The new findings have the potential to improve our understanding of cancers and a multitude of other diseases. Researchers at La Jolla Institute for Immunology (LJI) have finally discovered the role of an enzyme named O-GlcNAc transferase (OGT) in maintaining cell health. The findings, which were p
Image of breast cancer cells. Credit: National Cancer Institute’s Cancer Close Up project
The new study, spearheaded by Li and co-led by LJI Professor Anjana Rao, Ph.D., and LJI Assistant Professor Samuel Myers, Ph.D., is the first to show that OGT controls cell survival by regulating a critical protein called mTOR. In fact, OGT’s job of glycosylation is so important that embryonic cells will die without it. But until now, scientists were in the dark as to why.
For the new study, Li was able to get around that problem by using an inducible system to delete the OGT gene. He worked with mouse embryonic stem cells and then used an inducible version of a protein known as Cre to delete the gene for OGT. This meant that the cells could grow normally until the scientists decided to activate the process, after which cells that had lost the OGT gene began to stop proliferating and die.
Fortunately, OGT safeguards mTOR activity and mitochondrial fitness by keeping protein synthesis running smoothly and regulating aminolevels within cells. Importantly, the researchers discovered the same protective role for OGT in CD8+ T cells, which suggests the enzyme works the same way across mammalian cell types, not just in mouse embryonic stem cells.Even the dysfunctional cells lacking OGT weren’t doomed forever.
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