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Adventitious root initiation (ARI) is a de novo organogenesis program and a key adaptive trait in plants. Several hormones regulate ARI but the underlying genetic architecture that integrates the hormonal crosstalk governing this process remains largely elusive. In this study, we use genetics, genome editing, transcriptomics, hormone profiling and cell biological approaches to demonstrate a crucial role played by the APETALA2/ETHYLENE RESPONSE FACTOR 115 transcription factor. We demonstrate that ERF115 functions as a repressor of ARI by activating the cytokinin (CK) signaling machinery. We also demonstrate that ERF115 is transcriptionally activated by jasmonate (JA), an oxylipin-derived phytohormone, which represses ARI in NINJA-dependent and independent manners. Our data indicate that NINJA-dependent JA signaling in pericycle cells blocks early events of ARI. Altogether, our results reveal a previously unreported molecular network involving cooperative crosstalk between JA and CK machineries that represses ARI.

Jasmonate (JA), an oxylipin-derived phytohormone, plays crucial roles not only in plant immunity and defense against herbivorous insects but also in plant growth and developmental processes, including regeneration and organogenesis. However, the mechanistic basis of its mode of action and precise role in integrating other signaling cues are poorly understood. Here we provide genetic evidences that JA signaling acts in both NINJA-dependent and -independent modulation of the transcriptional activity of MYC transcription factors involved in the inhibition of adventitious root initiation (ARI). Our data show that NINJA-dependent JA signaling in pericycle cells blocks early events of ARI. Moreover, transcriptomic comparison of ninja-1myc2-322B double mutant (which produce extremely few ARs) and wild type seedlings identified a novel molecular network governed by the APETALA2/ETHYLENE RESPONSE FACTOR 115 (ERF115) transcription factor. We demonstrate that JA-induced ERF115 activates the cytokinin signaling machinery and thereby represses ARI. Altogether, our results reveal a molecular network involving cooperative crosstalk between JA and CK machineries that inhibits ARI. Footnotes * Added URL and accession number for RNAseq data Modified Acknowledgements * https://www.ebi.ac.uk/ena