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The plant root system consists of primary root, lateral roots and often adventitious roots (ARs). ARs derive from the aboveground organs in response to either intrinsic developmental cues or in response to the environmental ones. AR development is a pre-requisite step for vegetative propagation, which is widely used to multiply elite genotypes in forestry and horticulture. We used Arabidopsis hypocotyl as a model system to unravel the molecular networks controlling AR initiation. We showed that ARI in Arabidopsis hypocotyl is controlled by a complex hormone crosstalk between the positive regulator auxin (IAA) and the negative regulators jasmonate (JA) and cytokinins (CK). First, combining genetic, biochemical and hormonomics approaches, we identified the auxin coreceptor complexes involved in ARI. We found that IAA is perceived by two F-box proteins (TRANSPORT INHIBITOR1/AUXINSIGNALLING F-BOX (TIR1) and its closest homolog AFB2 as well as three Auxin/Inodole-3-acetic acid (Aux/IAA) repressors (IAA6, IAA9 and IAA17). These coreceptor proteins possibly act in combinatorial manner to fine-tune the auxin signaling machinery during ARI. In addition, in a genetic screen, we also revealed that the COP9 SIGNALOSOME SUBUNIT 4 (CSN4) protein plays a central role in ARI by modulating the function of the auxin perception machinery. In silico search for genes acting downstream of JA involved in ARI, we retrieved the recently characterized DIOXYGENASE FOR AUXIN OXIDATION (DAO1) and DAO2 genes. The DAOs encode for enzymes that catalyze the conversion of free IAA into 2-oxindole-3-acetic acid (oxIAA), a rate-limiting step in auxin degradation. We found that the DAO1 gene mediates a molecular circuit to stabilize the interaction between IAA and JA. Combining genetics, transcriptome profiling, hormononics and cell biological approaches, we found that MYC2-mediated JA signaling controls the expression of the ETHYLENE RESPONSE FACTOR 115 (ERF115) gene, which is a repressor of ARI. Our genetic data revealed that ERF115-mediated ARI inhibition requires cytokinins (CKs). CKs have long been established as inhibitors of ARI. Altogether, ARI seems to be controlled by a complex molecular network guided by three hormonal pathways (IAA, JA and CK), in which JA-induced ERF115 plays a role of “molecular switch”.