Complement-Like Protein TEP1 Is a Determinant of Vectorial Capacity in the Malaria Vector Anopheles gambiae

Anopheles mosquitoes are major vectors of human malaria in Africa. Large variation exists in the ability of mosquitoes to serve as vectors and to transmit malaria parasites, but the molecular mechanisms that determine vectorial capacity remain poorly understood. We report that the hemocyte-specific...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Cell 2004-03, Vol.116 (5), p.661-670
Hauptverfasser: Blandin, Stephanie, Shiao, Shin-Hong, Moita, Luis F, Janse, Chris J, Waters, Andrew P, Kafatos, Fotis C, Levashina, Elena A
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 670
container_issue 5
container_start_page 661
container_title Cell
container_volume 116
creator Blandin, Stephanie
Shiao, Shin-Hong
Moita, Luis F
Janse, Chris J
Waters, Andrew P
Kafatos, Fotis C
Levashina, Elena A
description Anopheles mosquitoes are major vectors of human malaria in Africa. Large variation exists in the ability of mosquitoes to serve as vectors and to transmit malaria parasites, but the molecular mechanisms that determine vectorial capacity remain poorly understood. We report that the hemocyte-specific complement-like protein TEP1 from the mosquito Anopheles gambiae binds to and mediates killing of midgut stages of the rodent malaria parasite Plasmodium berghei. The dsRNA knockdown of TEP1 in adults completely abolishes melanotic refractoriness in a genetically selected refractory strain. Moreover, in susceptible mosquitoes this knockdown increases the number of developing parasites. Our results suggest that the TEP1-dependent parasite killing is followed by a TEP1-independent clearance of dead parasites by lysis and/or melanization. Further elucidation of the molecular mechanisms of TEP1-mediated parasite killing will be of great importance for our understanding of the principles of vectorial capacity in insects.
doi_str_mv 10.1016/S0092-8674(04)00173-4
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71706756</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0092867404001734</els_id><sourcerecordid>71706756</sourcerecordid><originalsourceid>FETCH-LOGICAL-c491t-1b588226ad1067fa6761c921ed7a635be2980bb95b037c90d800293203cd2cfc3</originalsourceid><addsrcrecordid>eNqFkUFv1DAQhS1ERbeFnwDyCdFDytiJ7fiEqqVApUVUonC1HGdCTZM42F6k_nu87Ko9VhppDvO9N9J7hLxmcM6AyfffATSvWqmad9CcATBVV80zsmKgVdUwxZ-T1QNyTE5S-g0ArRDiBTlmAkDWjV6Ru3WYlhEnnHO18XdIr2PI6Gd6c3nN6FWiln7EjHHys50zDQP9iS6H6O1I13axzud7WvB8i_SrHW05HAh6MYflFkdM9JedOm_xJTka7Jjw1WGfkh-fLm_WX6rNt89X64tN5RrNcsU60bacS9szkGqwUknmNGfYKytr0SHXLXSdFh3UymnoWwCuaw6167kbXH1K3u59lxj-bDFlM_nkcBztjGGbjGKqGAv5JMiUZjWXdQHFHnQxpBRxMEv0k433hoHZ1WH-12F2WRsos6vDNEX35vBg203YP6oO-Rfgwx7Aksdfj9Ek53F22PtYUjR98E-8-Afx9ZiY</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17913263</pqid></control><display><type>article</type><title>Complement-Like Protein TEP1 Is a Determinant of Vectorial Capacity in the Malaria Vector Anopheles gambiae</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><source>Cell Press Free Archives</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Blandin, Stephanie ; Shiao, Shin-Hong ; Moita, Luis F ; Janse, Chris J ; Waters, Andrew P ; Kafatos, Fotis C ; Levashina, Elena A</creator><creatorcontrib>Blandin, Stephanie ; Shiao, Shin-Hong ; Moita, Luis F ; Janse, Chris J ; Waters, Andrew P ; Kafatos, Fotis C ; Levashina, Elena A</creatorcontrib><description>Anopheles mosquitoes are major vectors of human malaria in Africa. Large variation exists in the