Genetius

The study demonstrates that short‑term low phosphate treatment delays leaf senescence in rice by increasing photosynthetic pigments, enhancing antioxidant enzyme activities, and reducing oxidative damage, whereas high phosphate accelerates senescence. CRISPR/Cas9 editing of MIR827 to lower Pi levels also postpones senescence, while overexpression of MIR827 or MIR399, which raises Pi, speeds it up. Transcriptomic profiling reveals coordinated changes in senescence‑associated and metabolic pathways underlying the low‑phosphate response.

The study identifies the cysteine‑rich receptor‑like kinase CRK5 as a negative regulator of salicylic‑acid‑mediated cell death and a positive regulator of antioxidant homeostasis during dark‑induced leaf senescence in Arabidopsis. Loss‑of‑function crk5 mutants display accelerated senescence, elevated ROS and electrolyte leakage, and altered antioxidant enzyme activities, phenotypes that are rescued by suppressing SA biosynthesis or catabolism. Transcriptome analysis reveals extensive deregulation of senescence‑ and redox‑related genes, highlighting CRK5’s central role in coordinating hormonal and oxidative pathways.

The study shows that maize plants carrying autophagy-defective atg10 mutations exhibit delayed flowering and significant reductions in kernel size, weight, and number, culminating in lower grain yield. Reciprocal crossing experiments reveal that the maternal genotype, rather than the seed genotype, primarily drives the observed kernel defects, suggesting impaired nutrient remobilization from maternal tissues during seed development.

Using the bryophyte Physcomitrium patens, the study shows that loss of autophagy enhances auxin‑driven caulonemata differentiation and colony expansion under low nitrogen or imbalanced carbon/nitrogen conditions, accompanied by higher internal IAA, reduced PpPINA expression, and up‑regulated RSL transcription factors. Autophagy appears to suppress auxin‑induced differentiation during nutrient stress, acting as a hub that balances metabolic cues with hormonal signaling.

A two‑year field trial compared conventional and organic nutrient management on the Basmati rice cultivar Pant Basmati 1, revealing that conventional fertilizer enhanced later‑stage growth and grain yield, while organic inputs increased early plant height and markedly improved soil health and harvest index in the second year. Despite some yield differences, organic management achieved comparable productivity with superior soil macro‑ and micronutrient status, water‑holding capacity, aggregate stability, and enzyme activities, supporting its sustainability as an alternative nutrient regime.

Thermopriming enhances heat stress tolerance by orchestrating protein maintenance pathways: it activates the heat shock response (HSR) via HSFA1 and the unfolded protein response (UPR) while modulating autophagy to clear damaged proteins. Unprimed seedlings cannot mount these responses, leading to proteostasis collapse, protein aggregation, and death, highlighting the primacy of HSR and protein maintenance over clearance mechanisms.

The study examined the pre‑activation state of the rice NLR pair Pik‑1 (sensor) and Pik‑2 (helper) when transiently expressed in Nicotiana benthamiana leaves. Both wild‑type and engineered Pik‑1 variants constitutively associate with Pik‑2 to form ~1 MDa hetero‑oligomeric complexes that localize to the plasma membrane in the absence of effector. These results reveal that some NLRs exist as pre‑assembled membrane‑associated complexes prior to pathogen perception.

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 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 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.