Salt stress is an important environmental factor that limits plant growth and development. A better understanding of the molecular mechanisms underlying plant salt tolerance will help improve plant performance and crop production under saline conditions. Here, we found that the amino acid methionine significantly improves plant salt tolerance. The salinity-induced activation of key genes governing methionine biosynthesis, namely Hcy-S-methyltransferases (HMTs) and methionine synthases (MSs), is controlled by the concerted interplay of abscisic acid (ABA) and reactive oxygen species signaling. This orchestrated gene activation subsequently leads to methionine accumulation, activating ABA signaling and improving plant salt tolerance. Beyond its role in modulating ABA signaling, methionine affects root growth dynamics by suppressing auxin and cytokinin signaling and impeding cell cycle progression. These multiple effects on growth-related signaling pathways lead to an effective redistribution of energy resources to improve the plant's ability to combat salt-induced stress. Our findings underscore methionine's pivotal involvement in enhancing plant adaptation to salinity stress by establishing a delicate balance between growth and salt tolerance. This mechanistic understanding sheds light on a compelling way to increase crop yields in saline soils and provides a strategic framework for sustainable agricultural practices in challenging environments.

LEAFY COTYLEDON 2 (LEC2) acts throughout embryo morphogenesis and maturation phase to maintain embryogenic identity. Our previous study stated that Arabidopsis thaliana LEC2 (AtLEC2) driven by glucocorticoid receptor-dexamethasone (GR-DEX) inducible system (AtLEC2-GR) triggers embryogenic callus formation in tobacco (Nicotiana tabacum). In this study, the adenosine phosphate isopentenyltransferase genes AtIPT3, AtIPT7 and the tRNA isopentenyltransferase gene AtIPT9 were overexpressed in the AtLEC2-GR transgenic background. In the AtIPT7-OE AtLEC2-GR and AtIPT9-OE AtLEC2-GR seedlings, high-quality embryogenic callus was obtained under the DEX condition, and the shoot regeneration efficiency was 2 to 3.5 folds higher than AtLEC2-GR alone on hormone free medium without DEX. Transcriptome analyses showed that up-regulated BBM, L1L, ABI3, and FUS3 might function during embryogenic callus formation. However, at the shoot regeneration stage, BBM, L1L, ABI3, and FUS3 were down-regulated and Type-B ARRs were up-regulated, which might contribute to the increased shoot regeneration rate. A novel system for inducing shoot regeneration in tobacco has been developed using the GR-DEX system. Induced expression of AtLEC2 triggers embryogenic callus formation and overexpression of AtIPT7 or AtIPT9 improves shoot regeneration without exogenous cytokinin.

Ribosome biogenesis is an orchestrated process that relies on many assembly factors. The AAA-ATPase Midasin 1 (Mdn1) functions as a ribosome assembly factor in yeast (Saccharomyces cerevisiae), but the roles of MDN1 in Arabidopsis (Arabidopsis thaliana) are poorly understood. Here, we showed that the Arabidopsis null mutant of MDN1 is embryo-lethal. Using the weak mutant mdn1-1, which maintains viability, we found that MDN1 is critical for the regular pattern of auxin maxima in the globular embryo and functions in root meristem maintenance. By detecting the subcellular distribution of ribosome proteins, we noted that mdn1-1 impairs nuclear export of the pre-60S ribosomal particle. The processing of ribosomal precusor RNAs, including 35S, 27SB, and 20S, is also affected in this mutant. MDN1 physically interacts with PESCADILLO2 (PES2), an essential assembly factor of the 60S ribosome, and the observed mislocalization of PES2 in mdn1-1 further implied that MDN1 plays an indispensable role in 60S ribosome biogenesis. Therefore, the observed hypersensitivity of mdn1-1 to a eukaryotic translation inhibitor and high-sugar conditions might be associated with the defect in ribosome biogenesis. Overall, this work establishes a role of Arabidopsis MDN1 in ribosome biogenesis, which agrees with its roles in embryogenesis and root development.

To date, there has been no high-quality sequence for genomes of the East Asian grape species, hindering biological and breeding efforts to improve grape cultivars. This study presents ~522 Mb of the Vitis amurensis (Va) genome sequence containing 27 635 coding genes. Phylogenetic analysis indicated that Vitis riparia (Vr) may have first split from the other two species, Va and Vitis vinifera (Vv). Divergent numbers of duplicated genes reserved among grapes suggests that the core eudicot-common hexaploidy (ECH) and the subsequent genome instability still play a non-negligible role in species divergence and biological innovation. Prominent accumulation of sequence variants might have improved cold resistance in Va, resulting in a more robust network of regulatory cold resistance genes, explaining why it is extremely cold-tolerant compared with Vv and Vr. In contrast, Va has preserved many fewer nucleotide binding site (NBS) disease resistance genes than the other grapes. Notably, multi-omics analysis identified one trans-cinnamate 4-monooxygenase gene positively correlated to the resveratrol accumulated during Va berry development. A selective sweep analysis revealed a hypothetical Va sex-determination region (SDR). Besides, a PPR-containing protein-coding gene in the hypothetical SDR may be related to sex determination in Va. The content and arrangement order of genes in the putative SDR of female Va were similar to those of female Vv. However, the putative SDR of female Va has lost one flavin-containing monooxygenase (FMO) gene and contains one extra protein-coding gene uncharacterized so far. These findings will improve the understanding of Vitis biology and contribute to the improvement of grape breeding.

In plant cells, multiple paralogs from ribosomal protein (RP) families are always synchronously expressed, which is likely contributing to ribosome heterogeneity or functional specialization. However, previous studies have shown that most RP mutants share common phenotypes. Consequently, it is difficult to distinguish whether the phenotypes of the mutants have resulted from the loss of specific genes or a global ribosome deficiency. Here, to investigate the role of a specific RP gene, we employed a gene overexpression strategy. We found that Arabidopsis lines overexpressing RPL16D (L16D-OEs) display short and curled rosette leaves. Microscopic observations reveal that both the cell size and cell arrangement are affected in L16D-OEs. The severity of the defect is positively correlated with RPL16D dosage. By combining transcriptomic and proteomic profiling, we found that overexpressing RPL16D decreases the expression of genes involved in plant growth, but increases the expression of genes involved in immune response. Overall, our results suggest that RPL16D is involved in the balance between plant growth and immune response.

Ribosome biogenesis is tightly associated with plant growth and reproduction. Mutations in genes encoding ribosomal proteins (RPs) or ribosome biogenesis factors (RBFs) generally result in retarded growth and delayed flowering. However, the early-flowering phenotype resulting from the ribosome biogenesis defect is rarely reported. We previously identified that the AAA-ATPase MIDASIN 1 (MDN1) functions as a 60S RBF in Arabidopsis. Here, we found that its weak mutant mdn1-1 is early-flowering. Transcriptomic analysis showed that the expression of FLOWERING LOCUS C (FLC) is down-regulated, while that of some autonomous pathway genes and ABSCISIC ACID-INSENSITIVE 5 (ABI5) is up-regulated in mdn1-1. Phenotypic analysis revealed that the flowering time of mdn1-1 is severely delayed by increasing FLC expression, suggesting that the early flowering in mdn1-1 is likely associated with the downregulation of FLC. We also found that the photoperiod pathway downstream of CONSTANTS (CO) and FLOWERING LOCUS T (FT) might contribute to the early flowering in mdn1-1. Intriguingly, the abi5-4 allele completely blocks the early flowering in mdn1-1. Collectively, our results indicate that the ribosome biogenesis defect elicited by the mutation of MDN1 leads to early flowering by affecting multiple flowering regulation pathways.