Cell cycle reprogramming in plant symbiotic and pathogenic interactions.

Abstract

Intracellular plant-microbe interactions rely on host-derived interface membranes: as sites for reciprocal nutrient and signal exchange during symbiosis, or as conduits for asymmetrical nutrient acquisition and effector delivery by pathogens. Sustaining these dynamic structures places substantial metabolic and vesicular trafficking demands on host cells. This review examines how cell cycle reprogramming may help plants meet these demands. During plant-pathogen interactions, biotrophic pathogens can reprogram host cell cycle pathways to establish metabolically favorable niches, whereas plant immunity can engage cell cycle checkpoints to restrict resource allocation and reinforce physical barriers. In arbuscular mycorrhizal symbiosis, localized endoreduplication in host cells could function as a "metabolic amplification program" to boost biosynthetic output, whereas host cells may adopt a "division-restricted state" that enables extensive intracellular remodeling while preserving the transcellular infection pathway. Root nodule symbiosis and mycorrhizal symbiosis share several cellular programs for microbial accommodation and the cell cycle could be further activated during symbiotic nodule development. Thus, we speculate that interface formation-during either symbiotic or pathogenic infection-may rely on a shared cellular toolkit that is potentially governed by distinct regulatory thresholds, tentatively suggesting the possibility of engineering cell cycle programs to improve symbiotic efficiency or enhance resistance against pathogens.