Opportunities for new researchers

Positions are available within each research program for undergraduates, honours students, PhD students, and postdoctoral scientists, and we are happy to entertain new ideas. If you are interested in joining the lab, please contact Jo Bowles.

Current projects

Sex specific development of fetal germ cells

During fetal development, germ cell fate and behaviour is not intrinsically programmed, but instead depends on molecular cues from gonadal somatic cells. In a fetal ovary, germ cells enter meiosis and commit to oogenesis, whereas in a fetal testis, they avoid entry into meiosis and instead undergo mitotic arrest and begin to mature towards spermatogenesis. In mice, these fate decisions occur in the critical window 11.5-13.5 days post coitum (dpc), soon after the germ cells arrive in the nascent gonads.

1.Sex specific development of fetal germ cellsDuring this critical period of germ cell development, we aim to understand:

  • How meiosis is triggered in female germ cells
  • What makes female germ cells capable of responding to Retionic acid
  • How do male germ cells control pluripotency versus differentiation decisions

Germline stem cells

Spermatogonial stem cells (SSCs) generate millions of sperm each day throughout adult life and, therefore, underpin male fertility. Despite their obvious importance, little is known regarding how the SSC population is set aside and regulated. Germ cells are specified during early embryonic development and migrate to and colonise the nascent fetal testis. Although many thousand germ cells take up residence in the testis, only a small number of these will be earmarked as enduring SSCs; the surplus germ cells differentiate during the first wave of spermatogenesis at puberty (~6 days post partum in mice). Both the exact timing and molecular regulation of SSC allocation however, remains unknown.

During late embryonic and early postnatal male germ cell development, we aim to understand:

  • The exact timing of spermatogonial stem cell allocation
  • Molecularly, how are spermatogonial stem cells different from the greater germ cell population  
  • What signalling pathways are involved in spermatogoinal stem cell allocation and maintenance

Germline stem cells


The genesis of germline tumorigenes

The most common and deadly form of testis cancer is Type II germ cell cancer, which accounts for ~60% of all malignancies in men aged 20-40, and is rapidly on the increase in industrialised countries. The cell of origin or ‘cancer stem cell’, germ cell neoplasia in situ (GCNIS), is considered to be a germ cell that has failed to differentiate appropriately during embryonic development. After puberty, GCNIS cells that have remained dormant up until that point, invariably transform into either seminoma (SEM) or non-seminoma (N-SEM) germ cell cancer. Seminoma retains a fetal germ cell-like expression profile, while non-seminoma is the more deadly and invasive pluripotent tumour subtype. Understanding the origins of Type II GCC therefore rests on uncovering the mechanisms regulating male germ cell development during fetal life.

In fetal germ cell development, and in human germ cell tumours we aim to:

  • Identify factors that are responsible for restraining germ cell pluripotency
  • Identify developmental signalling pathways that become co-opted in cases of germ cell cancer
  • Develop novel diagnostics/therapeutics for GCNIS and germ cell cancer

The genesis of germline tumorigenes