Heat Shock (HS) signaling is activated in response to various types of cellular stress. This activation serves to protect cells from immediate threats in the surrounding environment. However, activation of HS signaling occurs in a heterogeneous manner within each cell population and can alter the epigenetic state of the cell, ultimately leading to long-term abnormalities in body function. Here, we summarize recent research findings obtained using molecular and genetic tools to track cells where HS signaling is activated. We then discuss the potential further applications of these tools, their limitations, and the necessary caveats in interpreting data obtained with these tools.
Keywords: Heat Shock Factor 1; Heat Shock Protein 70; Heat Shock signaling; detection of injury; epigenetics; genetic recombination; heterogeneity; reporter mice; transcriptional amplification; transcriptional bursting.