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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.

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comp-1 sperm have normal organization and size.(A–D) Wild-type (A, B) and comp-1(gk1149) (C, D) spermatozoa stained for mitochondria using Mitotracker. (E–H) Wild-type (E, F) and comp-1 (G, H) spermatozoa expressing PEEL-1::GFP (membranous organelles). (I–L) Wild-type (I, J) and comp-1(gk1149) (K, L) spermatozoa fixed and stained with α-GSP-3/4 antibody (green). (A–L) Scale bar, 5 μm. (M) comp-1 male spermatid size is not significantly different from wild-type. Cross sectional areas through the center of spermatids were measured. Error bars, 95% confidence interval; p = 0.41, Student's t test.DOI:http://dx.doi.org/10.7554/eLife.05423.015
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fig5: comp-1 sperm have normal organization and size.(A–D) Wild-type (A, B) and comp-1(gk1149) (C, D) spermatozoa stained for mitochondria using Mitotracker. (E–H) Wild-type (E, F) and comp-1 (G, H) spermatozoa expressing PEEL-1::GFP (membranous organelles). (I–L) Wild-type (I, J) and comp-1(gk1149) (K, L) spermatozoa fixed and stained with α-GSP-3/4 antibody (green). (A–L) Scale bar, 5 μm. (M) comp-1 male spermatid size is not significantly different from wild-type. Cross sectional areas through the center of spermatids were measured. Error bars, 95% confidence interval; p = 0.41, Student's t test.DOI:http://dx.doi.org/10.7554/eLife.05423.015

Mentions: One potential explanation for the male precedence defect in comp-1 mutants was that sperm do not undergo proper spermatogenesis or spermiogenesis necessary to mature into functional sperm. Loss of function of spe or fer genes required for spermatogenesis generally leads to hermaphrodite self sterility and male infertility, and reduction of gene function can result in partial fertility (Kadandale and Singson, 2004; Nishimura and L'Hernault, 2010). We thus examined available markers of sperm morphology to determine if comp-1 sperm harbor any general defects. Males and hermaphrodites both produce immotile, spherical spermatids that must be activated to become mature, pseudopod-bearing sperm competent for motility and fertility (Wolf et al., 1978). comp-1 mutant spermatids and sperm appear grossly normal by light microscopy (Figure 5A,C; Figure 5E,G and data not shown). In addition, several markers of sperm structures localized appropriately in the comp-1 mutant. As in wild-type sperm, mitochondria and membranous organelles were restricted to cell bodies (Figure 5A–H), and the GSP-3/4 phosphatase was polarized within pseudopodia (Figure 5I–L). The presence of properly polarized sperm structures in mutant sperm indicates that comp-1 is not required to complete spermatogenesis, nor is it necessary for proper localization of sperm structures in mature sperm cells. These findings are consistent with the absence of fertility or sperm usage defects in comp-1 animals in the absence of competition.10.7554/eLife.05423.015Figure 5.comp-1 sperm have normal organization and size.


COMP-1 promotes competitive advantage of nematode sperm.

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

comp-1 sperm have normal organization and size.(A–D) Wild-type (A, B) and comp-1(gk1149) (C, D) spermatozoa stained for mitochondria using Mitotracker. (E–H) Wild-type (E, F) and comp-1 (G, H) spermatozoa expressing PEEL-1::GFP (membranous organelles). (I–L) Wild-type (I, J) and comp-1(gk1149) (K, L) spermatozoa fixed and stained with α-GSP-3/4 antibody (green). (A–L) Scale bar, 5 μm. (M) comp-1 male spermatid size is not significantly different from wild-type. Cross sectional areas through the center of spermatids were measured. Error bars, 95% confidence interval; p = 0.41, Student's t test.DOI:http://dx.doi.org/10.7554/eLife.05423.015
© Copyright Policy
Related In: Results  -  Collection

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

fig5: comp-1 sperm have normal organization and size.(A–D) Wild-type (A, B) and comp-1(gk1149) (C, D) spermatozoa stained for mitochondria using Mitotracker. (E–H) Wild-type (E, F) and comp-1 (G, H) spermatozoa expressing PEEL-1::GFP (membranous organelles). (I–L) Wild-type (I, J) and comp-1(gk1149) (K, L) spermatozoa fixed and stained with α-GSP-3/4 antibody (green). (A–L) Scale bar, 5 μm. (M) comp-1 male spermatid size is not significantly different from wild-type. Cross sectional areas through the center of spermatids were measured. Error bars, 95% confidence interval; p = 0.41, Student's t test.DOI:http://dx.doi.org/10.7554/eLife.05423.015
Mentions: One potential explanation for the male precedence defect in comp-1 mutants was that sperm do not undergo proper spermatogenesis or spermiogenesis necessary to mature into functional sperm. Loss of function of spe or fer genes required for spermatogenesis generally leads to hermaphrodite self sterility and male infertility, and reduction of gene function can result in partial fertility (Kadandale and Singson, 2004; Nishimura and L'Hernault, 2010). We thus examined available markers of sperm morphology to determine if comp-1 sperm harbor any general defects. Males and hermaphrodites both produce immotile, spherical spermatids that must be activated to become mature, pseudopod-bearing sperm competent for motility and fertility (Wolf et al., 1978). comp-1 mutant spermatids and sperm appear grossly normal by light microscopy (Figure 5A,C; Figure 5E,G and data not shown). In addition, several markers of sperm structures localized appropriately in the comp-1 mutant. As in wild-type sperm, mitochondria and membranous organelles were restricted to cell bodies (Figure 5A–H), and the GSP-3/4 phosphatase was polarized within pseudopodia (Figure 5I–L). The presence of properly polarized sperm structures in mutant sperm indicates that comp-1 is not required to complete spermatogenesis, nor is it necessary for proper localization of sperm structures in mature sperm cells. These findings are consistent with the absence of fertility or sperm usage defects in comp-1 animals in the absence of competition.10.7554/eLife.05423.015Figure 5.comp-1 sperm have normal organization and size.

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