Host manipulation by parasitic endosymbionts: Combining proximate and ultimate approaches
Wolbachia
are intracellular bacteria that induce a cytoplasmic mating
incompatibility (CI) in many insect species. At the proximate level,
this phenomenon is intriguing because the bacteria implement it as a
modification-rescue system. That is, if an egg is fertilized by
Wolbachia-modified sperm, then Wolbachia must be present
in this egg to ensure regular embryonic development. Otherwise, CI
manifests itself in irregularities during the first cleavage mitosis
that typically lead to embryonic death. We aim to design a mechanistic
model of the bacterial strategies underlying these irregularities. The
model will be based on recent cytological studies of
Wolbachia-induced CI with special focus on the gonomeric spindle
and other particularities of the first cleavage mitosis in insects. We
seek to elucidate the role of checkpoints and developmental control
architecture in the evolution of bacterial host manipulations, paying
special attention to targets in cell cycle regulation, such as the
spindle assembly checkpoint. We hypothesize that the need for
developmental robustness with regard to internal perturbations opens
the door for external perturbance by certain parasitic agents. This
will help to address the ultimate question why Wolbachia are
highly persistent as parasitic endosymbionts of insects on an
evolutionary time scale.
CI is similarly intriguing at the ultimate level due to its potential catalyzing effect on host speciation. We aim to examine theoretically a recent field example from Drosophila recens and D. subquinaria where a unilateral Wolbachia-infection seems to have shaped female mating preferences, thereby reinforcing incipient speciation. In addition to suffering from CI, hybrids also face nuclear genetic incompatibilities, as typically found in speciation studies. Our study will thus focus on the potentially synergistic interplay of nuclear and cytoplasmic mating incompatibilities. We expect to show that such synergies can significantly contribute to Wolbachia’s impact on insect speciation and diversity, especially since our previous work estimates the percentage of Wolbachia-infected insect species to be of the order of 60 percent. Leading back to the mechanistic basis of CI, the field example raises a proximate issue: Transfection experiments demonstrate the conversion of Wolbachia-induced syndromes from CI SFB 618 C1 Hammerstein 295 to another phenomenon called male killing. Our efforts to model the mechanism of CI will include an attempt to explain this radical difference in syndromes caused by the same strain of bacteria in different host backgrounds.
CI is similarly intriguing at the ultimate level due to its potential catalyzing effect on host speciation. We aim to examine theoretically a recent field example from Drosophila recens and D. subquinaria where a unilateral Wolbachia-infection seems to have shaped female mating preferences, thereby reinforcing incipient speciation. In addition to suffering from CI, hybrids also face nuclear genetic incompatibilities, as typically found in speciation studies. Our study will thus focus on the potentially synergistic interplay of nuclear and cytoplasmic mating incompatibilities. We expect to show that such synergies can significantly contribute to Wolbachia’s impact on insect speciation and diversity, especially since our previous work estimates the percentage of Wolbachia-infected insect species to be of the order of 60 percent. Leading back to the mechanistic basis of CI, the field example raises a proximate issue: Transfection experiments demonstrate the conversion of Wolbachia-induced syndromes from CI SFB 618 C1 Hammerstein 295 to another phenomenon called male killing. Our efforts to model the mechanism of CI will include an attempt to explain this radical difference in syndromes caused by the same strain of bacteria in different host backgrounds.
description of the 1st period | german version |
description of the 2nd period |