Loss of ELM1B impairs mitochondrial fission, matrix redox state and stress tolerance in Physcomitrium patens

ELM1B loss diminishes mitochondrial fission, redox state, and stress resilience in Physcomitrium patens

Mitochondria orchestrate cellular metabolism, energy generation, and stress responses. As dynamic entities, they undergo fusion and fission, adjusting to stress conditions. The impact of stress on mitochondrial dynamics within plants and the subsequent effects on mitochondrial properties and plant resilience remains largely unexplored.

This study examines mitochondrial dynamics in response to oxidative stress in the non-vascular model plant Physcomitrium patens by creating mutants with impaired mitochondrial fission in various mitochondrial reporter lines.

PpMtPQ treatment augmented glutathione redox potential EGSH in mitochondria, cytosol, and chloroplasts, as detected by roGFP2-based genetically encoded biosensors. Mitochondria elongated within hours and exhibited a concurrent, heterogeneous elevation in matrix EOSred, which we propose as a marker for matrix protein damage. PpELM1B (elongated mitochondria) mutants displayed distinct alterations in mitochondrial morphology parameters, determined by automated 3D-segmentation and feature mapping of confocal z-stacks.

Ppelm1bge lines exhibited oxidative matrix EGSH shift and increased matrix EOSred, while matrix mixing persisted, albeit at the same slow rate as in wildtype, within days.

Ppelm1bge lines exhibited reduced growth, decreased respiration, and heightened sensitivity to oxidative stress. The findings demonstrate that plant mitochondrial morphology and physiological parameters specifically adapt to stress and impaired fission. Mitochondrial fission is crucial for preserving a healthy mitochondrial population that sustains plant oxidative stress tolerance.