SRAS1.1 E3 ligase mediates DSK2A degradation to regulate autophagy and drought tolerance in Arabidopsis.

Abstract

Drought stress significantly impacts plant growth and productivity, requiring complex adaptive responses to ensure survival. In eukaryotes, autophagy and the ubiquitin-proteasome system (UPS) are critical pathways for maintaining cellular homeostasis under stress. While their interaction is well-studied in animals, it remains poorly understood in plants, particularly under drought conditions. Here, we identify the E3 ubiquitin ligase SRAS1.1 as a key regulator of selective autophagy and drought tolerance in Arabidopsis, mediating its function through the ubiquitination and degradation of the autophagy receptor DSK2A. Loss of SRAS1.1 enhances drought tolerance by reducing water loss, increasing survival rates, and accelerating flowering. SRAS1.1 directly interacts with and ubiquitinates the autophagy receptor DSK2A, promoting its degradation via the 26S proteasome. Notably, under drought stress, SRAS1.1 relocates from the nucleus to the cytoplasm, associates with autophagosomes, and modulates autophagy-related gene expression and BES1 accumulation. These findings provide novel insights into UPS-autophagy crosstalk in plants and highlight SRAS1.1 as a promising target for genetic engineering to develop drought-resilient crops and to advance sustainable agriculture.