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28 results for “cytoplasmic incompatibility”
Rickettsia induces strong cytoplasmic incompatibility in a predatory insect
<p><em>Rickettsia</em>, a group of intracellular bacteria found in eukaryotes, exhibits diverse lifestyles, with some acting as vertebrate pathogens transmitted by arthropod vectors and others serving as maternally transmitted arthropod endosymbionts, some of which manipulate host reproduction for their own benefit. Two phenotypes, namely male killing and parthenogenesis induction are known as <em>Rickettsia</em>-induced host reproductive manipulations, but it remains unknown whether <em>Rickettsia</em> can induce other types of host manipulation. In this study, we discovered that <em>Rickettsia</em> induced strong cytoplasmic incompatibility (CI), in which uninfected females produce no offspring when mated with infected males, in the predatory insect <em>Nesidiocoris tenuis </em>(Hemiptera: Miridae). Molecular phylogenetic analysis revealed that the <em>Rickettsia</em> strain was related to <em>Rickettsia bellii</em>, a common insect endosymbiont. Notably, this strain carried plasmid-encoded homologues of the CI-inducing factors (namely <em>cifA</em>-like and <em>cifB</em>-like genes), typically found in <em>Wolbachia</em>, which are well-known CI-inducing endosymbionts. Protein domain prediction revealed that the <em>cifB</em>-like gene encodes PD-(D/E)XK nuclease and deubiquitinase domains, which are responsible for <em>Wolbachia</em>-induced CI, as well as OTU-like cysteine protease and ankyrin repeat domains. These findings suggest that <em>Rickettsia</em> and <em>Wolbachia</em> endosymbionts share underlying mechanisms of CI and that CI-inducing ability was acquired by microbes through horizontal plasmid transfer.</p>
Rickettsia induces strong cytoplasmic incompatibility in a predatory insect
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Supplementary data for Ün et. al. 2020 "Cytoplasmic incompatibility between New and Old World populations of a tramp ant"
<p>Supplementary annotation and phylogenetic data. See included README file for details.</p>
Data from: Loss of cytoplasmic incompatibility and minimal fecundity effects explain relatively low Wolbachia frequencies in Drosophila mauritiana
Maternally transmitted Wolbachia bacteria infect about half of all insect species. Many Wolbachia cause cytoplasmic incompatibility (CI), reduced egg hatch when uninfected females mate with infected males. Although CI produces a frequency-dependent fitness advantage that leads to high equilibrium Wolbachia frequencies, it does not aid Wolbachia spread from low frequencies. Indeed, the fitness advantages that produce initial Wolbachia spread and maintain non-CI Wolbachia remain elusive. wMau Wolbachia infecting Drosophila mauritiana do not cause CI, despite being very similar to CI-causing wNo from D. simulans (0.068% sequence divergence over 682,494 bp), suggesting recent CI loss. Using draft wMau genomes, we identify a deletion in a CI-associated gene, consistent with theory predicting that selection within host lineages does not act to increase or maintain CI. In the laboratory, wMau shows near-perfect maternal transmission; but we find no significant effect on host fecundity, in contrast to published data. Intermediate wMau frequencies on the island Mauritius are consistent with a balance between unidentified small, positive fitness effects and imperfect maternal transmission. Our phylogenomic analyses suggest that group-B Wolbachia, including wMau and wPip, diverged from group-A Wolbachia, such as wMel and wRi, 6–46 million years ago, more recently than previously estimated.
Supplementary material for Proctor et al., "Warm temperature inhibits cytoplasmic incompatibility induced by endosymbiotic Rickettsiella in a spider host"
<p>Included are two supplemental files: SupplementaryDocument1 includes primers and cycling conditions for qPCR quanitification of the symbiont Rickettsiella. SupplementaryDocument2 includes all raw data for the experiments included in this manuscript.</p>
Data from: Loss of cytoplasmic incompatibility and minimal fecundity effects explain relatively low Wolbachia frequencies in Drosophila mauritiana
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Suppression of cytoplasmic incompatibility in the leaf-mining fly Liriomyza sativae with a nuclear Wolbachia insert
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The facultative intracellular symbiont Lariskella is neutral for lifetime fitness and spreads through cytoplasmic incompatibility in the leaffooted bug, Leptoglossus zonatus
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Cardinium localization during its parasitoid wasp host's development provides insights into cytoplasmic incompatibility
