After priming, naïve CD8 T lymphocytes establish specific heritable transcription programs that define progression to long-lasting memory cells or to short-lived effector cells. Although lineage specification is critical for protection, it remains unclear how chromatin dynamics contributes to the control of gene expression programs. In murine CD8 T cells activated after Listeria monocytogenes infection, Suv39h1-dependent trimethylation of histone H3 lysine 9 controls the expression of a set of stem cell–related memory genes. Single-cell RNA sequencing revealed a defect in silencing of stem/memory genes selectively in Suv39h1-defective T cell effectors. As a result, Suv39h1-defective CD8 T cells show sustained survival and increased long-term memory reprogramming capacity.

For people living with post-traumatic stress disorder (PTSD), erasing distressing memories is something that could only be dreamed of. But researchers believe they may have found a way of turning those dreams into reality. Scientists have pinpointed an enzyme in the brain that is critical in the storage of long-term memories. While the enzyme has only been studied in mice so far, the researchers are optimistic that it could be targeted to remove distressing memories in people with PTSD in the future. The enzyme, called acetyl-CoA synthetase 2, or ACSS2 'fuels' gene expression in the nucleus of nerve cells to turn on key memory genes after learning.