Genetius

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.

The study examined the roles of AtKUP2, AtKUP6, AtKUP8, and GORK potassium transport proteins in guard cell function by performing gas-exchange measurements on mature Arabidopsis leaves. Loss of KUP2/6/8 reduced stomatal conductance, whereas a GORK loss‑of‑function mutant showed increased conductance, yet the magnitude of light‑ and ABA‑induced transpiration changes remained similar across genotypes, suggesting a limited dynamic range for rapid stomatal movements that relies on small ionic osmolytes.

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 demonstrates that subfamily I ethylene receptors form the core ethylene‑sensing module and act epistatically over subfamily II receptors, uniquely possessing Ca2+‑permeable channel activity that drives ethylene‑induced cytosolic calcium influx. This reveals a mechanistic link whereby subfamily I receptors integrate hormone perception with calcium signaling in plants.

The study shows that Arabidopsis root tips adapt to hypoxia by increasing H3K4me3 levels, linked to the inhibition of group 7 demethylases (KDM7s). Genetic loss of KDM7s mimics hypoxic conditions, activating genes that sustain meristem survival, suggesting KDM7s act as root‑specific oxygen sensors that prime epigenetic tolerance mechanisms.

The study shows that inoculation with the non‑diazotrophic bacterium Enterobacter sp. SA187 significantly improves Arabidopsis thaliana growth under low nitrate conditions by increasing fresh weight, primary root length, and lateral root density, while enhancing nitrate accumulation and reducing shoot C:N ratios. Transcriptomic and mutant analyses reveal that these benefits depend on ethylene signaling and the activity of high‑affinity nitrate transporters NRT2.5 and NRT2.6, indicating an ethylene‑mediated, HATS‑dependent reprogramming of nitrogen uptake.

The study reveals that Arabidopsis ethylene receptors ETR1 and ERS1 function as Ca²⁺-permeable channels, with ETR1 specifically mediating ethylene‑induced cytosolic Ca²⁺ spikes that influence hypocotyl elongation. Homologous receptors from diverse land plants and algae also show Ca²⁺ permeability, and ethylene further enhances this activity, indicating a conserved regulatory role across the green lineage.

The study demonstrates that ethylene signaling contributes to host resistance against the root parasitic plant Phelipanche aegyptiaca, as both water stress and parasitism activate ethylene responses in Arabidopsis roots. Application of the ethylene precursor ACC reduced parasite attachment, and mutants in ethylene signaling components (ETR1, CTR1) showed altered tolerance, highlighting ethylene-mediated defenses as a potential strategy for crop protection.

The study uncovers a reciprocal regulatory loop between type one protein phosphatases (TOPPs) and EIN2 in ethylene signaling, showing that ethylene induces TOPPs expression and that TOPPs dephosphorylate EIN2 at S655 to stabilize it and promote nuclear accumulation. TOPPs act upstream of EIN2, while EIN3/EIL1 transcriptionally activates TOPPs, linking dephosphorylation to enhanced ethylene responses and improved salt tolerance.