Limits...
COMP-1 promotes competitive advantage of nematode sperm.

Hansen JM, Chavez DR, Stanfield GM - Elife (2015)

Bottom Line: In this study, we utilize a forward genetic screen in Caenorhabditis elegans to identify a gene, comp-1, whose function is specifically required in competitive contexts.We show that comp-1 functions in sperm to modulate their migration through and localization within the reproductive tract, thereby promoting their access to oocytes.Contrary to previously described models, comp-1 mutant sperm show no defects in size or velocity, thereby defining a novel pathway for preferential usage.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Genetics, University of Utah, Salt Lake City, United States.

ABSTRACT
Competition among sperm to fertilize oocytes is a ubiquitous feature of sexual reproduction as well as a profoundly important aspect of sexual selection. However, little is known about the cellular mechanisms sperm use to gain competitive advantage or how these mechanisms are regulated genetically. In this study, we utilize a forward genetic screen in Caenorhabditis elegans to identify a gene, comp-1, whose function is specifically required in competitive contexts. We show that comp-1 functions in sperm to modulate their migration through and localization within the reproductive tract, thereby promoting their access to oocytes. Contrary to previously described models, comp-1 mutant sperm show no defects in size or velocity, thereby defining a novel pathway for preferential usage. Our results indicate not only that sperm functional traits can influence the outcome of sperm competition, but also that these traits can be modulated in a context-dependent manner depending on the presence of competing sperm.

Show MeSH

Related in: MedlinePlus

Model: comp-1 sperm have localization defects that result in failure to compete with wild-type sperm.(A) Wild-type male sperm (blue) migrate to the region of the spermathecae, where they displace hermaphrodite self sperm (pink) and preferentially fertilize oocytes. Oocytes fertilized by male sperm are shown in blue; oocytes fertilized by self sperm are shown in pink. (B) comp-1 mutant male sperm (light blue) migrate to the spermathecae, but remain outside while wild-type sperm (pink) are present, and are thus excluded from opportunities to fertilize oocytes. They also show delayed migration to the spermathecal region and increased localization in the periphery of the female reproductive tract.DOI:http://dx.doi.org/10.7554/eLife.05423.019
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4400581&req=5

fig8: Model: comp-1 sperm have localization defects that result in failure to compete with wild-type sperm.(A) Wild-type male sperm (blue) migrate to the region of the spermathecae, where they displace hermaphrodite self sperm (pink) and preferentially fertilize oocytes. Oocytes fertilized by male sperm are shown in blue; oocytes fertilized by self sperm are shown in pink. (B) comp-1 mutant male sperm (light blue) migrate to the spermathecae, but remain outside while wild-type sperm (pink) are present, and are thus excluded from opportunities to fertilize oocytes. They also show delayed migration to the spermathecal region and increased localization in the periphery of the female reproductive tract.DOI:http://dx.doi.org/10.7554/eLife.05423.019

Mentions: For males, reproductive success depends on several aspects of sperm function. To fertilize oocytes, sperm must be transferred, become motile, and migrate to the site of fertilization in response to guidance signals (Ward and Carrel, 1979; Kubagawa et al., 2006). Overall fecundity depends on the number of sperm that accomplish these behaviors as well as their ability to be stored so as to ensure long-term usage (Murray and Cutter, 2011). We have found that comp-1 sperm are transferred at rates comparable to the wild type, so they achieve initial entry into the reproductive tract, but they then show varying defects in the ensuing steps (Figure 8). Although comp-1 sperm show delays in migration toward the spermathecae, at least some sperm migrate rapidly and directionally, arguing against a defect in locomotion per se. Large numbers eventually accumulate in the spermathecal region, suggesting that they respond to directional cues, but they are generally found outside the spermathecal valve. Once self-sperm stores are depleted, comp-1 sperm concomitantly gain residency in the spermathecae and begin to fertilize oocytes. Since fertilization occurs only in these structures, it is likely that this localization defect underlies the reduced competitive ability and generally poor reproductive success of comp-1 males.10.7554/eLife.05423.019Figure 8.Model: comp-1 sperm have localization defects that result in failure to compete with wild-type sperm.


