The research that I am conducting in the academic year of, 2016-2017 in the UGR research program is a continuation of the research I performed during the academic year of 2015-2016. That research involved looking into the potential function of the M05D6.2 gene and its connection to the TCP11 gene in humans. To perform this research, we used the model organism of C. elegans. We compared the M05D6.2 gene to the TCP11 gene, which is the human ortholog of M05D6.2, to see its impact on fertility. At the end of the year, the preliminary data that we collected allowed us to conclude that we believe the M05D6.2 gene plays a role in male infertility. The approach we used in making this conclusion was by using RNAi, more commonly known and RNA interference. What we were looking for was a decrease in progeny count in the C. elegans that were exposed to the M05D6.2 treatment.
Currently, we have commenced our research by first looking at the effect of RNAi on N2 hermaphrodites. The N2 strain, of C. elegans, is considered to be the wild-type of this organism. We have previously used RNAi on other C. elegans hermaphrodites, from different strains, but we have not yet seen that effect of RNAi on wild-type hermaphrodites. In the hermaphrodites, from the different strains, we saw no decrease in the amount of progeny that was produced. This means that in these hermaphrodites the RNAi had no effect on fertility. Another thing that we are interested in is looking at how the internal structure of the organism, more primarily the sperm, is being effected by the RNAi. To see this change we want to image the worms. We can do this because C. elegans are transparent and their transparency makes it easy to see their internal structure. In humans, it has been found that the TCP11 gene impacts the way in which a sperms tail coils, thus if this gene is mutated it makes the sperm infertile, because it can no longer function properly. The two ideas of interest, I have talked about here, are only two of many that my team wants to investigate.