Genetius

The study characterizes the chloroplast‑localized protein AT4G33780 in Arabidopsis thaliana using CRISPR/Cas9 knockout and overexpression lines, revealing tissue‑specific expression and context‑dependent effects on seed germination, seedling growth, vegetative development, and root responses to nickel stress. Integrated transcriptomic (RNA‑seq) and untargeted metabolomic analyses show extensive transcriptional reprogramming—especially of cell‑wall genes—and altered central energy metabolism, indicating AT4G33780 coordinates metabolic state with developmental regulation rather than controlling single pathways.

The study identifies the extended NT‑C2 domain of Plastid Movement Impaired 1 (PMI1) as the main membrane‑binding module that interacts with PI4P and PI(4,5)P2, requiring basic residues for plasma‑membrane association. Calcium binding by the NT‑C2 domain modulates its phosphoinositide preference, and cytosolic Ca2+ depletion blocks blue‑light‑induced PMI1 redistribution, indicating that both the NT‑C2 domain and adjacent intrinsically disordered regions are essential for PMI1’s role in chloroplast movement.

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 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 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.

The study demonstrates that constitutively active MLO (faNTA) can rescue the fer-4 root‑hair bursting and polarity defects, restoring tip‑focused cytosolic Ca2+ oscillations and ROS accumulation, highlighting a FERONIA‑MLO signaling module that governs Ca2+ influx and ROS production during root‑hair tip growth. Genetic analysis of mlo15-4 further confirms MLO15 as a key regulator of these Ca2+ and ROS dynamics. The findings suggest MLO proteins act downstream of FER to coordinate calcium and ROS signals essential for root‑hair integrity.

Using an Arabidopsis line expressing the CBL1‑mRuby2‑GCaMP6s calcium reporter, the study uncovered distinct calcium signatures in intact root tissues when exposed to high (5 mM) and low (0.25 mM) nitrate concentrations. Root hairs displayed prominent calcium waves and spikes, while non‑hair epidermal cells showed asynchronous or absent responses, indicating cell‑type‑specific and nitrate‑concentration‑dependent calcium signaling.

The study shows that the mechanosensitive ion channel PIEZO in Arabidopsis thaliana regulates root elongation in response to magnetic fields and blue light, with mutant plants displaying significantly shorter roots under these conditions. PIEZO expression is up‑regulated by a leaf‑derived blue‑light signal in the presence of a magnetic field, influencing calcium efflux and auxin transport via interactions with PIN3, PIN6 and PIN7, and requiring the blue‑light receptors CRY1 and CRY2. Transcriptome analysis reveals that PIEZO integrates multiple hormonal and microRNA pathways, including miR5648‑5p‑mediated negative regulation, to coordinate these environmental responses.