10.5061/DRYAD.SK805
Ma, Wen-Juan
University of Groningen
Pannebakker, Bart A.
Wageningen University & Research
van de Zande, Louis
University of Groningen
Schwander, Tanja
University of Groningen
Wertheim, Bregje
University of Groningen
Beukeboom, Leo W.
University of Groningen
Data from: Diploid males support a two-step mechanism of
endosymbiont-induced thelytoky in a parasitoid wasp
Dryad
dataset
2015
endosymbiont-induced parthenogenesis
Asobara japonica
2015-05-13T15:58:10Z
2015-05-13T15:58:10Z
en
https://doi.org/10.1186/s12862-015-0370-9
278875 bytes
1
CC0 1.0 Universal (CC0 1.0) Public Domain Dedication
Background Haplodiploidy, where females develop from diploid, fertilized
eggs and males from haploid, unfertilized eggs, is abundant in some insect
lineages. Some species in these lineages reproduce by thelytoky that is
caused by infection with endosymbionts: infected females lay haploid eggs
that undergo diploidization and develop into females, while males are very
rare or absent. It is generally assumed that in thelytokous wasps,
endosymbionts merely diploidize the unfertilized eggs, which would then
trigger female development. Results We found that females in the
parasitoid wasp Asobara japonica infected with thelytoky-inducing
Wolbachia produce 0.7–1.2 % male offspring. Seven to 39 % of these males
are diploid, indicating that diploidization and female development can be
uncoupled in A. japonica. Wolbachia titer in adults was correlated with
their ploidy and sex: diploids carried much higher Wolbachia titers than
haploids, and diploid females carried more Wolbachia than diploid males.
Data from introgression lines indicated that the development of diploid
individuals into males instead of females is not caused by
malfunction-mutations in the host genome but that diploid males are most
likely produced when the endosymbiont fails to activate the female sex
determination pathway. Our data therefore support a two-step mechanism by
which endosymbionts induce thelytoky in A. japonica: diploidization of the
unfertilized egg is followed by feminization, whereby each step correlates
with a threshold of endosymbiont titer during wasp development.
Conclusions Our new model of endosymbiont-induced thelytoky overthrows the
view that certain sex determination mechanisms constrain the evolution of
endosymbiont-induced thelytoky in hymenopteran insects. Endosymbionts can
cause parthenogenesis through feminization, even in groups in which
endosymbiont-diploidized eggs would develop into males following the
hosts’ sex determination mechanism. In addition, our model broadens our
understanding of the mechanisms by which endosymbionts induce thelytoky to
enhance their transmission to the next generation. Importantly, it also
provides a novel window to study the yet-poorly known haplodiploid sex
determination mechanisms in haplodiploid insects.
Figure2_maleproductionFigure3_mothers_woltiterFigure4_progeny_woltiterFigure5_introgression
Japan