Copper Stress Trigger Organelles Communication and Chromatin Condensation Leading to Cell Death in Solanum lycopersicum

Copper (Cu) is a vital micronutrient for plants but becomes highly toxic when present in excess, disrupting redox balance and damaging cellular structures. While the physiological and mitochondrial responses to Cu toxicity are well-documented, the nuclear-level consequences, particularly chromatin remodeling and gene regulatory changes, remain poorly understood. In this study, we used the root apex of Solanum lycopersicum as a model system to explore how increasing copper concentrations affect organelle integrity, stress signaling, and nuclear architecture. Using confocal and super-resolution imaging with organelle-specific markers and immunostaining, we observed that mitochondria was the earliest affected to Cu stress, exhibiting fragmentation, membrane depolarization, and cytochrome c release led to reactive oxygen species (ROS) accumulation, activation of AMPK, suppression of mTOR signaling, and nuclear translocation of NRF2. Critically, we found that copper exposure induced profound nuclear alterations, including shrinkage, lobulation, peripheral chromatin tethering, and global condensation events tightly correlated with stress signaling. H3K4me3 immunostaining revealed a shift from active euchromatin to condensed, transcriptionally silent states, leading to membrane rupture and cell death in root tip cells. Our findings show that the nucleus actively integrates organelle-derived stress signals, with chromatin remodeling as a key marker of copper toxicity. This highlights potential for chromatin-based diagnostics and stress-resilient crop breeding.