for fusion, however the host process involved are uncharacterized.
Here, through live imaging studies, we determined that the nascent inclusions clustered tightly at the cell microtubule organizing center (MTOC) where they eventually fused to form a single inclusion. We established that factors involved in trafficking were required for efficient fusion as both disruption of the microtubule network and inhibition of microtubule trafficking reduced the efficiency of fusion. Additionally, fusion occurred at multiple sites in the cell and was delayed when the microtubule minus ends were either no longer anchored at a single MTOC or when a cell possessed multiple MTOCs.
The data presented demonstrates that efficient homotypic fusion requires the inclusions to be in close proximity and that this proximity is dependent on chlamydial microtubule trafficking to the minus ends of microtubules. |
doi_str_mv | 10.1186/1471-2180-13-185 |
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Here, through live imaging studies, we determined that the nascent inclusions clustered tightly at the cell microtubule organizing center (MTOC) where they eventually fused to form a single inclusion. We established that factors involved in trafficking were required for efficient fusion as both disruption of the microtubule network and inhibition of microtubule trafficking reduced the efficiency of fusion. Additionally, fusion occurred at multiple sites in the cell and was delayed when the microtubule minus ends were either no longer anchored at a single MTOC or when a cell possessed multiple MTOCs.
The data presented demonstrates that efficient homotypic fusion requires the inclusions to be in close proximity and that this proximity is dependent on chlamydial microtubule trafficking to the minus ends of microtubules.</description><identifier>ISSN: 1471-2180</identifier><identifier>EISSN: 1471-2180</identifier><identifier>DOI: 10.1186/1471-2180-13-185</identifier><identifier>PMID: 23919807</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Bacterial Proteins - genetics ; Bacterial Proteins - metabolism ; Cell culture ; Cell Line ; Chlamydia ; Chlamydia Infections - metabolism ; Chlamydia Infections - microbiology ; Chlamydia trachomatis ; Chlamydia trachomatis - genetics ; Chlamydia trachomatis - physiology ; Cloning ; Colleges & universities ; Dynein ; Epithelial cells ; Host-Pathogen Interactions ; Humans ; Inclusion Bodies - microbiology ; Infections ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Microbiology ; Microscopy ; Microtubule-Organizing Center - microbiology ; Microtubules - microbiology ; Migration ; Physiological aspects ; Plasmids ; Protein Transport ; Proteins ; Risk factors ; Sexually transmitted diseases ; STD</subject><ispartof>BMC microbiology, 2013-08, Vol.13 (1), p.185-185, Article 185</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 Richards et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2013 Richards et al.; licensee BioMed Central Ltd. 2013 Richards et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c558t-6886529eb054d7fd0ffe7c71598a9efcee5d47040bd87f9d5671e10fdcaee8783</citedby><cites>FETCH-LOGICAL-c558t-6886529eb054d7fd0ffe7c71598a9efcee5d47040bd87f9d5671e10fdcaee8783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3750546/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3750546/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23919807$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Richards, Theresa S</creatorcontrib><creatorcontrib>Knowlton, Andrea E</creatorcontrib><creatorcontrib>Grieshaber, Scott S</creatorcontrib><title>Chlamydia trachomatis homotypic inclusion fusion is promoted by host microtubule trafficking</title><title>BMC microbiology</title><addtitle>BMC Microbiol</addtitle><description>The developmental cycle of the obligate intracellular pathogen Chlamydia is dependant on the formation of a unique intracellular niche termed the chlamydial inclusion. The inclusion is a membrane bound vacuole derived from host cytoplasmic membrane and is modified significantly by the insertion of chlamydial proteins. A unique property of the inclusion is its propensity for homotypic fusion. The vast majority of cells infected with multiple chlamydial elementary bodies (EBs) contain only a single mature inclusion. The chlamydial protein IncA is required for fusion, however the host process involved are uncharacterized.
Here, through live imaging studies, we determined that the nascent inclusions clustered tightly at the cell microtubule organizing center (MTOC) where they eventually fused to form a single inclusion. We established that factors involved in trafficking were required for efficient fusion as both disruption of the microtubule network and inhibition of microtubule trafficking reduced the efficiency of fusion. Additionally, fusion occurred at multiple sites in the cell and was delayed when the microtubule minus ends were either no longer anchored at a single MTOC or when a cell possessed multiple MTOCs.
