Background: Soil salinity is a primary factor limiting soybean (Glycine max) productivity. Breeding soybean for tolerance to high salt conditions is therefore critical for increasing yield. To explore the molecular mechanism of soybean responses to salt stress, we performed a comparative transcriptome time-series analysis of root samples collected from two soybean cultivars with contrasting salt sensitivity. Results: The salt-tolerant cultivar ‘Qi Huang No.34’ (QH34) showed more differential expression of genes than the salt-sensitive cultivar ‘Dong Nong No.50’ (DN50). We identified 17,477 genes responsive to salt stress, of which 6644 exhibited distinct expression differences between the two soybean cultivars. We constructed the corresponding co-expression network and performed Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. The results suggested that phytohormone signaling, oxidoreduction, phenylpropanoid biosynthesis, the mitogen-activated protein kinase pathway and ribosome metabolism may play crucial roles in response to salt stress. Conclusions: Our comparative analysis offers a comprehensive understanding of the genes involved in responding to salt stress and maintaining cell homeostasis in soybean. The regulatory gene networks constructed here also provide valuable molecular resources for future functional studies and breeding of soybean with improved tolerance to salinity.

Background: Anastomosis group 1 IA (AG1-IA) of Rhizoctonia solani is the major agent of banded leaf and sheath blight (BLSB) disease that causes severe yield loss in many worldwide crops. MicroRNAs (miRNAs) are ~ 22 nt non-coding RNAs that negatively regulate gene expression levels by mRNA degradation or translation inhibition. A better understanding of miRNA function during AG1-IA infection can expedite to elucidate the molecular mechanisms of fungi-host interactions. Results: In this study, we sequenced three small RNA libraries obtained from the mycelium of AG1-IA isolate, non-infected maize sheath and mixed maize sheath 3 days after inoculation. In total, 137 conserved and 34 novel microRNA-like small RNAs (milRNAs) were identified from the pathogen. Among these, one novel and 17 conserved milRNAs were identified as potential virulence-associated (VA) milRNAs. Subsequently, the prediction of target genes for these milRNAs was performed in both AG1-IA and maize, while functional annotation of these targets suggested a link to pathogenesis-related biological processes. Further, expression patterns of these virulence-associated milRNAs demonstrated that theyparticipate in the virulence of AG1-IA. Finally, regulation of one maize targeting gene, GRMZM2G412674 for Rhi-milRNA-9829-5p, was validated by dual-luciferase assay and identified to play a positive role in BLSB resistance in two maize mutants. These results suggest the global differentially expressed milRNAs of R. solani AG1-IA that participate in the regulation of target genes in both AG1-IA and maize to reinforce its pathogenicity. Conclusions: Our data have provided a comprehensive overview of the VA-milRNAs of R. solani and identified that they are probably the virulence factors by directly interfered in host targeting genes. These results offer new insights on the molecular mechanisms of R.solani-maize interactions during the process of infection.

Mesocotyl elongation is the key determinant of deep-sowing tolerance in maize. Sowing at an appropriate depth allows the seedling to exploit water and nutrients stored in deeper soil layers, thereby enhancing its ability to withstand drought and other abiotic stresses. Mesocotyl elongation is regulated by the phytohormones brassinosteroid (BR), auxin (IAA), gibberellin (GA), and reactive oxygen species (ROS). However, whether and how BR coordinates IAA, GA, and ROS to control mesocotyl elongation in maize remains unclear. Here, we demonstrated that BRs orchestrate ROS, IAA, and GA signaling to remodel cell-wall metabolism in mesocotyl cells, promote cell elongation, and, consequently, strengthen deep-sowing tolerance. BR promoted mesocotyl elongation through multiple routes: (1) decreasing the contents of cell-wall components (hemicellulose, cellulose, and pectin); (2) activating cell-wall-loosening enzymes (cellulase, pectinase, and acidic xylanase); and (3) disturbing ROS homeostasis by elevating superoxide dismutase (SOD) activity. Combined treatments of BR with either IAA or GA further enhanced mesocotyl elongation in a concentration-dependent manner. In deep-sowing trials (15 cm), application of BR alone or in combination with IAA or GA markedly increased mesocotyl length and emergence rate, thereby improving deep-sowing tolerance. Our work indicated that BR integrated ROS, IAA, and GA signals to restructure the cell wall and derived mesocotyl cell elongation, providing both theoretical insights and practical strategies for breeding maize varieties with enhanced deep-sowing tolerance.