Recurrent drought stress seriously threatens plant growth and crop production, but plant drought adaptation often comes at a yield penalty, known as the growth-defense trade-off. Therefore, deciphering the mechanisms of trade-off between plant growth and drought tolerance is of great importance for plant survival and crop yield in fluctuating environments. Our recent studies have shown that U-box E3 ubiquitin ligase OsPUB33 reduces rice (Oryza sativa L.) grain yield via ubiquitination and degradation of the transcription factor OsNAC120, a positive regulator of grain size, whereas OsNAC120 compromises rice drought tolerance through transcriptionally repressing drought-responsive genes. In the present study, we found the OsPUB33-OsNAC120 module acts as a molecular switch between drought response and growth recovery in rice. OsPUB33 enhanced ABA-induced drought tolerance, and its protein abundance rapidly increased at the early stage of drought stress and returned to normal at the rehydration stage, whereas OsNAC120 acted oppositely. Genetic evidence showed that OsPUB33 and OsNAC120 regulate rice drought response through a common pathway. Notably, OsNAC120 phosphorylation mediated by OsSAPK9, a key SnRK2 kinase in ABA signaling, enhanced its interaction with OsPUB33, thus promoting OsNAC120 ubiquitination for degradation under drought stress and increasing rice drought tolerance. When drought stress was relieved, OsPUB33 abundance declined while OsNAC120 levels increased, consequently achieving growth recovery. These findings indicate that the OsPUB33-OsNAC120 module, which is controlled by OsSAPK9, is a molecular switch between the drought response and growth recovery, revealing a key mechanism of plant growth regulation under drought stress in rice.
The early nodulin-like (ENODL) subfamily, part of the phytocyanin, arabinogalactan protein, and nodulin-like families, is involved in plant growth and stress resistance. However, its role in symbiotic nodulation remains poorly understood. In barrel medic (Medicago truncatula), we found MtENODL29 was strongly activated at the late stages of nodule development, particularly in the infection zone of nodules. Both RNA interference (RNAi) and mutation of MtENODL29 caused a considerable reduction in nodule numbers, an increase in cysteine protease activity, a dramatic decrease in leghemoglobin content, and signs of premature senescence in nodule cells, suggesting that disruption of MtENODL29 accelerates nodule aging. Transcriptome analysis of 7-dpi (day post inoculation) inoculated roots and 28-dpi nodules in enodl29 mutants showed significant downregulation of symbiotic genes, accompanied by differential expression of genes associated with lipid metabolism and transport. MtENODL29 mutation also negatively impacted plant growth and development. MtENODL29 bound to MtnsLTP (non-specific lipid transfer protein), MtKCR (very-long-chain 3-oxoacyl-CoA reductase), and MtSec61γ (gamma subunit of the translocase complex Sec61) through its ALR (arabinogalactan protein-like region) domain. MtENODL29 co-localized with these proteins in the plasma membrane and endoplasmic reticulum. Notably, MtnsLTP showed high expression in the nodules, similar to MtENODL29, while MtKCR and MtSec61γ were also highly expressed in the leaves and stems. These results suggest that MtENODL29 participates in membrane lipid modification and transport by interacting with MtnsLTP, MtKCR, and MtSec61γ, facilitating the formation of symbiosome membranes as alfalfa rhizobium (Sinorhizobium meliloti) strain 1021 are released into nodule cells. Moreover, MtENODL29 influences plant growth, highlighting its role in coordinating plant development and symbiosis.

