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.

Genetic diversity is a cornerstone of crop improvement, However, cultivated soybean (Glycine max) has undergone several genetic bottlenecks, including domestication in China, the introduction of landraces to other areas of the world and, latterly, selective breeding, leading to low genetic diversity the poses a major obstacle to soybean improvement. By contrast, there remains a relatively high level of genetic diversity in soybean’s wild relatives, especially the perennial soybeans (Glycine subgenus Glycine), which could serve as potential gene pools for improving soybean cultivars. Wild soybeans are phylogenetically diversified and adapted to various habitats, harboring resistance to various biotic and abiotic stresses. Advances in genome and transcriptome sequencing enable alleles associated with desirable traits that were lost during domestication of soybean to be discovered in wild soybean. The collection and conservation of soybean wild relatives and the dissection of their genomic features will accelerate soybean breeding and facilitate sustainable agriculture and food production.

Unusually low temperatures caused by global climate change adversely affect rice production. Sensing cold to trigger signal network is a key base for improvement of chilling tolerance trait. Here, we report that Oryza sativa Calreticulin 3 (OsCRT3) localized at the endoplasmic reticulum (ER) exhibits conformational changes under cold stress, thereby enhancing its interaction with CBL‐interacting protein kinase 7 (OsCIPK7) to sense cold. Phenotypic analyses of OsCRT3 knock‐out mutants and transgenic overexpression lines demonstrate that OsCRT3 is a positive regulator in chilling tolerance. OsCRT3 localizes at the ER and mediates increases in cytosolic calcium levels under cold stress. Notably, cold stress triggers secondary structural changes of OsCRT3 and enhances its binding affinity with OsCIPK7, which finally boosts its kinase activity. Moreover, Calcineurin B‐like protein 7 (OsCBL7) and OsCBL8 interact with OsCIPK7 specifically on the plasma membrane. Taken together, our results thus identify a cold‐sensing mechanism that simultaneously conveys cold‐induced protein conformational change, enhances kinase activity, and Ca²⁺ signal generation to facilitate chilling tolerance in rice.

While the genetic regulation of nodule formation has been well explored, the molecular mechanisms by which abiotic stresses, such as salt stress, impede nodule formation remain largely elusive. Here, we identify four APETALA2/Ethylene Responsive Factor (AP2/ERF) transcription factors, GmERF13s, that are induced by salt stress and play key roles in salt-repressed nodulation. Loss of GmERF13 function increases nodule density, while its overexpression suppresses nodulation. Moreover, salt stress-inhibited nodule formation is greatly attenuated in GmERF13 loss-of-function mutants, whereas it becomes more pronounced when GmERF13 is overexpressed. Furthermore, GmERF13s can interact with Lateral Organ Boundaries Domain 16 (GmLBD16a), which attenuates GmLBD16a’s binding capacity on Expansin17c (GmEXP17c) promoter. Additionally, salt-induced GmERF13s expression relies on abscisic acid signaling, with direct promotion facilitated by GmABI5, illustrating their direct involvement in enhancing GmERF13s expression. Collectively, our study reveals a molecular mechanism by which salt stress impedes nodulation through the GmERF13-GmLBD16a-GmEXP17 module in soybean.