Originally published as Genetics Published Articles Ahead of Print on February 1, 2008.

Genetics, Vol. 178, 1003-1011, February 2008, Copyright © 2008
doi:10.1534/genetics.107.083071

Population Biology of Cytoplasmic Incompatibility: Maintenance and Spread of Cardinium Symbionts in a Parasitic Wasp

Steve J. Perlman*,1, Suzanne E. Kelly{dagger} and Martha S. Hunter{dagger}

* Department of Biology, University of Victoria, Victoria, British Columbia V8W 3N5, Canada and {dagger} Department of Entomology, The University of Arizona, Tucson, Arizona 85721

1 Corresponding author: Department of Biology, University of Victoria, P.O. Box 3020, Stn. CSC, Victoria, BC V8W 3N5, Canada.
E-mail: stevep{at}uvic.ca

Bacteria that cause cytoplasmic incompatibility (CI) are perhaps the most widespread parasites of arthropods. CI symbionts cause reproductive failure when infected males mate with females that are either uninfected or infected with a different, incompatible strain. Until recently, CI was known to be caused only by the {alpha}-proteobacterium Wolbachia. Here we present the first study of the population biology of Cardinium, a recently discovered symbiont in the Bacteroidetes that causes CI in the parasitic wasp Encarsia pergandiella (Hymenoptera: Aphelinidae). Cardinium occurs at high frequency (~92%) in the field. Using wasps that were recently collected in the field, we measured parameters that are crucial for understanding how CI spreads and is maintained in its host. CI Cardinium exhibits near-perfect rates of maternal transmission, causes a strong reduction in viable offspring in incompatible crosses, and induces a high fecundity cost, with infected females producing 18% fewer offspring in the first 4 days of reproduction. We found no evidence for paternal transmission or horizontal transmission of CI Cardinium through parasitism of an infected conspecific. No evidence for cryptic parthenogenesis in infected females was found, nor was sex allocation influenced by infection. We incorporated our laboratory estimates into a model of CI dynamics. The model predicts a high stable equilibrium, similar to what we observed in the field. Interestingly, our model also predicts a high threshold frequency of CI invasion (20% for males and 24% for females), below which the infection is expected to be lost. We consider how this threshold may be overcome, focusing in particular on the sensitivity of CI models to fecundity costs. Overall our results suggest that the factors governing the dynamics of CI Wolbachia and Cardinium are strikingly similar.


Related articles in Genetics:

ISSUE HIGHLIGHTS

Genetics 2008 178: NP. [Full Text]