Mechanisms for the epigenetic inheritance of stress response in single cells

Abstract

Cells have evolved to dynamically respond to different types of environmental and physiological stress conditions. The information about a previous stress stimulus experience by a mother cell can be passed to its descendants, allowing them to better adapt to and survive in new environments. In recent years, live-cell imaging combined with cell-lineage tracking approaches has elucidated many important principles that guide stress inheritance at the single-cell and population level. In this review, we summarize different strategies cells can employ to pass the ‘memory’ of previous stress responses to their descendants. Among these strategies, we focus on a recent discovery of how specific features of Msn2 nucleo-cytoplasmic shuttling dynamics could be inherited across cell lineages. We also discuss how stress response can be transmitted to progenies through changes in chromatin and through partitioning of anti-stress factors and/or damaged macromolecules between mother and daughter cells during cell division. Finally, we highlight how emergent technologies will help address open questions in the field.

Stochastic modeling of aging cells reveals how damage accumulation, repair, and cell-division asymmetry affect clonal senescence and population fitness

“…For instance, carbonylated proteins can form aggregates that are resistant to proteasome digestion [33, 34], and ERCs are self-replicating, suggesting that their effective repair rate – accounting for such self-replication – is probably also low [15, 35]. Finally, for asymmetric partitioning of damage in particular, it has been reported that some organisms like S. pombe and E. coli only exhibit this behavior during high levels of external stress [14, 17, 32, 36], suggesting that they may actually have evolved mechanisms to activate or inactivate damage partitioning depending on the region of parameter space they are in, just like other stress response mechanisms that are only activated in the presence of stress and can be epigenetically inherited by daughter cells [37, 38].…”

Histone Methylation and Memory of Environmental Stress

“…In specific cases, survival is improved when yeast cells “remember” a previous stressful experience, and are capable not only of a more rapid reactivation of the appropriate transcriptional stress response, but also of transmitting this response to their descendants. Here, we focus on examples of epigenetic transcriptional memory implicating chromatin modifications, although alternative mechanisms have been reported [4].…”

Stochastic modeling of aging cells reveals how damage accumulation, repair, and cell-division asymmetry affect clonal senescence and population fitness

“…For instance, carbonylated proteins can form aggregates that are resistant to proteasome digestion [33,34], and ERCs are self-replicating, suggesting that their effective repair rate – accounting for such self-replication – is probably also low [15,35]. Finally, for asymmetric partitioning of damage in particular, it has been reported that some organisms like S. pombe and E. coli only exhibit this behavior during high levels of external stress [14,18,32,36], suggesting that they may actually have evolved mechanisms to activate or inactivate damage partitioning depending on the region of parameter space they are in, just like other stress response mechanisms that are only activated in the presence of stress and can be epigenetically inherited by daughter cells [37,38].…”