Cytoplasmic incompatibility and host population structure
Many arthropod species are infected by maternally inherited bacteria that induce cytoplasmic incompatibility (CI). CI causes embryonic mortality in offspring when infected males mate with either uninfected females or with females that are infected with a different strain of bacteria. Here, we review...
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Veröffentlicht in: | Heredity 2009-09, Vol.103 (3), p.196-207 |
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description | Many arthropod species are infected by maternally inherited bacteria that induce cytoplasmic incompatibility (CI). CI causes embryonic mortality in offspring when infected males mate with either uninfected females or with females that are infected with a different strain of bacteria. Here, we review theoretical and empirical studies concerning the infection dynamics of CI-inducing bacteria, focusing in particular on the impact of the host population structure on the spread of CI. As different theoretical models have often produced divergent predictions with regard to issues such as the speed of CI spread and the stability of infection polymorphisms, we specifically aim to clarify how the various assumptions concerning population structure that underlie these models affect these predictions. We also discuss several implications of population structure, including the impact of CI on host gene flow reduction and speciation, the evolutionary dynamics of CI and strategies to control insect pest populations by means of CI-inducing microbes. |
doi_str_mv | 10.1038/hdy.2009.53 |
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CI causes embryonic mortality in offspring when infected males mate with either uninfected females or with females that are infected with a different strain of bacteria. Here, we review theoretical and empirical studies concerning the infection dynamics of CI-inducing bacteria, focusing in particular on the impact of the host population structure on the spread of CI. As different theoretical models have often produced divergent predictions with regard to issues such as the speed of CI spread and the stability of infection polymorphisms, we specifically aim to clarify how the various assumptions concerning population structure that underlie these models affect these predictions. We also discuss several implications of population structure, including the impact of CI on host gene flow reduction and speciation, the evolutionary dynamics of CI and strategies to control insect pest populations by means of CI-inducing microbes.</description><identifier>ISSN: 0018-067X</identifier><identifier>EISSN: 1365-2540</identifier><identifier>DOI: 10.1038/hdy.2009.53</identifier><identifier>PMID: 19436325</identifier><identifier>CODEN: HDTYAT</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Animals ; Arthropoda ; Arthropods ; Bacteria ; bacterial infections ; Biomedical and Life Sciences ; Biomedicine ; Cardinium ; Cytogenetics ; Cytoplasm ; Cytoplasm - genetics ; Cytoplasm - microbiology ; cytoplasmic incompatibility ; Ecology ; endosymbionts ; Evolutionary Biology ; Female ; Gene Flow ; Host-Pathogen Interactions ; Human Genetics ; Insecta - genetics ; Insecta - microbiology ; Insecta - physiology ; Insects ; literature reviews ; Male ; Models, Genetic ; Mortality ; Offspring ; Parasites ; Pest control ; Pest Control, Biological ; Pests ; Plant Genetics and Genomics ; Population structure ; review ; Speciation ; Theory ; Wolbachia ; Wolbachia - physiology</subject><ispartof>Heredity, 2009-09, Vol.103 (3), p.196-207</ispartof><rights>The Genetics Society 2009</rights><rights>Copyright Nature Publishing Group Sep 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-e20cd03532077d3ca83f2fd45b0d77b702bcc0b4d72f67a5ed2623d7fca045733</citedby><cites>FETCH-LOGICAL-c509t-e20cd03532077d3ca83f2fd45b0d77b702bcc0b4d72f67a5ed2623d7fca045733</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/hdy.2009.53$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/hdy.2009.53$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19436325$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Engelstadter, J</creatorcontrib><creatorcontrib>Telschow, A</creatorcontrib><title>Cytoplasmic incompatibility and host population structure</title><title>Heredity</title><addtitle>Heredity</addtitle><addtitle>Heredity (Edinb)</addtitle><description>Many arthropod species are infected by maternally inherited bacteria that induce cytoplasmic incompatibility (CI). CI causes embryonic mortality in offspring when infected males mate with either uninfected females or with females that are infected with a different strain of bacteria. Here, we review theoretical and empirical studies concerning the infection dynamics of CI-inducing bacteria, focusing in particular on the impact of the host population structure on the spread of CI. As different theoretical models have often produced divergent predictions with regard to issues such as the speed of CI spread and the stability of infection polymorphisms, we specifically aim to clarify how the various assumptions concerning population structure that underlie these models affect these predictions. 