ability of mosquitoes to serve as vectors and to transmit malaria parasites, but the molecular mechanisms that determine vectorial capacity remain poorly understood. We report that the hemocyte-specific complement-like protein TEP1 from the mosquito Anopheles gambiae binds to and mediates killing of midgut stages of the rodent malaria parasite Plasmodium berghei. The dsRNA knockdown of TEP1 in adults completely abolishes melanotic refractoriness in a genetically selected refractory strain. Moreover, in susceptible mosquitoes this knockdown increases the number of developing parasites. Our results suggest that the TEP1-dependent parasite killing is followed by a TEP1-independent clearance of dead parasites by lysis and/or melanization. Further elucidation of the molecular mechanisms of TEP1-mediated parasite killing will be of great importance for our understanding of the principles of vectorial capacity in insects.</description><identifier>ISSN: 0092-8674</identifier><identifier>EISSN: 1097-4172</identifier><identifier>DOI: 10.1016/S0092-8674(04)00173-4</identifier><identifier>PMID: 15006349</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Amino Acid Sequence ; Animals ; Anopheles - anatomy &amp; histology ; Anopheles - metabolism ; Anopheles - parasitology ; Anopheles gambiae ; Female ; Humans ; Insect Proteins - chemistry ; Insect Proteins - genetics ; Insect Proteins - metabolism ; Insect Vectors - genetics ; Insect Vectors - parasitology ; Insect Vectors - physiology ; Malaria - epidemiology ; Models, Molecular ; Molecular Sequence Data ; Plasmodium berghei ; Plasmodium berghei - cytology ; Plasmodium berghei - physiology ; Polymorphism, Genetic ; Protein Structure, Tertiary ; RNA - metabolism ; Sequence Alignment</subject><ispartof>Cell, 2004-03, Vol.116 (5), p.661-670</ispartof><rights>2004 Cell Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c491t-1b588226ad1067fa6761c921ed7a635be2980bb95b037c90d800293203cd2cfc3</citedby><cites>FETCH-LOGICAL-c491t-1b588226ad1067fa6761c921ed7a635be2980bb95b037c90d800293203cd2cfc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0092-8674(04)00173-4$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15006349$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Blandin, Stephanie</creatorcontrib><creatorcontrib>Shiao, Shin-Hong</creatorcontrib><creatorcontrib>Moita, Luis F</creatorcontrib><creatorcontrib>Janse, Chris J</creatorcontrib><creatorcontrib>Waters, Andrew P</creatorcontrib><creatorcontrib>Kafatos, Fotis C</creatorcontrib><creatorcontrib>Levashina, Elena A</creatorcontrib><title>Complement-Like Protein TEP1 Is a Determinant of Vectorial Capacity in the Malaria Vector Anopheles gambiae</title><title>Cell</title><addtitle>Cell</addtitle><description>Anopheles mosquitoes are major vectors of human malaria in Africa. Large variation exists in the ability of mosquitoes to serve as vectors and to transmit malaria parasites, but the molecular mechanisms that determine vectorial capacity remain poorly understood. We report that the hemocyte-specific complement-like protein TEP1 from the mosquito Anopheles gambiae binds to and mediates killing of midgut stages of the rodent malaria parasite Plasmodium berghei. The dsRNA knockdown of TEP1 in adults completely abolishes melanotic refractoriness in a genetically selected refractory strain. Moreover, in susceptible mosquitoes this knockdown increases the number of developing parasites. Our results suggest that the TEP1-dependent parasite killing is followed by a TEP1-independent clearance of dead parasites by lysis and/or melanization. Further elucidation of the molecular mechanisms of TEP1-mediated parasite killing will be of great importance for our understanding of the principles of vectorial capacity in insects.