<p>Arthropods harbor heritable intracellular symbionts that may manipulate host reproduction to favor symbiont transmission. In cytoplasmic incompatibility (CI), the symbiont sabotages the reproduction of infected males such that high levels of offspring mortality result when they mate with uninfected females. In crosses with infected males and infected females, however, (the "rescue" cross), normal numbers of offspring are produced. A common CI-inducing symbiont, <i>Cardinium hertigii</i>, causes variable levels of CI mortality in the parasitoid wasp, <i>Encarsia</i> <i>suzannae. </i>Previous work correlated CI-induced mortality with male development time in this system, although the timing of <i>Cardinium</i> CI-induction and the relationship between development time and CI mortality was not well understood. Here, using a combination of crosses, manipulation of development time, and fluorescence microscopy, we identify the localization and the timing of the CI-induction step in the <i>Cardinium-E. suzannae </i>system. Antibiotic treatment of adult <i>Cardinium-</i>infected males did not reduce the mortality associated with the CI phenotype, suggesting that CI-alteration occurs prior to adulthood. Our results suggest that the alteration step occurs during the pupal period, and is limited by the duration of pupal development: 1) <i>Encarsia </i>produces most sperm prior to adulthood, 2), FISH localization of <i>Cardinium </i>in testes showed an association with sperm nuclei throughout spermatogenesis but not with mature sperm and 3) two methods of prolonging the pupal period (cool temperatures and the juvenile hormone analog methoprene) both caused greater CI mortality, suggesting the degree of alteration is limited by the duration of the pupal stage. Based on these results, we compare two models for potential mechanisms of <i>Cardinium</i> sperm modification in the context of what is known about analogous mechanisms of <i>Wolbachia, </i>a more extensively studied CI-inducing symbiont.</p>
Data from: "Darwin's corollary" and cytoplasmic incompatibility induced by Cardinium may contribute to speciation in Encarsia wasps (Hymenoptera: Aphelinidae)
The potential importance of cytoplasmic incompatibility (CI) – inducing bacterial symbionts in speciation of their arthropod hosts has been debated. Theoretical advances have led to a consensus that a role is plausible when CI is combined with other isolating barriers. However, the insect model systems Nasonia and Drosophila are the only two experimental examples documented. Here we analyzed the components of reproductive isolation between the parasitoid wasp Encarsia suzannae, which is infected by the CI-inducing symbiont Cardinium, and its uninfected sibling species Encarsia gennaro. Laboratory crosses demonstrated that: 1) sexual isolation is incomplete; 2) hybrid offspring production is greatly reduced in the interspecific CI cross; 3) viable hybrids may be produced by curing E. suzannae males of Cardinium with antibiotics; 4) hybrid offspring production in the reciprocal cross is greatly reduced by hybrid inviability due to genetic incompatibilities; 5) hybrid sterility is nearly complete in both directions at the F1 stage. Thus, asymmetrical hybrid incompatibilities and CI act as complementary isolating mechanisms. We propose a new model for contributions of CI symbionts to speciation, with CI reducing gene flow between species in one direction, and in the other, a symbiont sweep resulting in accelerated mtDNA evolution, negative cytonuclear interactions and hybrid incompatibilities.
Data from: Wolbachia in the Drosophila yakuba complex: pervasive frequency variation and weak cytoplasmic incompatibility, but no apparent effect on reproductive isolation
Three hybridizing species-the clade ((Drosophila yakuba, D. santomea), D. teissieri) -comprise the yakuba complex in the D. melanogaster subgroup. Their ranges overlap on Bioko and São Tomé, islands off west Africa. All three species are infected with Wolbachia, maternally inherited, endosymbiotic bacteria, best known for manipulating host reproduction to favor infected females. Previous analyses reported no cytoplasmic incompatibility (CI) in these species. However, we discovered that Wolbachia from each species cause intra- and interspecific CI. In D. teissieri, analyses of F1 and backcross genotypes show that both host genotype and Wolbachia variation modulate CI intensity. Wolbachia-infected females seem largely protected from intra- and interspecific CI, irrespective of Wolbachia and host genotypes. Wolbachia do not affect host mating behavior or female fecundity, within or between species. The latter suggests little apparent effect of Wolbachia on premating or gametic RI between host species. In nature, Wolbachia frequencies varied spatially for D. yakuba in 2009, with 76% (N = 155) infected on São Tomé, and only 3% (N = 36) infected on Bioko; frequencies also varied temporally in D. yakuba and D. santomea on São Tomé between 2009 and 2015. These temporal frequency fluctuations could generate asymmetries in interspecific mating success, and contribute to postzygotic RI. However, the fluctuations in Wolbachia frequencies that we observe also suggest that asymmetries are unlikely to persist. Finally, we address theoretical questions that our empirical findings raise about Wolbachia persistence when conditions fluctuate and about the stable coexistence of Wolbachia and host variants that modulate Wolbachia effects.
