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Wolbachia infections and superinfections in cytoplasmically incompatible populations of the European cherry fruit fly Rhagoletis cerasi (Diptera, Tephritidae)
Author(s) -
Riegler Markus,
Stauffer Christian
Publication year - 2002
Publication title -
molecular ecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.619
H-Index - 225
eISSN - 1365-294X
pISSN - 0962-1083
DOI - 10.1046/j.1365-294x.2002.01614.x
Subject(s) - wolbachia , tephritidae , biology , cytoplasmic incompatibility , biological dispersal , host (biology) , rhagoletis , prophage , zoology , ecology , population , botany , genetics , pest analysis , demography , gene , escherichia coli , bacteriophage , sociology
Wolbachia is an obligately intracellular, maternally inherited bacterium which has been detected in many arthropods. Wolbachia infections disperse in host populations by mechanisms such as cytoplasmic incompatibility (CI). CI leads to embryonic mortality which occurs when infected males mate with uninfected females or females with a different Wolbachia strain. Populations of the European cherry fruit fly Rhagoletis cerasi (Diptera, Tephritidae) were found to be infected by two different Wolbachia strains, w Cer1 and w Cer2. Superinfections with both strains occurred throughout southern and central Europe and infections with w Cer1 were found in northern, western and eastern Europe. Strong unidirectional CI between European populations of R. cerasi were first reported in the 1970s. From the conformity in the recent geographical distribution of the Wolbachia infections and the CI expression patterns found 25 years ago it was deduced that w Cer2 potentially causes CI in R. cerasi . The comparison of the geographical distributions indicated that w Cer1 + 2 must have spread into w Cer1‐infected populations in some areas. In other regions, a spread of w Cer1 + 2 was probably prevented by dispersal barriers. There, a sharp transition from infected to superinfected populations suggested regional isolation between w Cer1 and w Cer1 + 2‐infected populations.