Targeted Gene Deletion and Phenotypic Analysis of the <i>Drosophila melanogaster</i> Seminal Fluid Protease Inhibitor Acp62F

Mueller, Jacob L.; Linklater, Jon R.; Ram, K. Ravi; Chapman, Tracey; Wolfner, Mariana F.

doi:10.1534/genetics.107.083766

Cited by 73 publications

(99 citation statements)

References 53 publications

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“…When testing whether females were either pregnant or not, the models were fitted with a binomial distribution. To test for an effect of genotype on sperm competition success, we assessed the percentage of offspring sired by the male in the offensive sperm competition position (Mueller et al 2008, Firman & Simmons 2011, Klemme & Firman 2013. A binomial distribution was used when examining this percentage, because all values were either 100 or 0% (effectively either 0 or 1) due to Sod1 C/C males siring all the offspring regardless of being the first or second to mate.…”

Section: Discussionmentioning

confidence: 99%

Copper-zinc superoxide dismutase deficiency impairs sperm motility and in vivo fertility

et al. 2013

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Oxidative stress, overproduction of reactive oxygen species (ROS) in relation to defence mechanisms, is considered to be a major cause of male infertility. For protection against the deleterious effects of ROS, animals have a variety of enzymatic antioxidants that reduce these molecules to less reactive forms. The physiological role of these antioxidants in vivo has been explored extensively through genetic inhibition of gene expression; surprisingly, many of these animals remain fertile in spite of increased oxidative stress. Copper-zinc superoxide dismutase-deficient (Sod1) male mice are one such example for which in vivo fertility has been repeatedly reported as normal, although examination of fertility has consisted of simply pairing animals of the same strain and checking for litters. This is a fairly low criterion by which to assess fertility. Herein, we show that Sod1-deficient males have zero fertilisation success in sperm competition trials that pit them against wild-type males of an otherwise identical genetic background and are almost completely infertile when mated singly with females of a different genotype. We also show that various aspects of sperm motility and function are impaired in Sod1-deficient mice. Testing the breeding capabilities of mice under more ecologically relevant conditions and with females of different genotypes may help reveal additional physiological causes of infertility.

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Section: Discussionmentioning

confidence: 99%

Copper-zinc superoxide dismutase deficiency impairs sperm motility and in vivo fertility

et al. 2013

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“…Phenotypic analysis of the Acp29AB 1 mutant: To assess the effects of the Acp29AB 1 mutation on sperm storage, sperm counts were carried out as in Neubaum and Wolfner (1999a) and Mueller et al (2008). Sperm stored in the storage organs (spermathecae and seminal receptacle) of females mated to control or mutant males were counted at 2 hr ASM and at 4 days ASM.…”

Section: Methodsmentioning

confidence: 99%

A Role for Acp29AB, a Predicted Seminal Fluid Lectin, in Female Sperm Storage inDrosophila melanogaster

et al. 2008

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Females of many animal species store sperm for taxon-specific periods of time, ranging from a few hours to years. Female sperm storage has important reproductive and evolutionary consequences, yet relatively little is known of its molecular basis. Here, we report the isolation of a loss-of-function mutation of the Drosophila melanogaster Acp29AB gene, which encodes a seminal fluid protein that is transferred from males to females during mating. Using this mutant, we show that Acp29AB is required for the normal maintenance of sperm in storage. Consistent with this role, Acp29AB localizes to female sperm storage organs following mating, although it does not appear to associate tightly with sperm. Acp29AB is a predicted lectin, suggesting that sugar-protein interactions may be important for D. melanogaster sperm storage, much as they are in many mammals. Previous association studies have found an effect of Acp29AB genotype on a male's sperm competitive ability; our findings suggest that effects on sperm storage may underlie these differences in sperm competition. Moreover, Acp29AB's effects on sperm storage and sperm competition may explain previously documented evidence for positive selection on the Acp29AB locus.

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“…Females remained alone in their vials for 2 hr, 4 days, or 10 days ASM (as in Ravi Ram and Wolfner 2007b) at which time they were frozen until processed for sperm counts. To visualize sperm, female reproductive tracts were removed, processed, and stained with orcein using previously described methods (Neubaum and Wolfner 1999;Mueller et al 2008;Bloch Qazi and Hogdal 2010). Sperm in the female storage organs were counted using a transillumination microscope with 31000 magnification.…”

Section: Fliesmentioning

confidence: 99%

Sex Peptide Is Required for the Efficient Release of Stored Sperm in Mated Drosophila Females

et al. 2010

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The Drosophila seminal fluid protein (SFP) sex peptide (SP) elicits numerous post-mating responses, including increased egg laying and decreased sexual receptivity, in the mated female. Unlike other SFPs, which are detectable in mated females for only a few hours post mating, SP is maintained-and its effects are sustained-for several days. The persistence of SP in the mated female's reproductive tract is thought to be a consequence of its binding to, and gradual release from, sperm in storage, which maintains SP's ability to act within the female reproductive tract. Recent studies have shown that several other SFPs, acting in a network, are needed for SP's localization to sperm and are necessary for the efficient release of sperm from storage. This result suggested an additional new role for SP modulating the release of sperm from storage. We tested for this possibility by examining sperm storage parameters in mated females that did not receive SP. We found that while sperm accumulation into storage was unaffected, sperm depletion from storage sites was significantly decreased (or impaired) in the absence of SP. Mates of males expressing a modified SP that is unable to be released from sperm showed a similar phenotype, indicating that release of sperm-bound SP is a necessary component of normal sperm depletion. Additionally, SP null males were more successful in a sperm competitive environment when they were first to mate, which is likely a consequence of higher retention of their sperm due to defective sperm release. Our findings illustrate a direct role for SP in the release of sperm from storage.

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Targeted Gene Deletion and Phenotypic Analysis of the Drosophila melanogaster Seminal Fluid Protease Inhibitor Acp62F

Cited by 73 publications

References 53 publications

Copper-zinc superoxide dismutase deficiency impairs sperm motility and in vivo fertility

Copper-zinc superoxide dismutase deficiency impairs sperm motility and in vivo fertility

A Role for Acp29AB, a Predicted Seminal Fluid Lectin, in Female Sperm Storage inDrosophila melanogaster

Sex Peptide Is Required for the Efficient Release of Stored Sperm in Mated Drosophila Females

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