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The widespread use of plant grafting enables eudicots and gymnosperms to join with closely related species and grow as one. Gymnosperms have dominated forests for over 200 million years, and despite their economic and ecological relevance, we know little about how they graft. Here we developed a micrografting method in conifers using young tissues that allowed efficient grafting with closely related species and between distantly related genera. Conifer graft junctions rapidly connected vasculature and differentially expressed thousands of genes including auxin and cell-wall-related genes. By comparing these genes to those induced during Arabidopsis thalianagraft formation, we found a common activation of cambium, cell division, phloem and xylem-related genes. A gene regulatory network analysis in Norway spruce (Picea abies) predicted that PHYTOCHROME A SIGNAL TRANSDUCTION 1(PAT1) acted as a core regulator of graft healing. This gene was strongly up-regulated during both spruce and Arabidopsisgrafting, and Arabidopsismutants lacking PATgenes failed to attach tissues or successfully graft. Complementing ArabidopsisPAT mutants with the spruce PAT1homolog rescued tissue attachment and enhanced callus formation. Together, our data show an ability for young tissues to graft with distantly related species and identifies the PAT gene family as conserved regulators of graft healing and tissue regeneration.

Plant somatic cells are generally acknowledged to retain totipotency, the potential to develop into any cell type within an organism. This astonishing plasticity may contribute to a high regenerative capacity on severe damage, but how plants control this potential during normal post-embryonic development remains largely unknown1,2. Here we show that POLYCOMB REPRESSIVE COMPLEX 2 (PRC2), a chromatin regulator that maintains gene repression through histone modification, prevents dedifferentiation of mature somatic cells in Arabidopsis thaliana roots. Loss-of-function mutants in PRC2 subunits initially develop unicellular root hairs indistinguishable from those in wild type but fail to retain the differentiated state, ultimately resulting in the generation of an unorganized cell mass and somatic embryos from a single root hair. Strikingly, mutant root hairs complete the normal endoreduplication programme, increasing their nuclear ploidy, but subsequently reinitiate mitotic division coupled with successive DNA replication. Our data show that the WOUND INDUCED DEDIFFERENTIATION3 (WIND3) and LEAFY COTYLEDON2 (LEC2) genes are among the PRC2 targets involved in this reprogramming, as their ectopic overexpression partly phenocopies the dedifferentiation phenotype of PRC2 mutants. These findings unveil the pivotal role of PRC2-mediated gene repression in preventing unscheduled reprogramming of fully differentiated plant cells.