Sperm of the wasted mutant are wasted when females utilize the stored sperm in Drosophila melanogaster

Abstract

Females of many animal species store sperm after copulation for use in fertilization, but the mechanisms controlling sperm storage and utilization are largely unknown. Here we describe a novel male sterile mutation of Drosophila melanogaster, wasted (wst), which shows defects in various processes of sperm utilization. The sperm of wst mutant males are stored like those of wild-type males in the female sperm storage organs, the spermathecae and seminal receptacles, after copulation and are released at each ovulation. However, an average of thirteen times more wst sperm than wild type sperm are released at each ovulation, resulting in rapid loss of sperm stored in seminal receptacles within a few days after copulation. wst sperm can enter eggs efficiently at 5 hr after copulation, but the efficiency of sperm entry decreases significantly by 24 hr after copulation, suggesting that wst sperm lose their ability to enter eggs during storage. Furthermore, wst sperm fail to undergo nuclear decondensation, which prevents the process of fertilization even when sperm enter eggs. Our results indicate that the wst gene is essential for independent processes in the utilization of stored sperm; namely, regulation of sperm release from female storage organs, maintenance of sperm efficiency for entry into eggs, and formation of the male pronucleus in the egg at fertilization.

A requirement for the neuromodulators octopamine and tyramine in Drosophila melanogaster female sperm storage

“…The recent identification of wasted mutants reported that sperm release is severely defective in these mutants, with sperm rapidly lost during each ovulation. However, sperm depletion from the seminal receptacle occurs much more rapidly than from the spermathecae in these mutants (58). In other cases, only storage in the seminal receptacle is disrupted.…”

The Homeodomain Protein Defective Proventriculus Is Essential for Male Accessory Gland Development to Enhance Fecundity in Drosophila

“…Therefore, it is assumed that the low fecundity of dve-A mutant males reflects the defects of seminal fluid proteins that are secreted from accessory gland cells. We examined two potential reasons for the low fecundity: (1) failure of egg-laying stimulation, and (2) reduced rate of fertilization as reported in wasted mutant sperm [28]. Females mated with dve-A mutant males laid substantially fewer eggs than those mated with control males, although the hatching rate was indistinguishable between females mated with dve-A mutant or control males (Figure 4B and data not shown).…”

Unlocking sperm chromatin at fertilization requires a dedicated egg thioredoxin in Drosophila

“…2a). Pronuclear migration also fails in eggs fertilized by sperm from paternal effect male sterile mutants affecting sperm plasma membrane (SPM) breakdown, such as sneaky ( snky ), misfire ( mfr ) and wasted ( wst )272829. SPM breakdown is indeed not only critical for sperm nuclear decondensation but is also required for the release of paternal centrioles in the egg cytoplasm and the formation of the sperm aster.…”