Plant genomic and epigenomic integrity are perpetually threatened by exogenous and endogenous DNA damage. However, the interplay between DNA damage, DNA methylation (5mC), and transposable element (TE) activity remains poorly understood. Here, we demonstrate that defective single-strand break (SSB) repair acts as a potent trigger for genome-wide TE derepression and extensive de novo DNA methylation in Arabidopsis. Mutations in ZDP/APE2, which encode conserved DNA 3'-end repair enzymes, impair the repair of 3'-blocked SSBs arising from base excision repair, ultimately leading to widespread TE activation. Concurrently, inefficient SSB repair activates the ATR-SOG1-mediated DNA damage response, which enhances the RNA-directed DNA methylation (RdDM) pathway to counteract TE activation by depositing 5mC. Paradoxically, the resulting methylation is excised by the DNA demethylase ROS1-a process that itself generates 3'-blocked SSBs requiring resolution by ZDP/APE2. In zdp ape2 mutants, ROS1-mediated 5mC excision produces additional SSBs, which in turn reactivate RdDM. This establishes a self-sustaining SSB-5mC cycle that perpetuates DNA damage and drives massive TE activation in the mutant. Our findings reveal a critical mechanistic link between SSB repair, DNA methylation dynamics, and TE derepression, positioning defective SSB repair as a major inducer of epigenomic instability.
Wenjie Liang, Haokai Cao, Chen Zou et al.· Proceedings of the National...· 0 citations
Plant viral symptoms are not merely passive consequences of infection but can represent adaptive strategies for enhancing transmission. The molecular mechanisms and ecological consequences of such virus-induced symptoms, particularly in perennial crops such as kiwifruit, require exploration. Here, in field experiments, we discovered a kiwifruit infected with a novel virus, Actinidia yellow ringspot virus (AYRSpV), which exhibits severe yellowing symptoms and significantly increases the attractiveness of pollinating insects such as bees and aphids during the flowering season. Given that AYRSpV is pollen-transmissible, this visual manipulation may facilitate the pollinator-mediated spread of the virus. We further explored whether the AYRSpV coat protein (CP) is a key virulence determinant that interacts with and targets the chlorophyll metabolic enzyme magnesium protoporphyrin IX methyltransferase (ChlM) for degradation, leading to a significant reduction in chlorophyll content and systemic leaf yellowing. Knockout of kiwifruit ChlM recapitulated the yellowing phenotype and further enhanced plant susceptibility to AYRSpV. Our study elucidates a pathway whereby a viral CP protein directly disrupts chlorophyll biosynthesis to induce leaf yellowing. Furthermore, we reveal a strategy wherein the virus exploits this symptom as a visual signal to manipulate pollinator behavior, thus creating a ‘symptom-mediated transmission’ loop. These findings provide a comprehensive understanding of the molecular and ecological mechanisms driving the spread of an emerging kiwifruit virus.
Ruotong Wang, Jierou Li, Xiaoling Li et al.· Horticulture Research· 0 citations
