This project aims to understand the role of the transcription factor A-myb and its targets in spermatogenesis. If the project is successful, we will know how a mutation in the MybL1 gene leads to male sterility in the mouse. This information will give us a more detailed picture of the processes of meiosis and spermatogenesis, not just in the mouse but in all organisms with homologous genes and mechanisms.

I used bioinformatics to pinpoint genes which were being directly affected by A-myb using microarray data from 14 and 17 day wild-type and mutant testes. In addition, antibody staining for A-MYB protein was much lower in mutant mice, suggesting protein destabilization in mutants. Several differences in histone composition were observed through antibody staining. Expression of genes that seemed to be affected in the microarray were studied using real-time PCR to determine if they have overlapping roles in spermatogenesis.

The mutation in A-Myb affected many genes, most of which became downregulated. These affected genes may be transcribed by A-Myb directly or may be affected indirectly through expression of mediating genes. As more data is collected, we will be able to construct a model of A-Myb?s function in spermatogenesis and understand which genes play key roles in meiosis and spermatogenesis.

Ultimately, knowledge of the inner workings of meiosis and spermatogenesis will allow for advances in human and veterinary medicine. This knowledge is especially applicable to males who are sterile.