Interacting host modifier systems control Wolbachia-induced cytoplasmic incompatibility in a haplodiploid mite
<p><span>Reproductive parasites such as <em>Wolbachia</em> spread within host populations by inducing cytoplasmic incompatibility (CI). CI occurs when parasite-modified sperm fertilizes uninfected eggs and is typified by great variation in strength across biological systems. In haplodiploid hosts, CI has different phenotypic outcomes depending on whether the fertilized eggs die or develop into males. Genetic conflict theories predict the evolution of host modulation of CI, which in turn influences the stability of reproductive parasitism. Yet, despite the ubiquity of CI-inducing parasites in nature, there is scarce evidence for intraspecific host modulation of CI strength and phenotype. Here, we tested for intraspecific host modulation of <em>Wolbachia</em>-induced CI in haplodiploid <em>Tetranychus urticae </em>mites. Using a single CI-inducing <em>Wolbachia </em>variant and mitochondrion, a nuclear panel was created that consisted of infected and cured near-isogenic lines. We performed a highly replicated age-synchronized full diallel cross comprised of incompatible and compatible control crosses. We uncovered host modifier systems that cause striking variation in CI strength when carried by infected <em>T. urticae </em>males. We observed a continuum of CI phenotypes in our crosses and identified strong intraspecific female modulation of CI phenotype. Crosses established a recessive genetic basis for the maternal effect and were consistent with polygenic Mendelian inheritance. Both male and female modulation interacted with the genotype of the mating partner. Our findings identify spermatogenesis as an important target of selection for host modulation of CI strength and underscore the importance of maternal genetic effects for the CI phenotype. Our findings reveal that intraspecific host modulation of CI is underpinned by complex genetic architectures and confirm that the evolution of reproductive parasitism is contingent on host genetics.</span></p>
Data from: Exposure to opposing temperature extremes causes comparable effects on Cardinium density but contrasting effects on Cardinium-induced cytoplasmic incompatibility
Terrestrial arthropods, including insects, commonly harbor maternally inherited intracellular symbionts that confer benefits to the host or manipulate host reproduction to favor infected female progeny. These symbionts may be especially vulnerable to thermal stress, potentially leading to destabilization of the symbiosis and imposing costs to the host. For example, increased temperatures can reduce the density of a common reproductive manipulator, Wolbachia, and the strength of its crossing incompatibility (cytoplasmic incompatibility, or CI) phenotype. Another manipulative symbiont, Cardinium hertigii, infects ~ 6-10% of Arthropods, and also can induce CI, but there is little homology between the molecular mechanisms of CI induced by Cardinium and Wolbachia. Here we investigated whether temperature disrupts the CI phenotype of Cardinium in a parasitic wasp host, Encarsia suzannae. We examined the effects of both warm (32°C day/ 29°C night) and cool (20°C day/ 17°C night) temperatures on Cardinium CI and found that both types of temperature stress modified aspects of this symbiosis. Warm temperatures reduced symbiont density, pupal developmental time, vertical transmission rate, and the strength of both CI modification and rescue. Cool temperatures also reduced symbiont density, however this resulted in stronger CI, likely due to cool temperatures prolonging the host pupal stage. The opposing effects of cool and warm-mediated reductions in symbiont density on the resulting CI phenotype indicates that CI strength may be independent of density in this system. Temperature stress also modified the CI phenotype only if it occurred during the pupal stage, highlighting the likely importance of this stage for CI induction in this symbiosis.
Testing the potential contribution of Wolbachia to speciation when cytoplasmic incompatibility becomes associated with host‐related reproductive isolation
<p>Endosymbiont induced cytoplasmic incompatibility (CI) may play an important role in arthropod speciation. However, whether CI consistently becomes associated or coupled with other host-related forms of reproductive isolation (RI) to impede the transfer of endosymbionts between hybridizing populations and further the divergence process remains an open question. Here, we show varying degrees of pre- and post-mating RI exist among allopatric populations of two interbreeding cherry-infesting tephritid fruit flies (<i>Rhagoletis cingulata</i> and <i>R. indifferens</i>) across North America. These flies display allochronic and sexual isolation among populations, as well as unidirectional reductions in egg hatch in hybrid crosses involving southwestern USA males. All populations are infected by a <i>Wolbachia </i>strain, <i>w</i>Cin2, whereas a second strain, <i>w</i>Cin3, only coinfects flies from the Southwest USA and Mexico. Strain <i>w</i>Cin3 is associated with a unique mtDNA haplotype and unidirectional postmating RI, implicating the strain as the cause of CI. When coupled with non-endosymbiont RI barriers, we estimate the strength of CI associated with <i>w</i>Cin3 would not prevent the strain from introgressing from infected Southwestern to uninfected populations elsewhere in the USA if populations were to come into secondary contact and hybridize. In contrast, cytoplasmic-nuclear coupling may be sufficient to impede the transfer of <i>w</i>Cin3 if Mexican and USA populations were to come into contact. We discuss our results in the context of the general paucity of examples demonstrating stable <i>Wolbachia</i> hybrid zones and whether the spread of <i>Wolbachia</i> among taxa can be constrained in natural hybrid zones long enough for the endosymbiont to participate in speciation.</p>
Data from: “Darwin’s corollary” and cytoplasmic incompatibility induced by Cardinium may contribute to speciation in Encarsia wasps (Hymenoptera: Aphelinidae)
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Cardinium localization during its parasitoid wasp host’s development provides insights into cytoplasmic incompatibility
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Interacting host modifier systems control Wolbachia-induced cytoplasmic incompatibility in a haplodiploid mite
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Data from: Exposure to opposing temperature extremes causes comparable effects on Cardinium density but contrasting effects on Cardinium-induced cytoplasmic incompatibility
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Cytoplasmic incompatibility between Old and New World populations of a tramp ant
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Testing the potential contribution of Wolbachia to speciation when cytoplasmic incompatibility becomes associated with host‐related reproductive isolation
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