Sexual Drive of Normal and SR Flies of Drosophila nebulosa

Malogolowkin-Cohen, Ch.; Rodrigues-Pereira, M. A. Q.

doi:10.2307/2407271

Cited by 8 publications

(4 citation statements)

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“…In previous studies, neither Drosophila bifasciata infected by male-killing Wolbachia nor Drosophila nebulosa infected by malekilling Spiroplasma presented different development time from their uninfected counterparts (Ikeda, 1970;Malogolowkin-Cohen and Rodrigues-Pereira, 1975). Fitness effects that could explain a relative increase of infected females in Drosophila species in which male-killers naturally occur have been previously reported for two cases.…”

Section: Discussionmentioning

confidence: 88%

“…Ebbert (1991) reported that Spiroplasma-infected females of D. willistoni produced more offspring in early broods than uninfected females. Malogolowkin-Cohen and Rodrigues-Pereira (1975) reported that Spiroplasma-infected females of D. nebulosa became receptive to mating earlier than uninfected females. In all cases the fitness effects are not strong.…”

Section: Discussionmentioning

confidence: 99%

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Spiroplasma infection in Drosophila melanogaster: What is the advantage of killing males?

Martins

Ventura

Klaczko

2010

Journal of Invertebrate Pathology

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Male-killing bacteria are maternally inherited agents that cause death of sons of infected females. Their transmission rate is commonly high but imperfect and also sensitive to different environmental factors. Therefore, the proportion of infected females should be reduced in each generation. In order to explain male-killers spread and persistence in host population, a mechanism resulting in the relative increase of infected females must outweigh the losses caused by the imperfect transmission. The resource release hypothesis states that the males' death results in increased resources available to sibling females which would otherwise be used by their male siblings. Infected females are then expected: to be larger than uninfected females in natural populations; or to have higher viability; or to have shorter development times; or any combination of these outcomes. Here, we tested the resource release hypothesis by measuring body size of infected and uninfected wild-caught Drosophila melanogaster females and carried out other fitness related measures in the laboratory. Wild-caught infected females produced more daughters than uninfected females in their first days in the laboratory. However, although no significant difference in viability was found in a controlled experiment with infected and uninfected flies from a standard laboratory strain, there was a decrease in development time probably mediated by reduced competition. Fitness effects conditioned by the host genetic background are pointed out as a possible explanation for this difference between wild and laboratory flies. Our findings are discussed in the context of the resource advantage hypothesis.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Spiroplasma infection in Drosophila melanogaster: What is the advantage of killing males?

Martins

Ventura

Klaczko

2010

Journal of Invertebrate Pathology

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“…Infection with spiroplasmas may affect fitness components of the host insects, such as body size, reproduction, and longevity (9,13,40). In this study, the titers of ef1␣, an index of the cell number in the host insect, were for the most part similar for female insects infected with NSRO and female insects infected with NSRO-A throughout the developmental course (data not shown), suggesting that the fitness effects, if there are any, are not drastically different between NSRO and NSRO-A.…”

Section: Discussionmentioning

confidence: 99%

Population Dynamics of Male-Killing and Non-Male-Killing Spiroplasmas in Drosophila melanogaster

