Background: Soybean is one of the most important oil crops in the world. The domestication of wild soybean has resulted in significant changes in the seed oil content and seed size of cultivated soybeans. To better understand the molecular mechanisms of seed formation and oil content accumulation, WDD01514 (E1), ZYD00463 (E2), and two extreme progenies (E23 and E171) derived from RILs were used for weighted gene coexpression network analysis (WGCNA) combined with transcriptome analysis. Results: In this study, both seed weight and oil content in E1 and E171 were significantly higher than those in E2 and E23, and 20 DAF and 30 DAF may be key stages of soybean seed oil content accumulation and weight increase. Pathways such as “Photosynthesis”, “Carbon metabolism”, and “Fatty acid metabolism”, were involved in oil content accumulation and grain formation between wild and cultivated soybeans at 20 and 30 DAF according to RNA-seq analysis. A total of 121 oil content accumulation and 189 seed formation candidate genes were screened from differentially expressed genes. WGCNA identified six modules related to seed oil content and seed weight, and 76 candidate genes were screened from modules and network. Among them, 16 genes were used for qRT-PCR and tissue specific expression pattern analysis, and their expression-levels in 33-wild and 23-cultivated soybean varieties were subjected to correlation analysis; some key genes were verified as likely to be involved in oil content accumulation and grain formation. Conclusions: Overall, these results contribute to an understanding of seed lipid metabolism and seed size during seed development, and identify potential functional genes for improving soybean yield and seed oil quantity.

Heat stress caused by global warming requires the development of thermotolerant crops to sustain yield. It is necessary to understand the molecular mechanisms that underlie heat tolerance in plants. Strigolactones (SLs) are a class of carotenoid-derived phytohormones that regulate plant development and responses to abiotic or biotic stresses. Although SL biosynthesis and signaling processes are well established, genes that directly regulate SL biosynthesis have rarely been reported. Here, we report that the MYB-like transcription factor AtMYBS1/AtMYBL, whose gene expression is repressed by heat stress, functions as a negative regulator of heat tolerance by directly inhibiting SL biosynthesis in Arabidopsis. Overexpression of AtMYBS1 led to heat hypersensitivity, whereas atmybs1 mutants displayed increased heat tolerance. Expression of MAX1, a critical enzyme in SL biosynthesis, was induced by heat stress and downregulated in AtMYBS1-overexpression (OE) plants but upregulated in atmybs1 mutants. Overexpression of MAX1 in the AtMYBS1-OE background reversed the heat hypersensitivity of AtMYBS1-OE plants. Loss of MAX1 function in the atmyb1 background reversed the heat-tolerant phenotypes of atmyb1 mutants. Yeast one-hybrid assays, chromatin immunoprecipitation‒qPCR, and transgenic analyses demonstrated that AtMYBS1 directly represses MAX1 expression through the MYB binding site in the MAX1 promoter in vivo. The atmybs1d14 double mutant, like d14 mutants, exhibited hypersensitivity to heat stress, indicating the necessary role of SL signaling in AtMYBS1-regulated heat tolerance. Our findings provide new insights into the regulatory network of SL biosynthesis, facilitating the breeding of heat-tolerant crops to improve crop production in a warming world.

Soybean cyst nematode (SCN) is a serious damaging disease in soybean worldwide. Peking- and PI 88788-type sources of resistance are two most important germplasm used in breeding resistant soybean cultivars against this disease. However, until now, no comparisons of constitutive resistances to soybean cyst nematode between these two types of sources had been conducted, probably due to the influences of different backgrounds. In this study, we used pooled-sample analysis strategy to minimize the influence of different backgrounds and directly compared the molecular mechanisms underlying constitutive resistance to soybean cyst nematode between these two types of sources via transcriptomic and metabolomic profilings. Six resistant soybean accessions that have identical haplotypes as Peking at Rgh1 and Rhg4 loci were pooled to represent Peking-type sources. The PI88788-type and control pools were also constructed in a same way. Through transcriptomic and metabolomics anaylses, differentially expressed genes and metabolites were identified. The molecular pathways involved in the metabolism of toxic metabolites were predicted to play important roles in conferring soybean cyst nematode resistance to soybean. Functions of two resistant candidate genes were confirmed by hairy roots transformation methods in soybean. Our studies can be helpful for soybean scientists to further learn about the molecular mechanism of resistance to soybean cyst nematode in soybean.

The Whirly (WHY) gene family, functioning as transcription factors, plays an essential role in the regulation of plant metabolic responses, which has been demonstrated across multiple species. However, the WHY gene family and its functions in soybean remains unclear. In this paper, we conducted genome-wide screening and identification to characterize the WHY gene family. Seven WHY members were identified and randomly distributed across six chromosomes. The phylogenetic evolutionary tree of WHY genes in soybean and other species was divided into five clades. An in-depth analysis revealed that segmental duplications significantly contributed to the expansion of GmWHYs, and the GmWHY gene members may have experienced evolutionary pressure for purifying selection in soybeans. The analysis of promoter Cis-elements in GmWHYs suggested their potential significance in addressing diverse stress conditions. The expression patterns of GmWHYs exhibited tissue-specific variations throughout the different stages of soybean development. Additionally, six GmWHY genes exhibited different responses to low phosphate stress. These findings will provide a theoretical basis and valuable reference for the future exploration of WHY gene function.