Genetius

Using a microfluidic valve rootchip, the study simultaneously tracked ROS and calcium dynamics in compressed roots and found three kinetic phases linking mechanosensitive channel activity, NADPH oxidase‑dependent ROS accumulation, and secondary calcium influx. Pharmacological inhibition revealed that a fast calcium response is mediated by plasma‑membrane mechanosensitive channels, while a slower calcium increase is driven by ROS production.

The study demonstrates that a rapid increase in cytosolic Ca²⁺ is the primary and sufficient signal mediating auxin‑induced root growth inhibition in Arabidopsis. Using live imaging, microfluidics, and optogenetic control of Ca²⁺ influx, the authors show that blocking Ca²⁺ entry prevents growth responses, while light‑triggered Ca²⁺ influx from the apoplast or ER mimics inhibition, indicating that diverse stimuli converge on a Ca²⁺‑dependent mechanism.

The study uses an optogenetic ChannelRhodopsin 2 variant (XXM2.0) to generate defined cytosolic Ca²⁺ transients in Arabidopsis root cells, revealing that these Ca²⁺ signatures suppress auxin‑induced membrane depolarization, Ca²⁺ spikes, and auxin‑responsive transcription, leading to reversible inhibition of cell division and elongation. This demonstrates that optogenetically imposed Ca²⁺ signals act as dynamic regulators of auxin sensitivity in roots.

The study investigates how auxin signaling influences aluminium tolerance using tomato mutants with altered auxin sensitivity, showing that the auxin‑hypersensitive entire mutant tolerates Al stress while the auxin‑reduced dgt mutant is more sensitive. Differences in reactive oxygen species accumulation and root transition‑zone cell differentiation correlate with distinct metabolic responses, suggesting that modifying auxin perception can enhance crop Al tolerance.

The study demonstrates that jasmonate (JA) enhances Arabidopsis thaliana responses to extracellular ATP (eATP) by upregulating the eATP receptor P2K1 and amplifying eATP‑induced cytosolic Ca²⁺ spikes and transcriptional reprogramming in a COI1‑dependent manner, whereas salicylic acid pretreatment suppresses these responses. These findings reveal a JA‑mediated priming mechanism that potentiates eATP signaling during stress.

The study characterizes a plasma membrane-localized, calcium‑permeable force‑gated channel named Rapid Mechanically Activated (RMA) in plants, using patch‑clamp and pressure‑clamp to elucidate its rapid activation, inactivation, and irreversible adaptation upon repeated mechanical stimulation. Kinetic modeling shows the channel functions as a pass‑band filter for frequencies between 10 Hz and 1 kHz, supporting its role in transducing high‑frequency mechano‑stimuli such as insect vibrations.

The study reveals that the endoplasmic reticulum‑associated degradation (ERAD) pathway governs the proteasome‑dependent turnover of PIN‑LIKES (PILS) auxin transport proteins under normal conditions, and that both internal and external cues modulate this process via the ERAD complex. These findings link ER protein homeostasis to auxin‑mediated growth regulation, highlighting a new mechanism by which plants adapt to environmental and developmental signals.

The study identifies fungal effectors from Ustilago maydis that interact with plant TOPLESS corepressors and induce gall formation by hijacking maize lateral root initiation pathways, notably through upregulation of LBD transcription factors. Transgenic expression of class II effectors derepresses auxin signaling, leading to pluripotent calli without external hormones, and maize mutants in LBD genes show reduced gall development.

The study visualizes subcellular dynamics following activation of the NRC4 resistosome, showing that NRC4 enrichment at the plasma membrane triggers calcium influx, followed by sequential disruption of mitochondria, plastids, endoplasmic reticulum, and cytoskeleton, culminating in plasma membrane rupture and cell death. These observations define a temporally ordered cascade of organelle and membrane events that execute plant immune cell death.

The study identified a suppressor mutation (sune42) in the Golgi-localized Ca2+ transporter CCX4 that alleviates the dominant‑negative root hair phenotype caused by the extensin‑less LRX1ΔE14 protein in Arabidopsis. Detailed Ca2+ imaging showed that LRX1ΔE14 disrupts tip‑focused cytoplasmic Ca2+ oscillations, a defect rescued by the sune42 mutation, highlighting the role of Golgi‑mediated Ca2+ homeostasis in root hair growth.