Characterization of spe-43 homologs: K05F1.1 and F57A8.6
Date
2025-12
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University of Delaware
Abstract
Sexual reproduction relies on the presence of a viable sperm cell, which fuses with an egg cell in the process of fertilization. To increase understanding of the molecular processes involved in sexual reproduction, a reverse genetics method can be utilized to learn the role of specific proteins in fertility. C. elegans are an excellent organism to model these processes with, as they reproduce through sexual reproduction. C. elegans exhibits two sexes: hermaphrodites, which can self-fertilize, as well as males, which produce sperm to fertilize eggs from the hermaphrodites. Sperm activation is the process through which post-meiotic spermatids are altered to become sperm suitable for fertilization. In C. elegans, the process is triggered through two different pathways: TRY-5 and SPE-8. The TRY-5 pathway and the SPE-8 pathway are active in the male reproductive tract, while only the SPE-8 pathway is active in hermaphrodites. Hermaphrodites with mutations in genes required for the SPE-8 pathway experience self-sterility. In contrast, males with non-functional TRY-5 pathway components show no fertility defect unless the SPE-8 pathway is also disabled. spe-43 is a protein-encoding gene required for sperm activation through the SPE-8 pathway. spe-43 has three different paralogs: K05F1.1, F57A8.6, and T10E9.4. All three paralogs are protein-encoding genes hypothesized to be involved in sperm activation. To study the role of K05F1.1 and F57A8.6 in C. elegans fertility, deletion mutants were made to knock out the genes’ function. Quantitative experiments, including hermaphrodite self-fertility assays and male fertility assays, display no significant difference in progeny produced by K05F1.1(syb4161) deletion mutants compared to wild type organisms. Similarly, imaging such as DAPI staining and sperm dissections have shown that loss of K05F1.1 has no visible impact on sperm production, localization, and sperm morphology. When knocking out K05F1.1 and spe-8 together, males were able to produce viable progeny. The result implies that the K05F1.1 protein is neither part of the TRY-5 pathway, nor the SPE-8 pathway. In contrast, F57A8.6(syb4189) deletion mutants had significantly fewer progeny produced compared to wild type organisms in quantitative experiments.