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physiology</subject><subject>Insects</subject><subject>literature reviews</subject><subject>Male</subject><subject>Models, Genetic</subject><subject>Mortality</subject><subject>Offspring</subject><subject>Parasites</subject><subject>Pest control</subject><subject>Pest Control, Biological</subject><subject>Pests</subject><subject>Plant Genetics and Genomics</subject><subject>Population structure</subject><subject>review</subject><subject>Speciation</subject><subject>Theory</subject><subject>Wolbachia</subject><subject>Wolbachia - physiology</subject><issn>0018-067X</issn><issn>1365-2540</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkE1r3DAQhkVpaDYfp94b00MujTejGctaH8uStoFADkkgNyFLcuJgW45kH_bfR8suBEKgp4GZh3dmHsa-c1hyoNXls90sEaBaCvrCFpxKkaMo4CtbAPBVDqV8PGRHMb4AAEmsvrFDXhVUEooFq9abyY-djn1rsnYwvh_11NZt106bTA82e_ZxykY_zl3q-yGLU5jNNAd3wg4a3UV3uq_H7OHP1f36X35z-_d6_fsmNwKqKXcIxgIJQpDSktErarCxhajBSllLwNoYqAsrsSmlFs5iiWRlYzQUQhIds_Nd7hj86-zipPo2Gtd1enB-jqqUoiKRXvsfiLACkAVP4M8P4Iufw5CeUEhJUokVJujXDjLBxxhco8bQ9jpsFAe19a6Sd7X1rsT2yB_7yLnunX1n96ITcLEDYhoNTy687_w872yHN9or_RTaqB7uEDgBl8ALrOgNrDKVQw</recordid><startdate>20090901</startdate><enddate>20090901</enddate><creator>Engelstadter, J</creator><creator>Telschow, A</creator><general>Springer International Publishing</general><general>Springer Nature B.V</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>3V.</scope><scope>7QL</scope><scope>7SN</scope><scope>7SS</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</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>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20090901</creationdate><title>Cytoplasmic incompatibility and host population structure</title><author>Engelstadter, J ; Telschow, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-e20cd03532077d3ca83f2fd45b0d77b702bcc0b4d72f67a5ed2623d7fca045733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Arthropoda</topic><topic>Arthropods</topic><topic>Bacteria</topic><topic>bacterial infections</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cardinium</topic><topic>Cytogenetics</topic><topic>Cytoplasm</topic><topic>Cytoplasm - genetics</topic><topic>Cytoplasm - microbiology</topic><topic>cytoplasmic incompatibility</topic><topic>Ecology</topic><topic>endosymbionts</topic><topic>Evolutionary Biology</topic><topic>Female</topic><topic>Gene Flow</topic><topic>Host-Pathogen Interactions</topic><topic>Human Genetics</topic><topic>Insecta - genetics</topic><topic>Insecta - microbiology</topic><topic>Insecta - physiology</topic><topic>Insects</topic><topic>literature reviews</topic><topic>Male</topic><topic>Models, Genetic</topic><topic>Mortality</topic><topic>Offspring</topic><topic>Parasites</topic><topic>Pest control</topic><topic>Pest Control, Biological</topic><topic>Pests</topic><topic>Plant Genetics and Genomics</topic><topic>Population structure</topic><topic>review</topic><topic>Speciation</topic><topic>Theory</topic><topic>Wolbachia</topic><topic>Wolbachia - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Engelstadter, J</creatorcontrib><creatorcontrib>Telschow, A</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</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</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>Research Library Prep</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>Research Library</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Heredity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Engelstadter, J</au><au>Telschow, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytoplasmic incompatibility and host population structure</atitle><jtitle>Heredity</jtitle><stitle>Heredity</stitle><addtitle>Heredity (Edinb)</addtitle><date>2009-09-01</date><risdate>2009</risdate><volume>103</volume><issue>3</issue><spage>196</spage><epage>207</epage><pages>196-207</pages><issn>0018-067X</issn><eissn>1365-2540</eissn><coden>HDTYAT</coden><abstract>Many arthropod species are infected by maternally inherited bacteria that induce cytoplasmic incompatibility (CI). CI causes embryonic mortality in offspring when infected males mate with either uninfected females or with females that are infected with a different strain of bacteria. Here, we review theoretical and empirical studies concerning the infection dynamics of CI-inducing bacteria, focusing in particular on the impact of the host population structure on the spread of CI. As different theoretical models have often produced divergent predictions with regard to issues such as the speed of CI spread and the stability of infection polymorphisms, we specifically aim to clarify how the various assumptions concerning population structure that underlie these models affect these predictions. We also discuss several implications of population structure, including the impact of CI on host gene flow reduction and speciation, the evolutionary dynamics of CI and strategies to control insect pest populations by means of CI-inducing microbes.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>19436325</pmid><doi>10.1038/hdy.2009.53</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Arthropoda Arthropods Bacteria bacterial infections Biomedical and Life Sciences Biomedicine Cardinium Cytogenetics Cytoplasm Cytoplasm - genetics Cytoplasm - microbiology cytoplasmic incompatibility Ecology endosymbionts Evolutionary Biology Female Gene Flow Host-Pathogen Interactions Human Genetics Insecta - genetics Insecta - microbiology Insecta - physiology Insects literature reviews Male Models, Genetic Mortality Offspring Parasites Pest control Pest Control, Biological Pests Plant Genetics and Genomics Population structure review Speciation Theory Wolbachia Wolbachia - physiology |
title | Cytoplasmic incompatibility and host population structure |
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