Poster
Yi-Feng Chen
Academia Sinica
Taipei, Nankang, TAIWAN
Kuan-Yu Lin
Institute of Plant and Microbial Biology, Academia Sinica
Taipei, Taipei, Taiwan (Republic of China)
Ching-Yi Huang
Max Plank Institute for Biology Tübingen
Tübingen, Baden-Wurttemberg, Germany
Liang-Yu Hou, PhD (he/him/his)
Postdoctoral researcher
Academia Sinica
Taipei, Taipei, Taiwan (Republic of China)
Chin-Wen Chang
Academia Sinica
Taipei, Taipei, Taiwan (Republic of China)
Hung-Yu Wang
Academia Sinica
Taipei, Taipei, Taiwan (Republic of China)
Tolga Bozkurt, PhD (he/him/his)
Reader
Imperial College London
London, England, United Kingdom
Chih-Hang Wu
Associate Research Fellow
Institute of Plant and Microbial Biology, Academia Sinica
Taipei City, Taipei, Taiwan (Republic of China)
Plant nucleotide-binding domain leucine-rich repeat (NLR) proteins function as immune receptors that recognize pathogens and confer resistance. Upon activation, many NLRs assemble into membrane-associated resistosomes that trigger immune signaling and lead to hypersensitive cell death. However, the sequential subcellular events that connect resistosome activation to cell death remain unclear. In this study, we explored the spatiotemporal dynamics of organelles upon activation of NLR required for cell death 4 (NRC4) resistosome. Using a copper-inducible system, we performed time-lapse imaging after triggering NRC4-mediated hypersensitive cell death. By employing various subcellular markers, we observed that cytoplasmic streaming and organelle movement were disrupted before visible resistosome puncta appeared. Coinciding with the emergence of resistosome puncta, both actin and microtubules were depolymerized. This was followed by a loss of plasma membrane (PM) integrity, fragmentation of the endoplasmic reticulum into vesicle-like structures, and nuclear envelope breakdown. Eventually, the cells collapsed, with the PM and tonoplast shrinking toward the cell center. This study provides a precise temporal sequence of subcellular dynamics during plant hypersensitive cell death and lays the foundation for future research on the molecular mechanisms underlying subcellular processes following immune activation.