Abstract

Wounding is a trigger for both regeneration and defense in plants, but it is not clear if the two responses are linked by common activation or regulated as tradeoffs. While plant glutamate-like receptors (GLRs) are known to mediate defense, here we implicate GLRs in regeneration through dynamic changes in chromatin and transcription in reprogramming cells near wound sites. We show that genetic and pharmacological inhibition of GLR activity increases regeneration efficiency in multiple organ repair systems and plant species. Perturbation of GLR-mediated function speeds cell division and re-specification of the stem cell niche while dampening defense responses. We show that the GLRs work through salicylic acid (SA) signaling in regeneration, with mutants in the SA receptor NPR1 partially resistant to GLR perturbation and hyper regenerative. These findings reveal a conserved mechanism that regulates a tradeoff between defense and regeneration and offer new strategies to improve regeneration in agriculture and conservation.

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