WOLBACHIA TRANSFER FROM DROSOPHILA-MELANOGASTER INTO DROSOPHILA-SIMULANS - HOST EFFECT AND CYTOPLASMIC INCOMPATIBILITY RELATIONSHIPS

Wolbachia are maternally transmitted endocellular bacteria causing a r eproductive incompatibility called cytoplasmic incompatibility (CI) in several arthropod species, including Drosophila. CI results in embryo nic mortality in incompatible crosses. The only bacterial strain known to infect Drosophila melanogaster (wDm) was transferred from a D. mel anogaster isofemale line into uninfected D. simulans isofemale Lines b y embryo microinjections. Males from the resulting transinfected lines induce >98% embryonic mortality when crossed with uninfected D. simul ans females. In contrast, males from the donor D. melanogaster line in duce only 18-32% CI on average when crossed with uninfected D. melanog aster females. Transinfected D. simulans lines do not differ from the D. melanogaster donor line in the Wolbachia load found in the embryo o r in the total bacterial load of young males. However, >80% of cysts a re infected by Wolbachia in the testes of young transinfected males, w hereas only 8% of cysts are infected in young males from the D. melano gaster donor isofemale line. This difference might be caused by physio logical differences between hosts, but it might also involve tissue-sp ecific control of Wolbachia density by D. melanogaster. The wDm-transi nfected D. simulans lines are unidirectionally incompatible with strai ns infected by the non-CI expressor Wolbachia strains wKi, wMau, or wA u, and they are bidirectionally incompatible with strains infected by the CI-expressor Wolbachia strains wHa or wNo. However, wDm-infected m ales do not induce CI toward females infected by the CI-expressor stra in wRi, which is found in D. simulans continental populations, while w Ri infected males induce partial CI toward wDm-infected females. This peculiar asymmetrical pattern could reflect an ongoing divergence betw een the CI mechanisms of wRi and wDm. Tt would also confirm other resu lts indicating that the factor responsible for CI induction in males i s distinct from the factor responsible for CI rescue in females.