The genetic basis of male fertility in relation to haplodiploid reproduction in Leptopilina clavipes (Hymenoptera:Figitidae)

Traits under relaxed selection are expected to become reduced or disappear completely, a process called vestigialization. In parthenogenetic populations, traits historically involved in sexual reproduction are no longer under selection and potentially subject to such reduction. In Leptopilina clavipes, thelytokous (parthenogenetic) populations are infected by Wolbachia bacteria. Arrhenotokous Populations do not harbor Wolbachia. When antibiotics are applied to infected females, they are cured from their infection and males arise. Such males are capable of producing offspring with uninfected females, but with lower fertilization success than sexual males. This can be attributed to the lack of selection on male fertility in thelytokous lines. In this study we used this variation in L. clavipes male fertility to determine the genetic basis of this trait. Males from Cured thelytokous populations were crossed to females from uninfected Populations. Using AFLP markers, a genetic linkage map was generated, consisting of five linkage groups and spanning a total distance of 219.9 cM. A single QTL of large effect (explaining 46.5% of the phenotypic variance) was identified for male fertility, which we call male fertility factor (mff). We discuss possible mechanisms underlying the effect of mff as well as mechanisms involved in vestigialization of traits involved in sexual reproduction.</p

Losing the desire: selection can promote obligate asexuality

Whilst parthenogenesis has evolved multiple times from sexual invertebrate and vertebrate lineages, the drivers and consequences of the sex-asex transition remain mostly uncertain. A model by Stouthamer et al. recently published in BMC Evolutionary Biology shows a pathway by which obligate asexuality could be selected for following endosymbiont infection

Genetics of decayed sexual traits in a parasitoid wasp with endosymbiont-induced asexuality.

Trait decay may occur when selective pressures shift, owing to changes in environment or life style, rendering formerly adaptive traits non-functional or even maladaptive. It remains largely unknown if such decay would stem from multiple mutations with small effects or rather involve few loci with major phenotypic effects. Here, we investigate the decay of female sexual traits, and the genetic causes thereof, in a transition from haplodiploid sexual reproduction to endosymbiont-induced asexual reproduction in the parasitoid wasp Asobara japonica. We take advantage of the fact that asexual females cured of their endosymbionts produce sons instead of daughters, and that these sons can be crossed with sexual females. By combining behavioral experiments with crosses designed to introgress alleles from the asexual into the sexual genome, we found that sexual attractiveness, mating, egg fertilization and plastic adjustment of offspring sex ratio (in response to variation in local mate competition) are decayed in asexual A. japonica females. Furthermore, introgression experiments revealed that the propensity for cured asexual females to produce only sons (because of decayed sexual attractiveness, mating behavior and/or egg fertilization) is likely caused by recessive genetic effects at a single locus. Recessive effects were also found to cause decay of plastic sex-ratio adjustment under variable levels of local mate competition. Our results suggest that few recessive mutations drive decay of female sexual traits, at least in asexual species deriving from haplodiploid sexual ancestors

Genetics of decayed sexual traits in a parasitoid wasp with endosymbiont-induced asexuality

Trait decay may occur when selective pressures shift, owing to changes in environment or life style, rendering formerly adaptive traits non-functional or even maladaptive. It remains largely unknown if such decay would stem from multiple mutations with small effects or rather involve few loci with major phenotypic effects. Here, we investigate the decay of female sexual traits, and the genetic causes thereof, in a transition from haplodiploid sexual reproduction to endosymbiont-induced asexual reproduction in the parasitoid wasp Asobara japonica. We take advantage of the fact that asexual females cured of their endosymbionts produce sons instead of daughters, and that these sons can be crossed with sexual females. By combining behavioral experiments with crosses designed to introgress alleles from the asexual into the sexual genome, we found that sexual attractiveness, mating, egg fertilization and plastic adjustment of offspring sex ratio (in response to variation in local mate competition) are decayed in asexual A. japonica females. Furthermore, introgression experiments revealed that the propensity for cured asexual females to produce only sons (because of decayed sexual attractiveness, mating behavior and/or egg fertilization) is likely caused by recessive genetic effects at a single locus. Recessive effects were also found to cause decay of plastic sex-ratio adjustment under variable levels of local mate competition. Our results suggest that few recessive mutations drive decay of female sexual traits, at least in asexual species deriving from haplodiploid sexual ancestors

Temporal variation in sex allocation in the mealybug <em>Planococcus citri</em>:Adaptation, constraint, or both?

Sex ratio theory has been very successful in predicting under which circumstances parents should bias their investment towards a particular offspring sex. However, most examples of adaptive sex ratio bias come from species with well-defined mating systems and sex determining mechanisms, while in many other groups there is still an on-going debate about the adaptive nature of sex allocation. Here we study the sex allocation in the mealybug Planococcus citri, a species in which it is currently unclear how females adjust their sex ratio, even though experiments have shown support for facultative sex ratio adjustment. Previous work has shown that the sex ratio females produce changes over the oviposition period, with males being overproduced early and late in the laying sequence. Here we investigate this complex pattern further, examining both the robustness of the pattern and possible explanations for it. We first show that this sex allocation behaviour is indeed consistent across lines from three geographical regions. Second, we test whether females produce sons first in order to synchronize reproductive maturation of her offspring, although our data provide little evidence for this adaptive explanation. Finally we test the age at which females are able to mate successfully and show that females are able to mate and store sperm before adult eclosion. Whilst early-male production may still function in promoting protandry in mealybugs, we discuss whether mechanistic constraints limit how female allocate sex across their lifetime

