Diploid males support a two-step mechanism of endosymbiont-induced thelytoky in a parasitoid wasp
Ma, W.J. ; Pannebakker, B.A. ; Zande, L. van de; Schwander, T. ; Wertheim, B. ; Beukeboom, L.W. - \ 2015
BMC Evolutionary Biology 15 (2015). - ISSN 1471-2148
leptopilina-clavipes hymenoptera - sex-determination - parthenogenetic populations - quantitative pcr - insect sex - wolbachia - host - reproduction - braconidae - determines
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.
A Caenorhabditis elegans Wild Type Defies the Temperature-Size Rule Owing to a Single Nucleotide Polymorphism in tra-3
Kammenga, J.E. ; Doroszuk, A. ; Riksen, J.A.G. ; Hazendonk, E. ; Spiridon, L.N. ; Petrescu, A.J. ; Tijsterman, M. ; Plasterk, R.H.A. ; Bakker, J. - \ 2007
Plos Genetics 3 (2007)3. - ISSN 1553-7404
quantitative trait loci - secondary structure prediction - life-history puzzle - drosophila-melanogaster - body-size - cell-size - c-elegans - transcription factor - sex-determination - cold-acclimation
Ectotherms rely for their body heat on surrounding temperatures. A key question in biology is why most ectotherms mature at a larger size at lower temperatures, a phenomenon known as the temperature¿size rule. Since temperature affects virtually all processes in a living organism, current theories to explain this phenomenon are diverse and complex and assert often from opposing assumptions. Although widely studied, the molecular genetic control of the temperature¿size rule is unknown. We found that the Caenorhabditis elegans wild-type N2 complied with the temperature¿size rule, whereas wild-type CB4856 defied it. Using a candidate gene approach based on an N2 × CB4856 recombinant inbred panel in combination with mutant analysis, complementation, and transgenic studies, we show that a single nucleotide polymorphism in tra-3 leads to mutation F96L in the encoded calpain-like protease. This mutation attenuates the ability of CB4856 to grow larger at low temperature. Homology modelling predicts that F96L reduces TRA-3 activity by destabilizing the DII-A domain. The data show that size adaptation of ectotherms to temperature changes may be less complex than previously thought because a subtle wild-type polymorphism modulates the temperature responsiveness of body size. These findings provide a novel step toward the molecular understanding of the temperature¿size rule, which has puzzled biologists for decades.