</description><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Anopheles - anatomy &amp; histology</subject><subject>Anopheles - metabolism</subject><subject>Anopheles - parasitology</subject><subject>Anopheles gambiae</subject><subject>Female</subject><subject>Humans</subject><subject>Insect Proteins - chemistry</subject><subject>Insect Proteins - genetics</subject><subject>Insect Proteins - metabolism</subject><subject>Insect Vectors - genetics</subject><subject>Insect Vectors - parasitology</subject><subject>Insect Vectors - physiology</subject><subject>Malaria - epidemiology</subject><subject>Models, Molecular</subject><subject>Molecular Sequence Data</subject><subject>Plasmodium berghei</subject><subject>Plasmodium berghei - cytology</subject><subject>Plasmodium berghei - physiology</subject><subject>Polymorphism, Genetic</subject><subject>Protein Structure, Tertiary</subject><subject>RNA - metabolism</subject><subject>Sequence Alignment</subject><issn>0092-8674</issn><issn>1097-4172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFv1DAQhS1ERbeFnwDyCdFDytiJ7fiEqqVApUVUonC1HGdCTZM42F6k_nu87Ko9VhppDvO9N9J7hLxmcM6AyfffATSvWqmad9CcATBVV80zsmKgVdUwxZ-T1QNyTE5S-g0ArRDiBTlmAkDWjV6Ru3WYlhEnnHO18XdIr2PI6Gd6c3nN6FWiln7EjHHys50zDQP9iS6H6O1I13axzud7WvB8i_SrHW05HAh6MYflFkdM9JedOm_xJTka7Jjw1WGfkh-fLm_WX6rNt89X64tN5RrNcsU60bacS9szkGqwUknmNGfYKytr0SHXLXSdFh3UymnoWwCuaw6167kbXH1K3u59lxj-bDFlM_nkcBztjGGbjGKqGAv5JMiUZjWXdQHFHnQxpBRxMEv0k433hoHZ1WH-12F2WRsos6vDNEX35vBg203YP6oO-Rfgwx7Aksdfj9Ek53F22PtYUjR98E-8-Afx9ZiY</recordid><startdate>20040305</startdate><enddate>20040305</enddate><creator>Blandin, Stephanie</creator><creator>Shiao, Shin-Hong</creator><creator>Moita, Luis F</creator><creator>Janse, Chris J</creator><creator>Waters, Andrew P</creator><creator>Kafatos, Fotis C</creator><creator>Levashina, Elena A</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20040305</creationdate><title>Complement-Like Protein TEP1 Is a Determinant of Vectorial Capacity in the Malaria Vector Anopheles gambiae</title><author>Blandin, Stephanie ; Shiao, Shin-Hong ; Moita, Luis F ; Janse, Chris J ; Waters, Andrew P ; Kafatos, Fotis C ; Levashina, Elena A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c491t-1b588226ad1067fa6761c921ed7a635be2980bb95b037c90d800293203cd2cfc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Anopheles - anatomy &amp; histology</topic><topic>Anopheles - metabolism</topic><topic>Anopheles - parasitology</topic><topic>Anopheles gambiae</topic><topic>Female</topic><topic>Humans</topic><topic>Insect Proteins - chemistry</topic><topic>Insect Proteins - genetics</topic><topic>Insect Proteins - metabolism</topic><topic>Insect Vectors - genetics</topic><topic>Insect Vectors - parasitology</topic><topic>Insect Vectors - physiology</topic><topic>Malaria - epidemiology</topic><topic>Models, Molecular</topic><topic>Molecular Sequence Data</topic><topic>Plasmodium berghei</topic><topic>Plasmodium berghei - cytology</topic><topic>Plasmodium berghei - physiology</topic><topic>Polymorphism, Genetic</topic><topic>Protein Structure, Tertiary</topic><topic>RNA - metabolism</topic><topic>Sequence Alignment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Blandin, Stephanie</creatorcontrib><creatorcontrib>Shiao, Shin-Hong</creatorcontrib><creatorcontrib>Moita, Luis F</creatorcontrib><creatorcontrib>Janse, Chris