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Within- and between-population variation for Wolbachia-induced reproductive incompatibility in a haplodiploid mite
1Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, The Netherlands. f.vala@ucl.ac.uk
Abstract:
Wolbachia pipientis is a bacterium that induces cytoplasmic incompatibility (CI), the phenomenon in which infected males are reproductively incompatible with uninfected females. CI spreads in a population of hosts because it reduces the fitness of uninfected females relative to infected females. CI encompasses two steps: modification (mod) of sperm of infected males and rescuing (resc) of these chromosomes by Wolbachia in the egg. Infections associated with CI have mod+ resa+ phenotypes. However, mod- resc+ phenotypes also exist; these do not result in CI. Assuming mod/resc phenotypes are properties of the symbiont, theory predicts that mod- resc+ infections can only spread in a host population where a mod+ resc+ infection already occurs. A mod- resc+ infection spreads if the cost it imposes on the infected females is lower than the cost inflicted by the resident (mod+ resc+) infection. Furthermore, introduction of a mod- Wolbachia eventually drives infection to extinction. The uninfected population that results can be recolonized by a CI-causing Wolbachia. Here, we investigated whether variability for induction of CI was present in two Tetranychus urticae populations. In one population all isofemale lines tested were mod-. In the other, mod+ resc+ and mod- resc+ isofemale lines coexisted. We found no evidence for a cost difference to females expressing either type (mod-/-). Infections in the two populations could not be distinguished based on sequences of two Wolbachia genes. We consider the possibility that mod- is a host effect through a population dynamics model. A mod- host allele leads to infection extinction in the absence of fecundity differences. Furthermore, the uninfected population that results is immune to reestablishment of the (same) CI-causing Wolbachia.
Insights
Wolbachia bacteria cause cytoplasmic incompatibility (CI) in Tetranychus urticae. This study found that non-CI causing Wolbachia (mod- resc+) can coexist with CI-causing strains (mod+ resc+), but may lead to extinction and prevent re-infection.
Area of Science:
- Microbiology
- Evolutionary Biology
- Genetics
Background:
- Wolbachia pipientis is an intracellular bacterium known to induce cytoplasmic incompatibility (CI) in its hosts.
- CI is a reproductive mechanism where infected males are incompatible with uninfected females, driving the spread of Wolbachia through host populations.
- CI involves sperm modification (mod) by Wolbachia in males and rescue (resc) in the egg, with CI-inducing infections exhibiting a mod+ resc+ phenotype.
Purpose of the Study:
- To investigate the variability of CI induction in two Tetranychus urticae populations.
- To determine if different Wolbachia phenotypes (mod+ resc+ and mod- resc+) coexist and how they interact within host populations.
- To explore the potential for host genetic factors influencing Wolbachia infection dynamics.
Main Methods:
- Testing of multiple isofemale lines from two Tetranychus urticae populations for Wolbachia infection phenotypes (mod+ resc+ and mod- resc+).
- Assessment of fitness costs associated with different Wolbachia phenotypes in infected females.
- Genetic sequencing of two Wolbachia genes to differentiate between infection types.
- Population dynamics modeling to evaluate the impact of host genetic effects on infection spread and extinction.
Main Results:
- One Tetranychus urticae population exclusively harbored mod- Wolbachia, while the other showed coexistence of mod+ resc+ and mod- resc+ isofemale lines.
- No significant fitness cost difference was observed for females infected with either mod- or mod+ resc+ Wolbachia.
- Sequencing of Wolbachia genes did not distinguish between the infection types found in the two populations.
- Population modeling suggested that a host allele associated with mod- infections can drive Wolbachia extinction, rendering the population immune to re-infection by CI-causing strains.
Conclusions:
- Variability in CI induction exists within Tetranychus urticae populations, with coexistence of CI-inducing and non-CI-inducing Wolbachia strains observed.
- The spread and persistence of Wolbachia infections may be influenced by host genetic factors rather than solely symbiont phenotypes.
- The extinction of Wolbachia infections, potentially mediated by host factors, can lead to a population resistant to subsequent CI-inducing infections.