The use of novel bioinformatic approaches to understand the sex-linked vs autosomal contributions to mouse sperm development.

Globally, populations are ageing, and birth rates are falling. This presents a variety of issues, including food shortages and a lack of working-age humans to sustain the older generations. This presents a global requirement for research into human and animal fertility: animal research to help with global food security allowing a larger population to be fed more effectively, and human research to help tackle the declining fertility rates to ensure that the population continues to grow at a level that can support the larger number of elderly people. The area of fertility research that needs to be investigated most is that of sperm development. There is traditionally a lot more female-factor research, leaving a knowledge gap for male-factor research. Sperm development in mice has been shown to be directly linked to successful fertilisation outcomes: mouse sperm with perturbed development do not produce viable embryos. In some cases, this has been shown to be a sex-I inked effect, whereby female mouse embryos are produced, but male mouse embryos are not. This study also shows that autosomal genes are critical for proper mouse sperm development, and so differential gene expression analysis methods are used to determine which genes have a greater impact: autosomal, or sex-linked, and to determine which specific genes may be the most implicated in poor mouse sperm development. The list of candidate genes found in this study to potentially be involved in poor mouse sperm development provides possible targets for gene therapy to improve fertilisation outcomes, and orthologues of these genes can be investigated in agricultural species such as pigs and cows, as well as humans.