Summary 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.

34Jasmonate (JA), an oxylipin-derived phytohormone, plays crucial roles not only in plant 35 immunity and defense against herbivorous insects but also in plant growth and developmental 36 processes, including regeneration and organogenesis. However, the mechanistic basis of its 37 mode of action and precise role in integrating other signaling cues are poorly understood. Here 38 we provide genetic indications that JA signaling acts in both NINJA-dependent and -39 independent modulation of the transcriptional activity of MYC transcription factors involved 40 in the inhibition of adventitious root initiation (ARI). Our data show that NINJA-dependent JA 41 signaling in pericycle cells blocks early events of ARI. Moreover, transcriptomic comparison 42 of ninja-1myc2-322B double mutant (which produce extremely few ARs) and wild type 43 seedlings identified a novel molecular network governed by the APETALA2/ETHYLENE 44 RESPONSE FACTOR 115 (ERF115) transcription factor. We demonstrate that JA-induced 45 ERF115 activates the cytokinin signaling machinery and thereby represses ARI. Altogether, 46 our results reveal a molecular network involving cooperative crosstalk between JA and CK 47 machineries that inhibits ARI. 48 49 Key words: 50 Jasmonate, cytokinins, adventitious rooting, AP2/ERF transcription factors, de novo 51 organogenesis. 52 53 Jasmonate (JA), a stress-induced phytohormone, plays crucial roles in plant immunity and 54 defense against herbivorous insects (Wasternack and Hause, 2013). It also participates in 55 control of diverse developmental processes, including tissue regeneration and rhizotaxis 56 (Wasternack and Hause, 2013;Lakehal et al., 2020). The isomer (+)-7-iso-JA-Ile (JA-Ile), the 57 bioactive form of JA (Fonseca et al., 2009), is perceived by the F-box protein CORONATINE 58 INSENSITIVE1 (COI1), which is an integral component of the Skp-Cullin-F-box (SCF) 59 complex (Xie et al., 1998). The COI1 receptor fine-tunes the function of the JA transcriptional 60 machinery in a simple manner. Briefly, in the resting state, marked by low JA-Ile contents, the 61 transcriptional activity of a number of transcription factors, including the basic-Helix-loop-62 Helix MYC, is repressed by JASMONATE ZIM DOMAIN (JAZ) repressors through either 63 physical interaction or recruitment of the general co-repressor TOPLESS (TPL) or TPL-related 64 proteins (TPRs) (Chini et al., 2007; Thines et al., 2007; Yan et al., 2007). The adaptor NOVEL 65 INTERACTOR OF JAZ (NINJA) mediates interaction of JAZs with TPL or TRPs (Pauwels et 66 al., 2010). During activation, marked by accumulation of JA-Ile, JAZs form co-receptor 67 complexes with COI1. This interaction is facilitated by JA-Ile, which acts as a molecular glue 68 (Sheard et al., 2010). Formation of the co-receptor complexes triggers ubiquitylation and 69 proteasome-dependent degradation of the targeted JAZs, thereby releasing the transcription 70 factors to transcriptionally induce or repress their downstream target genes. Biochemical 71 studies suggest that JAZ-dependent ...

Adventitious rooting is a post-embryonic developmental program governed by a multitude of endogenous and environmental cues. Auxin, along with other phytohormones, integrates and translates these cues into precise molecular signatures to provide a coherent developmental output. Auxin signaling guides every step of adventitious root (AR) development from the early event of cell reprogramming and identity transitions until emergence. We have previously shown that auxin signaling controls the early events of AR initiation (ARI) by modulating the homeostasis of the negative regulator jasmonate (JA). Although considerable knowledge has been acquired about the role of auxin and JA in ARI, the genetic components acting downstream of JA signaling and the mechanistic basis controlling the interaction between these two hormones are not well understood. Here we provide evidence that COI1-dependent JA signaling controls the expression of DAO1 and its closely related paralog DAO2. In addition, we show that the dao1-1 loss of function mutant produces more ARs than the wild type, probably due to its deficiency in accumulating JA and its bioactive metabolite JA-Ile. Together, our data indicate that DAO1 controls a sensitive feedback circuit that stabilizes the auxin and JA crosstalk during ARI.