Events and seminars

The aim of meiosis is to generate gametes, this involves introducing numerous DNA double-strand breaks facilitated by the formation of a multi-protein synaptonemal complex to recombine the chromosomes and reduce the genome from diploid to haploid. However, the occurrence of chromosomal recombination during mitosis causes oncogenic genetic instability, a hallmark of cancer. Consequently, for somatic cell division it is critical that meiotic synaptonemal complex genes are accurately and specifically silenced following the transition of cells to mitosis. Remarkably, the mechanisms of meiotic gene silencing are poorly understood even though the failure of this silencing process is common in cancer. I will discuss what implications re-expression of synaptonemal complex genes has for mitotic cells and how we think this is regulated. I will also focus on ways in which we can utilise cancer cell lines as models to learn more about certain aspects of meiotic features.

About the speaker: Ula graduated her PhD in gastric cancer cell biology from the University of Leeds, UK in 2013, she then moved to the British Northern Institute for Cancer Research for a Post-Doc to investigate how cell signalling regulates gene expression in prostate cancer. During that time Ula observed that it was common for cancers to express meiotic proteins. Consequently, this allowed her to form her groups’ research question and secure a junior Fellowship at Newcastle University mentored by Dr Owen Davies followed by a Tenure Track Position at the University of Liverpool. Ula’s group focuses on understanding how expression of meiotic homologous recombination machinery proteins is regulated during development and the effect this can have on mitotic cells in disease.

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