COMP-1 promotes competitive advantage of nematode sperm.

Hansen JM, Chavez DR, Stanfield GM - Elife (2015)

Model: comp-1 sperm have localization defects that result in failure to compete with wild-type sperm.(A) Wild-type male sperm (blue) migrate to the region of the spermathecae, where they displace hermaphrodite self sperm (pink) and preferentially fertilize oocytes. Oocytes fertilized by male sperm are shown in blue; oocytes fertilized by self sperm are shown in pink. (B) comp-1 mutant male sperm (light blue) migrate to the spermathecae, but remain outside while wild-type sperm (pink) are present, and are thus excluded from opportunities to fertilize oocytes. They also show delayed migration to the spermathecal region and increased localization in the periphery of the female reproductive tract.DOI:http://dx.doi.org/10.7554/eLife.05423.019
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4400581&req=5

fig8: Model: comp-1 sperm have localization defects that result in failure to compete with wild-type sperm.(A) Wild-type male sperm (blue) migrate to the region of the spermathecae, where they displace hermaphrodite self sperm (pink) and preferentially fertilize oocytes. Oocytes fertilized by male sperm are shown in blue; oocytes fertilized by self sperm are shown in pink. (B) comp-1 mutant male sperm (light blue) migrate to the spermathecae, but remain outside while wild-type sperm (pink) are present, and are thus excluded from opportunities to fertilize oocytes. They also show delayed migration to the spermathecal region and increased localization in the periphery of the female reproductive tract.DOI:http://dx.doi.org/10.7554/eLife.05423.019
Mentions: For males, reproductive success depends on several aspects of sperm function. To fertilize oocytes, sperm must be transferred, become motile, and migrate to the site of fertilization in response to guidance signals (Ward and Carrel, 1979; Kubagawa et al., 2006). Overall fecundity depends on the number of sperm that accomplish these behaviors as well as their ability to be stored so as to ensure long-term usage (Murray and Cutter, 2011). We have found that comp-1 sperm are transferred at rates comparable to the wild type, so they achieve initial entry into the reproductive tract, but they then show varying defects in the ensuing steps (Figure 8). Although comp-1 sperm show delays in migration toward the spermathecae, at least some sperm migrate rapidly and directionally, arguing against a defect in locomotion per se. Large numbers eventually accumulate in the spermathecal region, suggesting that they respond to directional cues, but they are generally found outside the spermathecal valve. Once self-sperm stores are depleted, comp-1 sperm concomitantly gain residency in the spermathecae and begin to fertilize oocytes. Since fertilization occurs only in these structures, it is likely that this localization defect underlies the reduced competitive ability and generally poor reproductive success of comp-1 males.10.7554/eLife.05423.019Figure 8.Model: comp-1 sperm have localization defects that result in failure to compete with wild-type sperm.

Bottom Line: In this study, we utilize a forward genetic screen in Caenorhabditis elegans to identify a gene, comp-1, whose function is specifically required in competitive contexts.We show that comp-1 functions in sperm to modulate their migration through and localization within the reproductive tract, thereby promoting their access to oocytes.Contrary to previously described models, comp-1 mutant sperm show no defects in size or velocity, thereby defining a novel pathway for preferential usage.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Genetics, University of Utah, Salt Lake City, United States.

ABSTRACT
Competition among sperm to fertilize oocytes is a ubiquitous feature of sexual reproduction as well as a profoundly important aspect of sexual selection. However, little is known about the cellular mechanisms sperm use to gain competitive advantage or how these mechanisms are regulated genetically. In this study, we utilize a forward genetic screen in Caenorhabditis elegans to identify a gene, comp-1, whose function is specifically required in competitive contexts. We show that comp-1 functions in sperm to modulate their migration through and localization within the reproductive tract, thereby promoting their access to oocytes. Contrary to previously described models, comp-1 mutant sperm show no defects in size or velocity, thereby defining a novel pathway for preferential usage. Our results indicate not only that sperm functional traits can influence the outcome of sperm competition, but also that these traits can be modulated in a context-dependent manner depending on the presence of competing sperm.

Show MeSH
Related in: MedlinePlus