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.

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.