Blog Post 3: Wrapping Up

This post is coming to you a little later than expected, but hopefully I can get you caught up on my last days in lab this summer. I spent a lot of time on excel, analyzing the data collected from the video analysis. If you remember from my last post, I took lots of videos of moving sperm from swm-1 and spe-6(hc187) mutants in order to compare how SPE-6 affected the motility of sperm that had activated precociously. While it meant a lot of time on the computer, I still really enjoyed it because it meant that I got to see an experiment through from beginning to end (with help from several lab members). I spent most of my spring semester and portions of my time this summer getting trained, so it was exciting to finally feel like I had completed an experiment fully.

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Blog Post 2: Motility Experiments and Results

In my last post, I mentioned the process by which nematode spermatids activate to form spermatozoa. Sperm activation in nematodes is characterized, among other changes, by the formation of a pseudopod. Whereas vertebrate sperm “swim” using a flagellum, C. elegans sperm “crawl” using a pseudopod. The goal of both is to locomote towards and ultimately fertilize an oocyte.  In C. elegans, the process by which male sperm activate is tightly regulated because successful fertilization requires sperm to activate at precisely the right moment – when the male sperm are transferred to the reproductive tract of the hermaphrodite (Stanfield and Villenueve, 2006). If sperm activate precociously (within the male), then they are often unable to be transferred to a hermaphrodite.  Many proteins control this process of sperm activation to ensure that spermatids activate properly. One such protein is SWM-1, a protein that functions outside of sperm to inhibit sperm activation in males prior to insemination of the hermaphrodites. In swm-1 mutants, however, sperm activate precociously and often fail to be transferred to a hermaphrodite. This precocious activation phenotype extends to other mutants as well, including spe-6 mutants. In spe-6(hc187), the sperm of males raised at 25°C lack SPE-6 protein and activate precociously within the seminal vesicle.

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Blog Post 1: Getting Started in Lab

I have been back in lab for a few days now, equipped with a list of goals for the week. Many of them revolve around working with other students in lab so that I can get up to speed on various projects. C. elegans provide a model through which genetic mutations can be connected to abnormalities in phenotype, which can elucidate how cellular processes occur and the components involved. Mutants can be used to understand the function of a gene. My main focus so far has been on mutations in spe-6, which is a gene that controls aspects of sperm production and fertility (WormBase). The prefix spe is used to indicate a mutation in any gene that can result in defective spermatogenesis. spe-6 mutations are loss of function mutations that prevent Major Sperm Protein (MSP) from localizing correctly (Muhlrad and Ward 2002). During normal C. elegans spermatogenesis, MSP is localized to fibrous bodies, which form complexes with membranous organelles. Young spermatids possess fibrous bodies containing MSP, but more mature spermatids have MSP throughout their cytoplasm. Mature spermatids undergo sperm activation to form spermatozoa, which have pseudopods, consisting of a cytoskeleton made of MSP, that allow them to crawl and fertilize oocytes. Sperm activation is controlled by a signaling pathway that is not completely understood, but somehow SPE-6, a casein kinase produced by the spe-6 gene, allows for proper movement of MSP throughout the development of spermatozoa.

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Defects in spermatogenesis and spermiogenesis in fer-6 mutants of Caenorhabditis elegans Abstract

The project, “Defects in Spermatogenesis and Spermiogenesis in fer-6 Mutants of Caenorhabditis elegans”, will attempt to identify where the earliest abnormalities occur in spermatogenesis and spermiogenesis of fer-6 mutants of C. elegans, a species of nematode commonly studied in molecular biology. In past research, fer-6 mutants have been shown to form abnormal sperm that often struggle to become fully motile due to improperly formed spermatozoa (1).

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