Figure 2.

Single cell ablation in the Arabidopsis root meristem triggers multiple local and regional wounding responses. (a) Ablation of cortex cells in the elongation zone triggers the induction of Ca²⁺, ROS, ethylene, and membrane depolarization. The increase in Ca²⁺ influx after ablation is dependent on ROS production in the apoplast by RBOH enzymes and allows the fast change in membrane polarization (1.5 s after ablation). Additionally, it induces an accumulation of ROS around the wound that occurs ∼6 min after the ablation. Both, Ca²⁺ influx and ROS production contribute to the ethylene signalling induction by an increased ACC SYNTHASE 6 (ACS6) expression starting three hours after ablation. Eventually, ethylene signalling via EIN2 increases the resistance against nematode infection [37^••]. (b) Laser ablation of epidermis cells in the transition zone triggers a Ca²⁺ influx that spreads throughout the adjacent tissue but results in different amplitudes depending on the distance from the harmed cell. Harmed cells (grey) exhibit a stronger Ca²⁺ influx than those directly adjacent to the eliminated cells (orange) and cells further away (white). Strong influx and complete destruction of membrane integrity activate METACASPASE4 (MC4) from inactive zMC4, which cleaves the PRECURSOR OF PEP1 (PROPEP1) into Pep1. By this, it becomes translocated from the vacuolar membrane to the cytosol to be perceived by the PEPR1 and PEPR2 receptors at the cell surface of neighboring (orange) cells [34^••]. (c) Ablation in the root meristem triggers restorative divisions to replace the eliminated cells. These divisions happen predominately in the inner adjacent cells. They are induced by the activation of stem cell programs (orange nuclei; here: SHR – CYCD6;1) and an accelerated progression through the cell cycle. They include the switch of the division plane from anticlinal to periclinal, and the newly generated outer daughter cells adopt the cell fate of the eliminated cells to eventually regenerate the disrupted tissue pattern [32^••]. (d) Ablations in the stem cell niche trigger a jasmonate induction within 30 s which is perceived by COI1 to activate MYC2, a JA-dependent transcription factor. MYC2 binds to the promoter of ERF115 to enhance its expression around the wound site [41^••]. ERF115 is also activated by its JA/MYC2-dependent homologue ERF109 [41^••] and by downstream signalling of auxin [41^••], ROS [49], and brassinosteroids (BL) [47,48]. In ablations outside the stem cell niche, ERF115 expression is confined to cells directly adjacent to the killed cell [31^••,32^••]. ERF115 can bind to RETINOBLASTOMA-RELATED1 (RBR1) and inhibit its activity to regulate the division rate in the quiescent centre and the stem cell niche [41^••]. Few downstream targets of ERF115 have been identified. One of them, PSK5, might be involved in the acceleration of the cell cycle progression [47]. Eventually, ERF115 transcription factor activity contributes greatly to tissue regeneration after single cell ablation as well as whole root tip removal [31^••,32^••,41^••]. Yellow thunderbolts indicate UV laser ablation.