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.

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 researchers created tomato lines overexpressing the autophagy gene SlATG8f and evaluated their performance under high-temperature stress. qRT‑PCR and physiological measurements revealed that SlATG8f overexpression enhances expression of autophagy‑related and heat‑shock protein genes, accelerates fruit ripening, and improves fruit quality under heat stress.

The study identifies an autophagy pathway that degrades plasma membrane-derived clathrin-coated vesicles (CCVs) during hyperosmotic stress, helping maintain membrane tension as cell volume decreases. Using live imaging and correlative microscopy, the authors show that the TPLATE complex subunits AtEH1/Pan1 and AtEH2/Pan1 act as selective autophagy receptors by directly binding ATG8, thereby removing excess membrane under drought or salt conditions.

The study investigates autophagy’s protective role against cadmium stress in Arabidopsis thaliana by comparing wild-type, atg5 and atg7 autophagy-deficient mutants, and ATG5/ATG7 overexpression lines. Cadmium exposure triggered autophagy, shown by ATG8a-PE accumulation, GFP-ATG8a fluorescence and ATG gene up-regulation, with atg5 mutants displaying heightened Cd sensitivity and disrupted metal ion homeostasis, whereas overexpression had limited impact. Genotype-specific differences between Col-0 and Ws backgrounds were also observed.

The study introduces a native‑condition method combining cell fractionation and immuno‑isolation to purify autophagic compartments from Arabidopsis, followed by proteomic and lipidomic characterisation of the isolated phagophore membranes. Proteomic profiling identified candidate proteins linked to autophagy, membrane remodeling, vesicular trafficking and lipid metabolism, while lipidomics revealed a predominance of glycerophospholipids, especially phosphatidylcholine and phosphatidylglycerol, defining the unique composition of plant phagophores.

The study performed comparative gene expression profiling across four rice accessions—from shoot apical meristem to primordia stage P5—to delineate developmental and photosynthetic transitions in leaf development. By integrating differential expression and gene regulatory network analyses, the authors identified stage-specific regulatory events and key transcription factors, such as RDD1, ARID2, and ERF3, especially in the wild rice Oryza australiensis, offering a comprehensive framework for optimizing leaf function.

The study identifies the Arabidopsis phospholipases LCAT3 and LCAT4 as essential components that hydrolyze membranes of autophagic bodies within the vacuole, a critical step for autophagy completion. Double mutants lacking both enzymes accumulate autophagic bodies and display diminished autophagic activity, while in vivo reconstitution shows LCAT3 initiates membrane hydrolysis, facilitating LCAT4’s function.

The study examined how osmotic stress and cytosolic Ca²⁺ signaling regulate autophagy in plants by monitoring the dynamics of RFP‑tagged ATG8i. Both stimuli altered the accumulation of RFP‑ATG8i‑labeled autophagosomes in an organ‑specific way, and colocalization with the ER marker HDEL indicated that ATG8i participates in ER‑phagy during stress.