Anbutsu

Fukatsu

2003

Appl Environ Microbiol

112

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The endosymbiotic bacteria Spiroplasma spp. are vertically transmitted through female hosts and are known to cause selective death of male offspring in insects. One strain of spiroplasma, NSRO, causes male killing in Drosophila species, and a non-male-killing variant of NSRO, designated NSRO-A, has been isolated. It is not known why NSRO-A does not kill males. In an attempt to understand the mechanism of male killing, we investigated the population dynamics of NSRO and NSRO-A throughout the developmental course of the laboratory host Drosophila melanogaster by using a quantitative PCR technique. In the early development of the host insect, the titers of NSRO were significantly higher than those of NSRO-A at the first-and second-instar stages, whereas at the egg, third-instar, and pupal stages, the titers of the two spiroplasmas were almost the same. Upon adult emergence, the titers of the two spiroplasmas were similar, around 2 ؋ 10 8 dnaA copy equivalents. However, throughout host aging, the two spiroplasmas showed strikingly different population growth patterns. The titers of NSRO increased exponentially for 3 weeks, attained a peak value of around 4 ؋ 10 9 dnaA copy equivalents per insect, and then decreased. In contrast, the titers of NSRO-A were almost constant throughout the adult portion of the life cycle. In adult females, consequently, the titer of NSRO was significantly higher than the titer of NSRO-A except for a short period just after emergence. Although infection of adult females with NSRO resulted in almost 100% male killing, production of some male offspring was observed within 4 days after emergence when the titers of NSRO were as low as those of NSRO-A. Based on these results, we proposed a threshold density hypothesis for the expression of male killing caused by the spiroplasma. The extents of the bottleneck in the vertical transmission through host generations were estimated to be 5 ؋ 10 ؊5 for NSRO and 3 ؋ 10 ؊4 for NSRO-A.Occasionally, female-biased sex ratios have been found in the progeny of wild-caught female insects. This trait has been referred to as the sex ratio (SR) trait. The mated daughters of such females were found to produce daughters and few or no sons. In many cases, the female-biased sex ratios are expressed through selective death of male offspring. Such SR traits have been reported for a wide variety of insect taxa (reviewed in references 22, 26, and 28). In some of these cases, it has been demonstrated that the SR traits are caused by maternally inherited endosymbiotic bacteria. These microorganisms are called male-killing bacteria and have been found in diverse bacterial taxa, such as the genus Spiroplasma of the class Mollicutes (24, 60), the genera Rickettsia and Wolbachia of the ␣ subdivision of the division Proteobacteria (25, 57), the genus Arsenophonus of the ␥ subdivision of the Proteobacteria (15), an unidentified bacterium belonging to the FlavobacteriumBacteroides group (23) (44). In the D. willistoni group of the genus Drosophila, the causative agents of the S...

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“…The majority of detected fitness effects have been negative (Majerus 1999). Only two cases of benefit have been reported, in the drosophilids Drosophila willistoni and Drosophila nebulosa (Malogolowkin-Cohen and Rodriguez-Pereira 1975;Ebbert 1991), in both of which infected larvae develop faster.…”

Section: Introductionmentioning

confidence: 99%

Male-killing in the Coccinellidae: testing the predictions

Majerus

Majerus²

2011

Evol Ecol

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Male-killing endosymbionts have been widely reported in the invertebrates and are highly prevalent in the Coccinellidae. The presence of male-killers can lead to extreme bias in host population sex ratios and may have important and far-reaching consequences for the life-history and evolution of their hosts. Male-killers may have direct and indirect effects on host fitness and reproductive behaviour, as well as affecting the host genome, either via strong selection pressure imposed by highly female-biased population sex ratios or by selective sweeps caused as a male-killer conferring an advantage to infected individuals spreads through a population. Criteria used to predict which species are liable to male-killer invasion, based on a variety of ecological factors, have been produced. In summary male-killers are predicted to occur in aphidophageous species, that lay eggs in clutches, show sibling egg consumption and are liable to neonatal larval mortality due to starvation. We assayed 30 species of Coccinellid for the presence of such male-killers to assess the predictive accuracy of the criteria. Male-killers were identified in 8 species in which they were predicted to occur and were absent from all 10 species predicted not to harbor them. Analysis of the remaining 12 species, where male-killers were predicted by the original criteria, but where they were not found, allowed us to identify areas where the criteria can be refined and improved. We conclude that whilst the original criteria give a reasonably accurate prediction, there are refinements and improvements, concerning details of host diet and life-history, which make them more robust, especially in the light of discoveries of male-killing suppressors and when incorporated give a better fit to our findings from field samples. Michael E. N. Majerus-deceased. Electronic supplementary material The online version of this article (

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Sexual Drive of Normal and SR Flies of Drosophila nebulosa

Cited by 8 publications

References 0 publications

Spiroplasma infection in Drosophila melanogaster: What is the advantage of killing males?

Spiroplasma infection in Drosophila melanogaster: What is the advantage of killing males?

Population Dynamics of Male-Killing and Non-Male-Killing Spiroplasmas in Drosophila melanogaster

Male-killing in the Coccinellidae: testing the predictions

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