Abstract
Environmental and genetic stress have well-known detrimental effects on ejaculate quality, but their concomitant effect on male fitness remains poorly understood. We used competitive fertilization assays to expose the effects of stress on offensive sperm competitive ability in the beetle Callosobruchus maculatus, a species where ejaculates make up more than 5% of male body mass. To examine the effects of environmental and genetic stress, males derived from outcrosses or sib matings were heat shocked at 50°C for 50 min during the pupal stage, while their siblings were maintained at a standard rearing temperature of 28°C. Heat-shocked males achieved only half the offensive paternity success of their siblings. While this population exhibited inbreeding depression in body size, sperm competitiveness was unaffected by inbreeding, nor did the effect of heat shock stress on sperm competitiveness depend on inbreeding status. In contrast, pupal emergence success was increased by 34% among heat-stressed individuals, regardless of their inbreeding status. Heat-shocked males' ejaculate size was 19% reduced, but they exhibited 25% increased mating duration in single mating trials. Our results highlight both the importance of stress in postcopulatory sexual selection, and the variability among stressors in affecting male fitness.
Highlights
As the vehicle for male gametes, the ejaculate plays a central role in determining male reproductive fitness
Stress induces the expression of heat shock proteins (Hsp), molecular chaperones that repair cellular damage associated with stress
Our results indicate that the observed decline in offensive sperm competitiveness in stressed males was associated with reduced ejaculate size
Summary
As the vehicle for male gametes, the ejaculate plays a central role in determining male reproductive fitness The importance of both the sperm and nonsperm components (seminal fluid proteins) of the ejaculate in postcopulatory natural and sexual selection are well recognized (Simmons and Fitzpatrick 2012). Stress induces the expression of heat shock proteins (Hsp), molecular chaperones that repair cellular damage associated with stress (reviewed in Sørensen et al 2003). Due to their resource requirements and demands on the transcriptional machinery, the expression of these gene products imposes its own costs (Feder et al 1992; Krebs and Feder 1998), and the survival benefits of expression typically trade-off against other fitness components (Hoffmann 1995). We examined whether any reductions in sperm competitive ability result from changes in ejaculate size
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