Researchers in the Faculty of Science have discovered that the gene BRAP-2 plays a key role in programmed cell death, also known as apoptosis, when there is DNA damage.
Apoptosis is an essential process that eliminates abnormal or unnecessary cells from an organism. For instance, it purges cells with irreparable DNA damage that can lead to tumour formation and cancer. Apoptosis is controlled by intricate cell signalling pathways that scientists are still trying to understand.
Using the nematode C. elegans and radiation to induce DNA damage, recent PhD graduate Dayana D’Amora, who worked under the supervision of Faculty of Science Professor Terry Kubiseski, has now discovered that the gene BRAP-2 is required for apoptosis in cells with DNA damage. Her experiments also show that when the BRAP-2 gene is mutated and nonfunctional, the worms not only evade apoptosis, but also display higher levels of cell survival gene expression.
C. elegans is very useful for developmental and genetic studies because it is easy to grow and modify genetically. In addition, the worm has many genes that are similar to humans’, making it a useful tool to study fundamental biological processes and diseases.
“The evasion of apoptosis is a hallmark of cancer, and this study has provided us with a genetic tool to better understand the signalling pathways that govern the balance between pro-death and pro-cell survival factors that lead to apoptosis activation,” said Kubiseski.
There are many questions to pursue following these research findings, adds Kubiseski, but one of them will be focused on understanding how pro-survival proteins are being activated when BRAP-2 is mutated.
The research findings were published in the journal Cell Death and Differentiation.