Plants grow on soils that not only provide support for root anchorage but also act as a reservoir of water and nutrients important for plant growth and development. However, environmental factors, such as high salinity, hinder the uptake of nutrients and water from the soil and reduce the quality and productivity of plants. Under high salinity, plants attempt to maintain cellular homeostasis through the production of numerous stress-associated endogenous metabolites that can help mitigate the stress. Both primary and secondary metabolites can significantly contribute to survival and the maintenance of growth and development of plants on saline soils. Existing studies have suggested that seed/plant-priming with exogenous metabolites is a promising approach to increase crop tolerance to salt stress without manipulation of the genome. Recent advancements have also been made in genetic engineering of various metabolic genes involved in regulation of plant responses and protection of the cells during salinity, which have therefore resulted in many more basic and applied studies in both model and crop plants. In this review, we discuss the recent findings of metabolic reprogramming, exogenous treatments with metabolites and genetic engineering of metabolic genes for the improvement of plant salt tolerance.

Sclerotinia sclerotiorum (Lib.) de Bary is a broad host-range fungus that infects an inclusive array of plant species and afflicts significant yield losses globally. Despite being a notorious pathogen, it has an uncomplicated life cycle consisting of either basal infection from myceliogenically germinated sclerotia or aerial infection from ascospores of carpogenically germinated sclerotia. This fungus is unique among necrotrophic pathogens in that it inevitably colonizes aging tissues to initiate an infection, where a saprophytic stage follows the pathogenic phase. The release of cell wall-degrading enzymes, oxalic acid, and effector proteins are considered critical virulence factors necessary for the effective pathogenesis of S. sclerotiorum. Nevertheless, the molecular basis of S. sclerotiorum pathogenesis is still imprecise and remains a topic of continuing research. Previous comprehensive sequencing of the S. sclerotiorum genome has revealed new insights into its genome organization and provided a deeper comprehension of the sophisticated processes involved in its growth, development, and virulence. This review focuses on the genetic and genomic aspects of fungal biology and molecular pathogenicity to summarize current knowledge of the processes utilized by S. sclerotiorum to parasitize its hosts. Understanding the molecular mechanisms regulating the infection process of S. sclerotiorum will contribute to devising strategies for preventing infections caused by this destructive pathogen.

Previous investigations have shown that the SUPPRESSORS OF MAX2 1-LIKE6, 7 and 8 (SMXL6, 7 and 8) proteins redundantly repress strigolactone (SL) signaling in plant growth and development. Recently, a growing body of evidence indicated that SLs positively regulate plant drought resistance through functional analyses of genes involved in SL biosynthesis and positive regulation of SL signaling. However, the functions of the SL-signaling negative regulators SMXL6, 7 and 8 in drought resistance and the associated mechanisms remain elusive. To reveal the functions of these SMXL proteins, we analyzed the drought-resistant phenotype of the triple smxl6,7,8 mutant plants and studied several drought resistance-related traits. Our results showed that the smxl6,7,8 mutant plants were more resistant to drought than wild-type plants. Physiological investigations indicated that the smxl6,7,8 mutant plants exhibited higher leaf surface temperature, reduced cuticle permeability, as well as decreases in drought-induced water loss and cell membrane damage in comparison with wild-type plants. Additionally, smxl6,7,8 mutant plants displayed an increase in anthocyanin biosynthesis during drought, enhanced detoxification capacity and increased sensitivity to abscisic acid in cotyledon opening and growth inhibition assays. A good correlation between the expression levels of some relevant genes and the examined physiological and biochemical traits was observed. Our findings together indicate that the SMXL6, 7 and 8 act as negative regulators of drought resistance, and that disruption of these SMXL genes in crops may provide a novel way to improve their drought resistance.

Verticillium wilt caused by Verticillium dahliae is a serious vascular disease in cotton (Gossypium spp.). V. dahliae induces the expression of the CAROTENOID CLEAVAGE DIOXYGENASE 7 (GauCCD7) gene involved in strigolactone (SL) biosynthesis in Gossypium australe, suggesting a role for SLs in Verticillium wilt resistance. We found that the SL analog rac-GR24 enhanced while the SL biosynthesis inhibitor TIS108 decreased cotton resistance to Verticillium wilt. Knock-down of GbCCD7 and GbCCD8b genes in island cotton (Gossypium barbadense) decreased resistance, whereas overexpression of GbCCD8b in upland cotton (Gossypium hirsutum) increased resistance to Verticillium wilt. Additionally, Arabidopsis (Arabidopsis thaliana) SL mutants defective in CCD7 and CCD8 putative orthologs were susceptible, whereas both Arabidopsis GbCCD7- and GbCCD8b-overexpressing plants were more resistant to Verticillium wilt than wild-type (WT) plants. Transcriptome analyses showed that several genes related to the jasmonic acid (JA)- and abscisic acid (ABA)-signaling pathways, such as MYELOCYTOMATOSIS 2 (GbMYC2) and ABA-INSENSITIVE 5, respectively, were upregulated in the roots of WT cotton plants in responses to rac-GR24 and V. dahliae infection but downregulated in the roots of both GbCCD7- and GbCCD8b-silenced cotton plants. Furthermore, GbMYC2 suppressed the expression of GbCCD7 and GbCCD8b by binding to their promoters, which might regulate the homeostasis of SLs in cotton through a negative feedback loop. We also found that GbCCD7- and GbCCD8b-silenced cotton plants were impaired in V. dahliae-induced reactive oxygen species (ROS) accumulation. Taken together, our results suggest that SLs positively regulate cotton resistance to Verticillium wilt through crosstalk with the JA- and ABA-signaling pathways and by inducing ROS accumulation.