J</creatorcontrib><creatorcontrib>Waters, Andrew P</creatorcontrib><creatorcontrib>Kafatos, Fotis C</creatorcontrib><creatorcontrib>Levashina, Elena A</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Blandin, Stephanie</au><au>Shiao, Shin-Hong</au><au>Moita, Luis F</au><au>Janse, Chris J</au><au>Waters, Andrew P</au><au>Kafatos, Fotis C</au><au>Levashina, Elena A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Complement-Like Protein TEP1 Is a Determinant of Vectorial Capacity in the Malaria Vector Anopheles gambiae</atitle><jtitle>Cell</jtitle><addtitle>Cell</addtitle><date>2004-03-05</date><risdate>2004</risdate><volume>116</volume><issue>5</issue><spage>661</spage><epage>670</epage><pages>661-670</pages><issn>0092-8674</issn><eissn>1097-4172</eissn><abstract>Anopheles mosquitoes are major vectors of human malaria in Africa. Large variation exists in the ability of mosquitoes to serve as vectors and to transmit malaria parasites, but the molecular mechanisms that determine vectorial capacity remain poorly understood. We report that the hemocyte-specific complement-like protein TEP1 from the mosquito Anopheles gambiae binds to and mediates killing of midgut stages of the rodent malaria parasite Plasmodium berghei. The dsRNA knockdown of TEP1 in adults completely abolishes melanotic refractoriness in a genetically selected refractory strain. Moreover, in susceptible mosquitoes this knockdown increases the number of developing parasites. Our results suggest that the TEP1-dependent parasite killing is followed by a TEP1-independent clearance of dead parasites by lysis and/or melanization. Further elucidation of the molecular mechanisms of TEP1-mediated parasite killing will be of great importance for our understanding of the principles of vectorial capacity in insects.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15006349</pmid><doi>10.1016/S0092-8674(04)00173-4</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0092-8674
ispartof Cell, 2004-03, Vol.116 (5), p.661-670
issn 0092-8674
1097-4172
language eng
recordid cdi_proquest_miscellaneous_71706756
source MEDLINE; Elsevier ScienceDirect Journals Complete; Cell Press Free Archives; EZB-FREE-00999 freely available EZB journals
subjects Amino Acid Sequence
Animals
Anopheles - anatomy & histology
Anopheles - metabolism
Anopheles - parasitology
Anopheles gambiae
Female
Humans
Insect Proteins - chemistry
Insect Proteins - genetics
Insect Proteins - metabolism
Insect Vectors - genetics
Insect Vectors - parasitology
Insect Vectors - physiology
Malaria - epidemiology
Models, Molecular
Molecular Sequence Data
Plasmodium berghei
Plasmodium berghei - cytology
Plasmodium berghei - physiology
Polymorphism, Genetic
Protein Structure, Tertiary
RNA - metabolism
Sequence Alignment
title Complement-Like Protein TEP1 Is a Determinant of Vectorial Capacity in the Malaria Vector Anopheles gambiae
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-28T04%3A24%3A15IST&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=Complement-Like%20Protein%20TEP1%20Is%20a%20Determinant%20of%20Vectorial%20Capacity%20in%20the%20Malaria%20Vector%20Anopheles%20gambiae&rft.jtitle=Cell&rft.au=Blandin,%20Stephanie&rft.date=2004-03-05&rft.volume=116&rft.issue=5&rft.spage=661&rft.epage=670&rft.pages=661-670&rft.issn=0092-8674&rft.eissn=1097-4172&rft_id=info:doi/10.1016/S0092-8674(04)00173-4&rft_dat=%3Cproquest_cross%3E71706756%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=17913263&rft_id=info:pmid/15006349&rft_els_id=S0092867404001734&rfr_iscdi=true