HSF/HSP Networks and Environmental Memory: From Molecular Persistence to a Recovery-Associated State
- 1Department of Biological and Environmental Sciences and Technologies, University of Salento, Via Monteroni 165, 73100 Lecce, Italy
- 2NBFC National Biodiversity Future Center, 90133 Palermo, Italy
Abstract
Plants encounter environmental stresses in sequences of exposure, recovery, and subsequent challenge. Persistent molecular changes alone do not establish how previous exposure influences later responsiveness. Sustained protection may contribute to memory, whereas unresolved physiological disturbance can complicate its interpretation. The heat shock factor/heat shock protein (HSF/HSP) system links transcriptional regulation with protein folding, quality control, and recovery, providing a framework for examining these distinctions. We assess evidence for HSF/HSP-dependent environmental memory through its temporal organisation. Recurrent heat provides the strongest causal evidence, implicating HSF activity, transcriptional and chromatin regulation, chaperone persistence, and protein turnover in distinct aspects of thermomemory. Broader stress histories reveal altered subsequent responses, but causal HSF/HSP involvement remains less clearly resolved. We define experimental criteria for characterising recovery, demonstrating history-dependent functional responses, and identifying when candidate processes contribute causally. We then propose a recovery-associated state as a heuristic working model, rather than a demonstrated discrete cellular entity, to examine how previous exposure changes the configuration of regulatory and proteostatic processes during recovery. Persistent protective components, altered relationships among processes, or consequences outlasting the initiating molecular change may shape the later response. This framework guides experiments across stress sequences and species while distinguishing established thermomemory mechanisms from hypotheses about broader environmental memory.
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BibTeX
@article{caroli2026hsfhsp,
title = {{HSF/HSP Networks and Environmental Memory: From Molecular Persistence to a Recovery-Associated State}},
author = {Monica De Caroli and Carla Perrotta and Patrizia Rampino},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms27219890},
url = {https://www.mdpi.com/1422-0067/27/21/9890},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - HSF/HSP Networks and Environmental Memory: From Molecular Persistence to a Recovery-Associated State
AU - Monica De Caroli
AU - Carla Perrotta
AU - Patrizia Rampino
PY - 2026
DA - 2026/11/04
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219890
UR - https://www.mdpi.com/1422-0067/27/21/9890
AB - Plants encounter environmental stresses in sequences of exposure, recovery, and subsequent challenge. Persistent molecular changes alone do not establish how previous exposure influences later responsiveness. Sustained protection may contribute to memory, whereas unresolved physiological disturbance can complicate its interpretation. The heat shock factor/heat shock protein (HSF/HSP) system links transcriptional regulation with protein folding, quality control, and recovery, providing a framework for examining these distinctions. We assess evidence for HSF/HSP-dependent environmental memory through its temporal organisation. Recurrent heat provides the strongest causal evidence, implicating HSF activity, transcriptional and chromatin regulation, chaperone persistence, and protein turnover in distinct aspects of thermomemory. Broader stress histories reveal altered subsequent responses, but causal HSF/HSP involvement remains less clearly resolved. We define experimental criteria for characterising recovery, demonstrating history-dependent functional responses, and identifying when candidate processes contribute causally. We then propose a recovery-associated state as a heuristic working model, rather than a demonstrated discrete cellular entity, to examine how previous exposure changes the configuration of regulatory and proteostatic processes during recovery. Persistent protective components, altered relationships among processes, or consequences outlasting the initiating molecular change may shape the later response. This framework guides experiments across stress sequences and species while distinguishing established thermomemory mechanisms from hypotheses about broader environmental memory.
SN - 1422-0067
ER -