Genetics, Vol. 150, 227-237, September 1998, Copyright © 1998

Wolbachia Transfer from Drosophila melanogaster into D. simulans: Host Effect and Cytoplasmic Incompatibility Relationships

Denis Poinsota, Kostas Bourtzisb,c, George Markakisd, Charalambos Savakisb,e, and Hervé Merçota
a Institut Jacques Monod, Laboratoire de Dynamique du Génome et Evolution, CNRS-Universités Paris 6 and 7, Paris Cedex 05, France,
b Insect Molecular Genetics Group, Institute of Molecular Biology and Biotechnology, FORTH, Heraklion 711 10-, Crete, Greece,
c Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut 06520
d Department of Biology, Medical School, University of Crete, Heraklion 711 10-, Crete, Greece
e Division of Medical Sciences, Medical School, University of Crete, Heraklion 711 10-, Crete, Greece

Corresponding author: Denis Poinsot, Institut Jacques Monod, Laboratoire de Dynamique du Génome et Evolution, CNRS - Université Paris 7, 2 place Jussieu 75251 Paris Cedex 05, France., poinsot{at}ccr.jussieu.fr (E-mail).

Communicating editor: A. A. HOFFMANN

Wolbachia are maternally transmitted endocellular bacteria causing a reproductive incompatibility called cytoplasmic incompatibility (CI) in several arthropod species, including Drosophila. CI results in embryonic mortality in incompatible crosses. The only bacterial strain known to infect Drosophila melanogaster (wDm) was transferred from a D. melanogaster isofemale line into uninfected D. simulans isofemale lines by embryo microinjections. Males from the resulting transinfected lines induce >98% embryonic mortality when crossed with uninfected D. simulans females. In contrast, males from the donor D. melanogaster line induce only 18–32% CI on average when crossed with uninfected D. melanogaster females. Transinfected D. simulans lines do not differ from the D. melanogaster donor line in the Wolbachia load found in the embryo or in the total bacterial load of young males. However, >80% of cysts are infected by Wolbachia in the testes of young transinfected males, whereas only 8% of cysts are infected in young males from the D. melanogaster donor isofemale line. This difference might be caused by physiological differences between hosts, but it might also involve tissue-specific control of Wolbachia density by D. melanogaster. The wDm-transinfected D. simulans lines are unidirectionally incompatible with strains infected by the non-CI expressor Wolbachia strains wKi, wMau, or wAu, and they are bidirectionally incompatible with strains infected by the CI-expressor Wolbachia strains wHa or wNo. However, wDm-infected males do not induce CI toward females infected by the CI-expressor strain wRi, which is found in D. simulans continental populations, while wRi-infected males induce partial CI toward wDm-infected females. This peculiar asymmetrical pattern could reflect an ongoing divergence between the CI mechanisms of wRi and wDm. It would also confirm other results indicating that the factor responsible for CI induction in males is distinct from the factor responsible for CI rescue in females.





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