Summary: Symbiotic nodulation is initiated in the roots of legumes in response to low nitrogen and rhizobial signal molecules and is dynamically regulated by a complex regulatory network that coordinates rhizobial infection and nodule organogenesis. It has been shown that the miR156‐SPL module mediates nodulation in legumes; however, conclusive evidence of how this module exerts its function during nodulation remains elusive. Here, we report that the miR156b‐GmSPL9d module regulates symbiotic nodulation by targeting multiple key regulatory genes in the nodulation signalling pathway of soybean. miR156 family members are differentially expressed during nodulation, and miR156b negatively regulates nodulation by mainly targeting soybean SQUAMOSA promoter‐binding protein‐like 9d (GmSPL9d), a positive regulator of soybean nodulation. GmSPL9d directly binds to the miR172c promoter and activates its expression, suggesting a conserved role of GmSPL9d. Furthermore, GmSPL9d was coexpressed with the soybean nodulation marker genes nodule inception a (GmNINa) and GmENOD40‐1 during nodule formation and development. Intriguingly, GmSPL9d can bind to the promoters of GmNINa and GmENOD40‐1 and regulate their expression. Our data demonstrate that the miR156b‐GmSPL9d module acts as an upstream master regulator of soybean nodulation, which coordinates multiple marker genes involved in soybean nodulation.

Symbiotic nitrogen fixation boosts legume growth and production in nitrogen-poor soils. It has long been assumed that fixed nitrogen increases reproductive success, but until now, the regulatory mechanism was unknown. Here, we report a symbiotic flowering pathway that couples symbiotic and nutrient signals to the flowering induction pathway in legumes. We show that the symbiotic microRNA–microRNA172c (miR172c) and fixed nitrogen systemically and synergistically convey symbiotic and nutritional cues from roots to leaves to promote soybean ( Glycine max ) flowering. The combinations of symbiotic miR172c and local miR172c elicited by fixed nitrogen and development in leaves activate florigen-encoding FLOWERING LOCUS T ( FT ) homologs ( GmFT2a/5a ) by repressing TARGET OF EAT1-like 4a ( GmTOE4a ). Thus, FTs trigger reproductive development, which allows legumes to survive and reproduce under low-nitrogen conditions.

Fusarium head blight (FHB) caused by Fusarium graminearum is a worldwide disease which has destructive effects on wheat production, resulting in severe yield reduction and quality deterioration, while FHB-infected wheat grains are toxic to people and animals due to accumulation of fungal toxins. Although impressive progress towards understanding host resistance has been achieved, our knowledge of the mechanism underlying host resistance is still quite limited due to the complexity of wheat–pathogen interactions. In recent years, disease epidemics, the resistance germplasms and components, the genetic mechanism of FHB, and disease management and control, etc., have been well reviewed. However, the resistance mechanism of FHB is quite complex with Type I, II to V resistances. In this review, we focus on the potential resistance mechanisms by linking different resistance types to multi-omics and emphasize the pathways or genes that may play significant roles in the different types of resistance. Deciphering the complicated mechanism of FHB resistance types in wheat at the integral levels based on multi-omics may help discover the genes or pathways that are critical for different FHB resistance, which could then be utilized and manipulated to improve FHB resistance in wheat breeding programs by using transgenic approaches, gene editing, or marker assisted selection strategies.

Fusarium head blight (FHB) caused by Fusarium graminearum not only results in severe yield losses, but also contaminates wheat grains with deoxynivalenol (DON) toxins. Prevention and control of FHB and DON contamination rely mainly on resistant varieties and fungicides. Selenium (Se) is an essential element for humans and animals, and also a beneficial element for plants. In this work, four Se compounds, i.e., sodium selenite (Na₂SeO₃), sodium selenate (Na₂SeO₄), selenomethionine (SeMet) and selenocysteine (SeCys₂), were supplemented in a trichothecene biosynthesis induction (TBI) solid medium at different dosages in in vitro experiments. The four Se compounds at the dosage of 20 mg∙L⁻¹ were sprayed onto wheat spikes immediately after inoculation at anthesis. All four of the Se compounds significantly inhibited the mycelial growth and DON production in the in vitro experiment; however, in planta, their effects on FHB severity and toxin accumulation in grains were compound-dependent. SeMet consistently negatively regulated fungal growth and DON accumulation both in vitro and in planta, which could be a novel and proconsumer strategy for reducing the detriment of wheat FHB disease and DON accumulation.

Fusarium head blight (FHB) caused by Fusarium species is a globally important wheat disease. Host resistance to FHB is composed of multiple mechanisms, including resistance to initial infection (type I), disease spread (type II), toxin accumulation (type III), kernel infection (type IV), and yield loss (type V), of which the last three have been less studied. Traditionally, the Fusarium-damaged kernel rate (FDK; percentage of Fusarium-infected grains) from point- or spray-inoculated experiments was used as the parameter for type IV resistance, which may be problematic because of the influence of type II resistance. Here we propose a new definition for type IV resistance: that is, the resistance against Fusarium infection expressed in wheat grains that have the same chance in contact with the pathogen, under favorable temperature and humidity for infection. Fhb1 confers strong type II resistance, leading to significantly reduced FHB severity and FDK. To investigate the role of Fhb1 in type IV resistance, a pair of near-isogenic lines, R22W (Fhb1 carrier, resistant in terms of type II resistance) and S22V (non-Fhb1, susceptible), along with eight wheat genotypes differing at Fhb1 were inoculated at different grain development stages with Fusarium macrospores both in vivo and in vitro. The in vivo experiments with all florets inoculated demonstrated a significant reduction in thousand kernel weight (TKW) in inoculated grains, regardless of their Fhb1 status and developmental stages. Surprisingly, R22W showed more TKW reduction than S22V, which was supported by the scanning electron microscopy observation that confirmed the more severe degradation of starch granules in R22W grains. The in vitro experiments demonstrated that grains from both R22W and S22V promoted fungal colonization, but no significant difference was found between the two lines. In summary, our results indicated that the proposed type IV evaluation system is effective in determining different grain resistance levels, providing novel tools for FHB resistance breeding. The finding that Fhb1 is not associated with type IV resistance enriches our understanding of this gene.

It has long been known that the gaseous plant hormone ethylene plays a key role in nodulation in legumes. The perception of ethylene by a family of five membrane-localized receptors is necessary to trigger the ethylene signaling pathway, which regulates various biological responses in Arabidopsis. However, a systematic analysis of the ethylene receptors in leguminous plants and their roles in nodule development is lacking. In this study, we performed a characterization of ethylene receptor genes based on the latest Glycine max genome sequence and a public microarray database. Eleven ethylene receptor family genes were identified in soybean through homology searches, and they were divided into two subgroups. Exon–intron analysis showed that the gene structures are highly conserved within each group. Further analysis of their expression patterns showed that these ethylene receptor genes are differentially expressed in various soybean tissues and organs, including functional nodules. Notably, the ethylene receptor genes showed different responses to rhizobial infection and Nod factors, suggesting a possible role for ethylene receptors and ethylene signaling in rhizobia–host cell interactions and nodulation in soybean. Together, these data indicate the functional divergence of ethylene receptor genes in soybean, and that some of these receptors mediate nodulation, including rhizobial infection, nodule development, and nodule functionality. These findings provide a foundation for further elucidation of the molecular mechanism by which the ethylene signaling pathway regulates nodulation in soybean, as well as other legumes.