Male development time influences the strength of Wolbachia-induced cytoplasmic incompatibility expression in Drosophila melanogaster.
Cytoplasmic incompatibility (CI) is the most widespread reproductive modification induced in insects by the maternally inherited intracellular bacteria, Wolbachia. Expression of CI in Drosophila melanogaster is quite variable. Published papers typically show that CI expression is weak and often varies between different Drosophila lines and different labs reporting the results. The basis for this variability is not well understood but is often considered to be due to unspecified host genotype interactions with Wolbachia. Here, we show that male development time can greatly influence CI expression in D. melanogaster. In a given family, males that develop fastest express very strong CI. The "younger brothers" of these males (males that take longer to undergo larval development) quickly lose their ability to express the CI phenotype as a function of development time. This effect is independent of male age effects and is enhanced when flies are reared under crowded conditions. No correlation is seen between this effect and Wolbachia densities in testes, suggesting that a more subtle interaction between host and symbiont is responsible. The observed younger brother effect may explain much of the reported variability in CI expression in this species. When male development time is controlled, it is possible to obtain consistently high levels of CI expression, which will benefit future studies that wish to use D. melanogaster as a model host to unravel CI mechanisms.
School of Integrative Biology, The University of Queensland, St. Lucia, QLD 4072, Brisbane, Australia.
Ryuichi
R
Yamada
Kevin D
KD
Floate
Markus
M
Riegler
Scott L
SL
O'Neill
D000818:Animals; D003593:Cytoplasm / Q000502:physiology*; D004331:Drosophila melanogaster / Q000254:growth & development / Q000382:microbiology*; D008297:Male; D010641:Phenotype; D013559:Symbiosis; D013737:Testis / Q000382:microbiology; D020577:Wolbachia / Q000472:pathogenicity*