Rapamycin-Reactivated Lipid Catabolism in Eruca sativa Mill. Exposed to Salt Stress

TL;DR

Rapamycin helps Eruca sativa seedlings under salt stress by reactivating lipid breakdown, improving their development.

Contribution

Rapamycin reactivates lipid catabolism in salt-stressed Eruca sativa embryos, potentially aiding stress tolerance.

Findings

Salt stress blocks lipid droplet catabolism and starch storage in Eruca sativa embryos.

Rapamycin restores lipid catabolism under salt stress, similar to control conditions.

Rapamycin induces autophagy, including pexophagy, to support the glyoxylate cycle.

Abstract

Salt stress is one of the most common factors reducing the productivity of crops. We tested the effect of Rapamycin, an mTOR inhibitor and autophagy inducer, for the possible amelioration of high-salinity stress in Eruca sativa. We analyzed the germination rate, the macro- and micro-morphology of seedlings, and the ultrastructure of cotyledons with a Transmission Electron Microscope. The most striking observation was that salt stress blocked the catabolism of the lipid droplets stored in the embryos of E. sativa, also dramatically reducing the starch storage capability in the plastids. As a consequence, lipid droplets remained in the developing seedlings until a late stage. On the contrary, the catabolism of the lipid storage in the embryos in the presence of rapamycin and salt stress was comparable to the control, even if the starch stored in the plastids was lower. Rapamycin-induced autophagic activity was shown by characteristic ultrastructural changes, such as increased membrane recycling. Part of this activity was interpreted as pexophagy, i.e., the autophagy of peroxisomes, where an increase in their turnover rate could be necessary to maintain an active glyoxylate cycle.

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