Adventitious roots form from non-root tissues as part of normal development or in response to stress or wounding. The root primordia form in the source tissue, and during emergence the adventitious roots penetrate the inner cell layers and the epidermis; however, the mechanisms underlying this emergence remain largely unexplored. Here, we report that a regulatory module composed of the AP2/ERF transcription factor ABSCISIC ACID INSENSITIVE 4 (ABI4), the MAP kinases MPK3 and MPK6, and the phosphatase PP2C12 plays an important role in the emergence of junction adventitious roots (J-ARs) from the root–hypocotyl junctions in Arabidopsis thaliana. ABI4 negatively regulates J-AR emergence, preventing the accumulation of reactive oxygen species and death of epidermal cells, which would otherwise facilitate J-AR emergence. Phosphorylation by MPK3/MPK6 activates ABI4 and dephosphorylation by PP2C12 inactivates ABI4. MPK3/MPK6 also directly phosphorylate and inactivate PP2C12 during J-AR emergence. We propose that this “double-check” mechanism increases the robustness of MAP kinase signaling and finely regulates the local programmed cell death required for J-AR emergence.

不定根从非根组织形成，作为正常发育的一部分或对压力或创伤的反应。根原基在源组织中形成，并且在出苗期间不定根穿透内部细胞层和表皮；但是，这种出现的潜在机制在很大程度上仍未得到探索。在这里，我们报告说，由AP2 / ERF转录因子ABSCISIC ACID INSENSITIVE 4（ABI4），MAP激酶MPK3和MPK6和磷酸酶PP2C12组成的调控模块在结不定根（J-ARs）的出现中起重要作用）从拟南芥的根-下胚轴交界处。ABI4负调节J-AR的出现，防止活性氧的积累和表皮细胞的死亡，否则会促进J-AR的出现。MPK3 / MPK6的磷酸化激活ABI4，PP2C12的去磷酸化使ABI4失活。在J-AR出现期间，MPK3 / MPK6也直接磷酸化PP2C12并使之失活。我们建议这种“双重检查”机制增加MAP激酶信号传导的鲁棒性，并精细调节J-AR出现所需的局部程序性细胞死亡。