The data presented demonstrates that efficient homotypic fusion requires the inclusions to be in close proximity and that this proximity is dependent on chlamydial microtubule trafficking to the minus ends of microtubules.</description><subject>Bacterial Proteins - genetics</subject><subject>Bacterial Proteins - metabolism</subject><subject>Cell culture</subject><subject>Cell Line</subject><subject>Chlamydia</subject><subject>Chlamydia Infections - metabolism</subject><subject>Chlamydia Infections - microbiology</subject><subject>Chlamydia trachomatis</subject><subject>Chlamydia trachomatis - genetics</subject><subject>Chlamydia trachomatis - physiology</subject><subject>Cloning</subject><subject>Colleges & universities</subject><subject>Dynein</subject><subject>Epithelial cells</subject><subject>Host-Pathogen Interactions</subject><subject>Humans</subject><subject>Inclusion Bodies - microbiology</subject><subject>Infections</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Microbiology</subject><subject>Microscopy</subject><subject>Microtubule-Organizing Center - microbiology</subject><subject>Microtubules - microbiology</subject><subject>Migration</subject><subject>Physiological aspects</subject><subject>Plasmids</subject><subject>Protein Transport</subject><subject>Proteins</subject><subject>Risk factors</subject><subject>Sexually transmitted diseases</subject><subject>STD</subject><issn>1471-2180</issn><issn>1471-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNks9vFCEUx4nR2Fq9ezKTeNHDVBhgYC4mzcZqkyYm_riZEAYeu9QZWAfGuP99mWxdu8aD4fAI7_O-Dx5fhJ4TfE6IbN8QJkjdEIlrQmsi-QN0ejh6eG9_gp6kdIMxEZKKx-ikoR3pJBan6NtqM-hxZ72u8qTNJo46-1SVGPNu603lgxnm5GOo3D6U7HZa0mCrflfIlKvRmynmuZ8HWGSc8-a7D-un6JHTQ4Jnd_EMfb1892X1ob7--P5qdXFdG85lrlspW9500GPOrHAWOwfCCMI7qTtwBoBbJjDDvZXCdZa3ggDBzhoNIMuTztDbve527kewBkK5xKC2kx_1tFNRe3WcCX6j1vGnooKXnm0ReHUnMMUfM6SsRp8MDIMOEOekCKMM04a37D_QBreYcdEV9OVf6E2cp1AmsVC8NJZU_qHWegDlg4vLRyyi6oJTxluCOSnU-T-osiyU4ccAzpfzo4LXRwWFyfArr_Wckrr6_OmYxXu2_GJKE7jD6AhWi9HU4iS1OEkRqorRSsmL-yM_FPx2Fr0FpeXNeg</recordid><startdate>20130807</startdate><enddate>20130807</enddate><creator>Richards, Theresa S</creator><creator>Knowlton, Andrea E</creator><creator>Grieshaber, Scott S</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7T7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130807</creationdate><title>Chlamydia trachomatis homotypic inclusion fusion is promoted by host microtubule trafficking</title><author>Richards, Theresa S ; Knowlton, Andrea E ; Grieshaber, Scott S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c558t-6886529eb054d7fd0ffe7c71598a9efcee5d47040bd87f9d5671e10fdcaee8783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Bacterial Proteins - genetics</topic><topic>Bacterial Proteins - metabolism</topic><topic>Cell culture</topic><topic>Cell Line</topic><topic>Chlamydia</topic><topic>Chlamydia Infections - metabolism</topic><topic>Chlamydia Infections - microbiology</topic><topic>Chlamydia trachomatis</topic><topic>Chlamydia trachomatis - genetics</topic><topic>Chlamydia trachomatis - physiology</topic><topic>Cloning</topic><topic>Colleges & universities</topic><topic>Dynein</topic><topic>Epithelial cells</topic><topic>Host-Pathogen Interactions</topic><topic>Humans</topic><topic>Inclusion Bodies - microbiology</topic><topic>Infections</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Microbiology</topic><topic>Microscopy</topic><topic>Microtubule-Organizing Center - microbiology</topic><topic>Microtubules - microbiology</topic><topic>Migration</topic><topic>Physiological aspects</topic><topic>Plasmids</topic><topic>Protein Transport</topic><topic>Proteins</topic><topic>Risk factors</topic><topic>Sexually transmitted diseases</topic><topic>STD</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Richards, Theresa S</creatorcontrib><creatorcontrib>Knowlton, Andrea E</creatorcontrib><creatorcontrib>Grieshaber, Scott S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Richards, Theresa S</au><au>Knowlton, Andrea E</au><au>Grieshaber, Scott S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chlamydia trachomatis homotypic inclusion fusion is promoted by host microtubule trafficking</atitle><jtitle>BMC microbiology</jtitle><addtitle>BMC Microbiol</addtitle><date>2013-08-07</date><risdate>2013</risdate><volume>13</volume><issue>1</issue><spage>185</spage><epage>185</epage><pages>185-185</pages><artnum>185</artnum><issn>1471-2180</issn><eissn>1471-2180</eissn><abstract>The developmental cycle of the obligate intracellular pathogen Chlamydia is dependant on the formation of a unique intracellular niche termed the chlamydial inclusion. The inclusion is a membrane bound vacuole derived from host cytoplasmic membrane and is modified significantly by the insertion of chlamydial proteins. A unique property of the inclusion is its propensity for homotypic fusion. The vast majority of cells infected with multiple chlamydial elementary bodies (EBs) contain only a single mature inclusion. The chlamydial protein IncA is required for fusion, however the host process involved are uncharacterized.
Here, through live imaging studies, we determined that the nascent inclusions clustered tightly at the cell microtubule organizing center (MTOC) where they eventually fused to form a single inclusion. We established that factors involved in trafficking were required for efficient fusion as both disruption of the microtubule network and inhibition of microtubule trafficking reduced the efficiency of fusion. Additionally, fusion occurred at multiple sites in the cell and was delayed when the microtubule minus ends were either no longer anchored at a single MTOC or when a cell possessed multiple MTOCs.
The data presented demonstrates that efficient homotypic fusion requires the inclusions to be in close proximity and that this proximity is dependent on chlamydial microtubule trafficking to the minus ends of microtubules.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>23919807</pmid><doi>10.1186/1471-2180-13-185</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Bacterial Proteins - genetics Bacterial Proteins - metabolism Cell culture Cell Line Chlamydia Chlamydia Infections - metabolism Chlamydia Infections - microbiology Chlamydia trachomatis Chlamydia trachomatis - genetics Chlamydia trachomatis - physiology Cloning Colleges & universities Dynein Epithelial cells Host-Pathogen Interactions Humans Inclusion Bodies - microbiology Infections Membrane Proteins - genetics Membrane Proteins - metabolism Microbiology Microscopy Microtubule-Organizing Center - microbiology Microtubules - microbiology Migration Physiological aspects Plasmids Protein Transport Proteins Risk factors Sexually transmitted diseases STD |
title | Chlamydia trachomatis homotypic inclusion fusion is promoted by host microtubule trafficking |
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