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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 transgenes rescue the male precedence defects of comp-1 mutants.(A, B) The jnSi109[Pcomp-1::COMP-1] transgene, which contains a 3.9 kb region surrounding F37E3.3, rescues the precedence defect of (A) comp-1(me69) and (B) comp-1(gk1149) males in crosses to dpy-4 hermaphrodites. (C) Expression of COMP-1::GFP rescues the precedence defect. comp-1(gk1149); jnSi171[Pcomp-1::COMP-1::GFP] males have a wild-type precedence pattern in crosses to dpy-4 hermaphrodites. Precedence assays were performed as in Figure 1D. ***, p < 0.001; **, p < 0.01; ns, not significant (Kolmogorov–Smirnov test). Lines indicate medians. In addition to the indicated genotypes, control strains contained the transgene oxSi221[Peft-3 ::GFP].DOI:http://dx.doi.org/10.7554/eLife.05423.005
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fig1s2: COMP-1 transgenes rescue the male precedence defects of comp-1 mutants.(A, B) The jnSi109[Pcomp-1::COMP-1] transgene, which contains a 3.9 kb region surrounding F37E3.3, rescues the precedence defect of (A) comp-1(me69) and (B) comp-1(gk1149) males in crosses to dpy-4 hermaphrodites. (C) Expression of COMP-1::GFP rescues the precedence defect. comp-1(gk1149); jnSi171[Pcomp-1::COMP-1::GFP] males have a wild-type precedence pattern in crosses to dpy-4 hermaphrodites. Precedence assays were performed as in Figure 1D. ***, p < 0.001; **, p < 0.01; ns, not significant (Kolmogorov–Smirnov test). Lines indicate medians. In addition to the indicated genotypes, control strains contained the transgene oxSi221[Peft-3 ::GFP].DOI:http://dx.doi.org/10.7554/eLife.05423.005

Mentions: We obtained a comp-1 deletion allele, gk1149, from the C. elegans Deletion Mutant Consortium (C. elegans Deletion Mutant Consortium, 2012). gk1149 eliminates a large region of the coding sequence and is likely a allele. To test if the me69 and gk1149 alleles result in a similar male precedence defect, we crossed gk1149 males to dpy-4 hermaphrodites and found that gk1149 mutant males indeed showed a reduction in male precedence as compared to the wild type (Figure 1D). Like me69, gk1149 is recessive; crosses with heterozygous gk1149/+ males showed a wild-type precedence pattern. However, me69/gk1149 heterozygotes had male precedence defects, indicating the two mutations failed to complement one another. To confirm that loss of comp-1 function is responsible for the male precedence defect, we performed rescue experiments. We generated animals harboring a Mos-mediated single copy insertion (MosSCI) transgene (Frøkjær-Jensen et al., 2008, 2012) encompassing a 3.9-kb genomic fragment surrounding F37E3.3 (Tables 3 and 4). This transgene rescued the male precedence defect of both me69 and gk1149 males (Figure 1—figure supplement 2), confirming that comp-1 is the gene affected in these mutants.10.7554/eLife.05423.008Table 3.


COMP-1 promotes competitive advantage of nematode sperm.

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

COMP-1 transgenes rescue the male precedence defects of comp-1 mutants.(A, B) The jnSi109[Pcomp-1::COMP-1] transgene, which contains a 3.9 kb region surrounding F37E3.3, rescues the precedence defect of (A) comp-1(me69) and (B) comp-1(gk1149) males in crosses to dpy-4 hermaphrodites. (C) Expression of COMP-1::GFP rescues the precedence defect. comp-1(gk1149); jnSi171[Pcomp-1::COMP-1::GFP] males have a wild-type precedence pattern in crosses to dpy-4 hermaphrodites. Precedence assays were performed as in Figure 1D. ***, p < 0.001; **, p < 0.01; ns, not significant (Kolmogorov–Smirnov test). Lines indicate medians. In addition to the indicated genotypes, control strains contained the transgene oxSi221[Peft-3 ::GFP].DOI:http://dx.doi.org/10.7554/eLife.05423.005
© Copyright Policy
Related In: Results  -  Collection

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

fig1s2: COMP-1 transgenes rescue the male precedence defects of comp-1 mutants.(A, B) The jnSi109[Pcomp-1::COMP-1] transgene, which contains a 3.9 kb region surrounding F37E3.3, rescues the precedence defect of (A) comp-1(me69) and (B) comp-1(gk1149) males in crosses to dpy-4 hermaphrodites. (C) Expression of COMP-1::GFP rescues the precedence defect. comp-1(gk1149); jnSi171[Pcomp-1::COMP-1::GFP] males have a wild-type precedence pattern in crosses to dpy-4 hermaphrodites. Precedence assays were performed as in Figure 1D. ***, p < 0.001; **, p < 0.01; ns, not significant (Kolmogorov–Smirnov test). Lines indicate medians. In addition to the indicated genotypes, control strains contained the transgene oxSi221[Peft-3 ::GFP].DOI:http://dx.doi.org/10.7554/eLife.05423.005
Mentions: We obtained a comp-1 deletion allele, gk1149, from the C. elegans Deletion Mutant Consortium (C. elegans Deletion Mutant Consortium, 2012). gk1149 eliminates a large region of the coding sequence and is likely a allele. To test if the me69 and gk1149 alleles result in a similar male precedence defect, we crossed gk1149 males to dpy-4 hermaphrodites and found that gk1149 mutant males indeed showed a reduction in male precedence as compared to the wild type (Figure 1D). Like me69, gk1149 is recessive; crosses with heterozygous gk1149/+ males showed a wild-type precedence pattern. However, me69/gk1149 heterozygotes had male precedence defects, indicating the two mutations failed to complement one another. To confirm that loss of comp-1 function is responsible for the male precedence defect, we performed rescue experiments. We generated animals harboring a Mos-mediated single copy insertion (MosSCI) transgene (Frøkjær-Jensen et al., 2008, 2012) encompassing a 3.9-kb genomic fragment surrounding F37E3.3 (Tables 3 and 4). This transgene rescued the male precedence defect of both me69 and gk1149 males (Figure 1—figure supplement 2), confirming that comp-1 is the gene affected in these mutants.10.7554/eLife.05423.008Table 3.

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