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The evolution of cytoplasmic incompatibility or when spite can be successful
1A.B.R.G., Department of Zoology, Oxford, U.K.
Journal of Theoretical Biology
|January 21, 1991
Summary
Prokaryotic symbionts may cause cytoplasmic incompatibility by producing a sperm toxin, wolbachin, that kills incompatible eggs. This "spiteful" symbiont strategy, where costs are borne by the host, can successfully invade and resist invasion in host populations.
Area of Science:
- Microbiology
- Evolutionary Biology
- Genetics
Background:
- Cytoplasmic incompatibility (CI) is a reproductive isolation mechanism often mediated by intracellular bacteria.
- The evolutionary drivers and mechanisms of CI, particularly the role of symbiont self-interest, remain incompletely understood.
Purpose of the Study:
- To propose and model a mechanism for cytoplasmic incompatibility based on the selfish interests of prokaryotic symbionts.
- To investigate the evolutionary stability of a
- spiteful
- symbiont strategy in the context of host reproduction.
Main Methods:
- Development of a theoretical model to simulate symbiont invasion dynamics.
- Analysis of symbiont behavior, focusing on the production of a toxin (wolbachin) and its neutralization.
Main Results:
- Symbionts producing wolbachin can invade populations of non-producing symbionts.
- Symbiont populations employing this spiteful strategy can resist invasion by other spiteful symbionts, even with less efficient transmission.
- The costs of spiteful symbiont behavior are externalized to the host, facilitating invasion.
Conclusions:
- Cytoplasmic incompatibility can be explained by selfish prokaryotic symbionts acting spitefully.
- Spiteful symbiont strategies can be evolutionarily stable when costs are borne by the host.
- This mechanism provides a novel perspective on the evolution of reproductive isolation and symbiont-host interactions.