A mobile lncRNA QingLattice mediates DML-IDN2 crosstalk via chromatin looping to reprogram DNA methylation and nutrient allocation

Vascular-mobile lncRNAs can function as systemic signals in abiotic stress adaptation. However, their direct molecular mechanisms—particularly the ability to recruit chromatin remodelers for modulating chromatin architecture at target loci—remain largely unexplored in sink tissues, where chromatin accessibility and transcriptional reprogramming are critical for systemic adaptation. Here, we show that the lncRNA QingLattice acts as a mobile signal during iron (Fe) deficiency, moving from shoot to root tissues where it reprograms target gene expression through two synergistic epigenetic pathways. Directly, QingLattice binds the MdNRAMP3 locus and recruits the demethylase MdDML1, catalyzing active DNA demethylation to activate MdNRAMP3 transcription. Indirectly, QingLattice induces alteration of chromatin looping at the MdIDN2 locus, repressing this core RdDM component and thereby relieving RdDM-mediated methylation suppression on MdNRAMP3. These two pathways coordinately reduce MdNRAMP3 methylation and ensure its robust expression, leading to enhanced vacuolar Fe export and systemic Fe-deficiency tolerance. Grafting experiments with QingLattice-overexpressing scions and wild-type rootstocks confirm that its mobility is necessary and sufficient for these epigenetic regulation-induced adaptive phenotypes. Our findings reveal a paradigm in which a mobile lncRNA integrates direct demethylase recruitment with indirect RdDM suppression to fine-tune target gene methylation, offering insight into systemic epigenetic regulation of plant–environment interactions.