Genetics of decayed sexual traits in a parasitoid wasp with endosymbiont-induced asexuality

Trait decay may occur when selective pressures shift, owing to changes in environment or life style, rendering formerly adaptive traits non-functional or even maladaptive. It remains largely unknown if such decay would stem from multiple mutations with small effects or rather involve few loci with major phenotypic effects. Here, we investigate the decay of female sexual traits, and the genetic causes thereof, in a transition from haplodiploid sexual reproduction to endosymbiont-induced asexual reproduction in the parasitoid wasp Asobara japonica. We take advantage of the fact that asexual females cured of their endosymbionts produce sons instead of daughters, and that these sons can be crossed with sexual females. By combining behavioral experiments with crosses designed to introgress alleles from the asexual into the sexual genome, we found that sexual attractiveness, mating, egg fertilization and plastic adjustment of offspring sex ratio (in response to variation in local mate competition) are decayed in asexual A. japonica females. Furthermore, introgression experiments revealed that the propensity for cured asexual females to produce only sons (because of decayed sexual attractiveness, mating behavior and/or egg fertilization) is likely caused by recessive genetic effects at a single locus. Recessive effects were also found to cause decay of plastic sex-ratio adjustment under variable levels of local mate competition. Our results suggest that few recessive mutations drive decay of female sexual traits, at least in asexual species deriving from haplodiploid sexual ancestors

Antibiotic treatment leads to the elimination of Wolbachia endosymbionts and sterility in the diplodiploid collembolan Folsomia candida

<p>Abstract</p> <p>Background</p> <p><it>Wolbachia </it>is an extremely widespread bacterial endosymbiont of arthropods and nematodes that causes a variety of reproductive peculiarities. Parthenogenesis is one such peculiarity but it has been hypothesised that this phenomenon may be functionally restricted to organisms that employ haplodiploid sex determination. Using two antibiotics, tetracycline and rifampicin, we attempted to eliminate <it>Wolbachia </it>from the diplodiploid host <it>Folsomia candida</it>, a species of springtail which is a widely used study organism.</p> <p>Results</p> <p>Molecular assays confirmed that elimination of <it>Wolbachia </it>was successfully achieved through continuous exposure of populations (over two generations and several weeks) to rifampicin administered as 2.7% dry weight of their yeast food source. The consequence of this elimination was total sterility of all individuals, despite the continuation of normal egg production.</p> <p>Conclusion</p> <p>Microbial endosymbionts play an obligatory role in the reproduction of their diplodiploid host, most likely one in which the parthenogenetic process is facilitated by <it>Wolbachia</it>. A hitherto unknown level of host-parasite interdependence is thus recorded.</p

Anti-filarial Activity of Antibiotic Therapy Is Due to Extensive Apoptosis after Wolbachia Depletion from Filarial Nematodes

Filarial nematodes maintain a mutualistic relationship with the endosymbiont Wolbachia. Depletion of Wolbachia produces profound defects in nematode development, fertility and viability and thus has great promise as a novel approach for treating filarial diseases. However, little is known concerning the basis for this mutualistic relationship. Here we demonstrate using whole mount confocal microscopy that an immediate response to Wolbachia depletion is extensive apoptosis in the adult germline, and in the somatic cells of the embryos, microfilariae and fourth-stage larvae (L4). Surprisingly, apoptosis occurs in the majority of embryonic cells that had not been infected prior to antibiotic treatment. In addition, no apoptosis occurs in the hypodermal chords, which are populated with large numbers of Wolbachia, although disruption of the hypodermal cytoskeleton occurs following their depletion. Thus, the induction of apoptosis upon Wolbachia depletion is non-cell autonomous and suggests the involvement of factors originating from Wolbachia in the hypodermal chords. The pattern of apoptosis correlates closely with the nematode tissues and processes initially perturbed following depletion of Wolbachia, embryogenesis and long-term sterilization, which are sustained for several months until the premature death of the adult worms. Our observations provide a cellular mechanism to account for the sustained reductions in microfilarial loads and interruption of transmission that occurs prior to macrofilaricidal activity following antibiotic therapy of filarial nematodes

Wolbachia endosymbiont is essential for egg hatching in a parthenogenetic arthropod.

Wolbachia pipientis can induce a range of sex ratio distortions including parthenogenesis. Recently Wolbachia has been detected in the diploid, parthenogenetic, collembolan species Folsomia candida. In this paper we address the effect of Wolbachia on reproduction in F. candida. Wolbachia infection was removed by antibiotic and heat treatment, and quantitative PCR techniques confirmed the success of the treatments. Complete loss of Wolbachia-infection led to the production of normal clutch sizes, but was associated with full egg hatching failure. Our results demonstrate that F. candida is strictly dependent on Wolbachia to produce viable offspring. This is one of the few cases of obligatory Wolbachia infection in arthropods. Our data suggest a unique mechanism underlying Wolbachia-dependence of egg development. One of our more salient results is that hatching success increased in consecutive egg clutches of antibiotic-treated individuals, probably due to restoration of bacterial densities over time. These observations suggest that reproduction in F. candida is a threshold effect requiring a critical Wolbachia density as is hypothesized by the bacterial dosage model. Quantitative PCR analysis showed that heat or antibiotic treated individuals with egg hatching failure had low average bacterial densities, but bacterial densities were not significantly different from those of treated individuals with successfully eclosing eggs. Additional experiments with partially cured F. candida are needed to prove the dosage model. © Springer Science+Business Media B.V. 2008