Genetius

The study demonstrates that FERONIA and phytochrome B physically interact with the NADPH oxidase RBOHD, and that FERONIA-mediated phosphorylation of phyB is essential for RBOHD-driven ROS production under excess light stress in Arabidopsis thaliana. Additional membrane proteins CRK10 and PIP2;6 also associate with this complex, forming a plasma‑membrane assembly that integrates multiple signaling pathways to regulate stress‑induced ROS.

The study elucidates the SPL/NZZ‑dependent regulatory pathway governing megaspore mother cell (MMC) differentiation, revealing that SPL/NZZ directly targets genes and interacts with ovule‑identity MADS‑domain transcription factor complexes. Integration of multi‑omics data with genetic complementation and mutant analyses uncovers an auxin‑dependent downstream network that drives MMC formation.

The study identifies wound‑induced proline transporters ProT2 and ProT3 as central regulators that link salicylic acid signaling to the suppression of de novo root regeneration (DNRR) via modulation of reactive oxygen species dynamics. Genetic loss of these transporters or pharmacological inhibition of proline transport alleviates SA‑mediated regeneration inhibition across several plant species without compromising disease resistance.

The study demonstrates that very long chain sphingolipids in the outer membrane leaflet interdigitate with inner‑leaflet phosphatidylserine, forming a vertical bridge that organizes PS nanodomains and enables auxin‑induced activation of the Rho‑GTPase ROP6. Disruption of sphingolipid biosynthesis disperses these nanodomains, impairing ROP6 signaling, cytoskeletal dynamics, and directional growth, highlighting interleaflet coupling as a key mechanism linking membrane asymmetry to plant signal transduction.

The study examined how Arabidopsis calcium‑dependent protein kinases AtCPK5 and AtCPK6 modulate immunity triggered by bacterial rhamnolipids, finding that RLs up‑regulate these kinases and that mutants, especially cpk5/6, show altered reactive oxygen species production and defense gene expression. However, these kinases did not influence RL‑induced electrolyte leakage or resistance to Pseudomonas syringae pv. tomato DC3000, indicating additional signaling components are involved.

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.

A comparative phosphoproteomics study using Arabidopsis thaliana ahk5 loss‑of‑function mutants and wild‑type seedlings revealed that the histidine kinase AHK5 mediates a rapid shift from multistep phosphorelay signaling to serine/threonine phosphorylation in response to H2O2. AHK5 controls ROS‑responsive phosphorylation of plasma‑membrane nanodomain proteins and orchestrates distinct ABA‑independent stomatal closure and ABA‑dependent root development pathways by modulating key components such as RBOHD, CAS, HPCA1, and auxin transporters.

The study identifies two maize genes, Discordia3a and Discordia3b, that encode the microtubule‑severing protein KATANIN. Loss‑of‑function allele combinations reduce microtubule severing, impair cell elongation, delay mitotic entry, and disrupt preprophase band and nuclear positioning, leading to dwarfed, misshapen plants.

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.