2025/07/01 by Yi‐Feng Chen, Kuan‐Yu Lin, Ching‐Yi Huang +8 · 1 voice · 2 citations
Biochemistry, Genetics and Molecular Biology · Chemistry · #Apoptosis #Biochemistry #Biology #Biophysics #CRISPR and Genetic Engineering #Calcium #Calcium signaling and nucleotide metabolism #Cell #Cell biology #Chemistry #Dynamics (music) #Organelle #Photosynthetic Processes and Mechanisms #Physics #Programmed cell death
paper · pdf · doi:10.1101/2025.06.27.662017
published in bioRxiv (Cold Spring Harbor Laboratory) (Cold Spring Harbor Laboratory)
openalex publication_date 2025/07/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/14
Abstract Plant nucleotide-binding domain leucine-rich repeat-containing (NLR) proteins act as intracellular immune receptors that assemble into resistosomes to execute immune responses. However, the subcellular processes during cell death following resistosome activation remain unclear. Here, we visualized the changes in calcium signaling and organelle behavior after activation of the NRC4 (NLR-required for cell death 4) resistosome. We found that NRC4 membrane enrichment coincided with calcium influx. This is followed by sequential mitochondria and plastid disruption, endoplasmic reticulum fragmentation and cytoskeleton depolymerization. Subsequent loss of plasma membrane integrity, nuclear shrinkage, and vacuolar collapse mark the terminal stage of cell death. Our findings reveal a spatiotemporally-resolved cascade of subcellular events downstream of resistosome activation, providing new mechanistic insight into the execution phase of plant immune cell death.