Clathrin-coated vesicles are targeted for selective autophagy during osmotic stress.
Authors: dragwidge, j., Buridan, M., Kraus, J., Kosuth, T., Chambaud, C., Brocard, L., Yperman, K., Mylle, E., Vandorpe, M., Eeckhout, D., De Jaeger, G., Pleskot, R., Bernard, A., Van Damme, D.
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.
A dual component system instructs membrane hydrolysis during the final stages of plant autophagy
Authors: Castets, J., Buridan, M., Toboso Moreno, I., Sanchez de Medina Hernandez, V., Gomez, R. E., Dittrich-Domergue, F., Lupette, J., Chambaud, C., Pascal, S., Ibrahim, T., Bozkurt, T. O., Dagdas, Y., Domergue, F., Joubes, J., Minina, A. E. A., Bernard, A.
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.
Gain and loss of gene function shaped the nickel hyperaccumulation trait in Noccaea caerulescens
Authors: Belloeil, C., Garcia de la Torre, V. S., Contreras Aguilera, R., Kupper, H., Lopez-Roques, C., Iampetro, C., Vandecasteele, C., Klopp, C., Launay-Avon, A., Leemhuis, W., Yamjabok, J., van den Heuvel, J., Aarts, M. G. M., Quintela Sabaris, C., Thomine, S., MERLOT, S.
The study presents a high-quality genome assembly for the nickel hyperaccumulator Noccaea caerulescens and uses it as a reference for comparative transcriptomic analyses across different N. caerulescens accessions and the non‑accumulating relative Microthlaspi perfoliatum. It identifies a limited set of metal transporters (NcHMA3, NcHMA4, NcIREG2, and NcIRT1) whose elevated expression correlates with hyperaccumulation, and demonstrates that frameshift mutations in NcIRT1 can abolish the trait, indicating an ancient, transporter‑driven origin of nickel hyperaccumulation.
The study integrates genome, transcriptome, and chromatin accessibility data from 380 soybean accessions to dissect the genetic and regulatory basis of symbiotic nitrogen fixation (SNF). Using GWAS, TWAS, eQTL mapping, and ATAC-seq, the authors identify key loci, co‑expression modules, and regulatory elements, and validate the circadian clock gene GmLHY1b as a negative regulator of nodulation via CRISPR and CUT&Tag. These resources illuminate SNF networks and provide a foundation for soybean improvement.
ATG8i Autophagy activation is mediated by cytosolic Ca2+ under osmotic stress in Arabidopsis thaliana
Authors: Castillo-Olamendi, L., Gutierrez-Martinez, J., Jimenez-Nopala, G., Galindo, A., Barrera-Ortiz, S., Rosas-Santiago, P., Cordoba, E., Leon, P., Porta, H.
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.
MdBRC1 and MdFT2 Interaction Fine-Tunes Bud Break Regulation in Apple
Authors: Gioppato, H. A., Estevan, J., Al Bolbol, M., Soriano, A., Garighan, J., Jeong, K., Georget, C., Soto, D. G., El Khoury, S., Falavigna, V. d. S., George, S., Perales, M., Andres, F.
The study identifies the transcription factor MdBRC1 as a key inhibitor of bud growth during the ecodormancy phase in apple (Malus domestica), directly regulating dormancy‑associated genes and interacting with the flowering promoter MdFT2 to modulate bud break. Comparative transcriptomic analysis and gain‑of‑function experiments in poplar demonstrate that MdFT2 physically binds MdBRC1, attenuating its repressive activity and acting as a molecular switch for the transition to active growth.
The study introduced full-length SOC1 genes from maize and soybean, and a partial SOC1 gene from blueberry, into tomato plants under constitutive promoters. While VcSOC1K and ZmSOC1 accelerated flowering, all three transgenes increased fruit number per plant mainly by promoting branching, and transcriptomic profiling revealed alterations in flowering, growth, and stress‑response pathways.
The study shows that the SnRK1 catalytic subunit KIN10 directs tissue-specific growth‑defense programs in Arabidopsis thaliana by reshaping transcriptomes. kin10 knockout mutants exhibit altered root transcription, reduced root growth, and weakened defense against Pseudomonas syringae, whereas KIN10 overexpression activates shoot defense pathways, increasing ROS and salicylic acid signaling at the cost of growth.