Fusarium sacchari, a key pathogen of sugarcane, is responsible for the Pokkah boeng disease (PBD) in China. The 14-3-3 proteins have been implicated in critical developmental processes, including dimorphic transition, signal transduction, and carbon metabolism in various phytopathogenic fungi. However, their roles are poorly understood in F. sacchari. This study focused on the characterization of two 14-3-3 protein-encoding genes, FsBmh1 and FsBmh2, within F. sacchari. Both genes were found to be expressed during the vegetative growth stage, yet FsBmh1 was repressed at the sporulation stage in vitro. To elucidate the functions of these genes, the deletion mutants ΔFsBmh1 and ΔFsBmh2 were generated. The ΔFsBmh2 exhibited more pronounced phenotypic defects, such as impaired hyphal branching, septation, conidiation, spore germination, and colony growth, compared to the ΔFsBmh1. Notably, both knockout mutants showed a reduction in virulence, with transcriptome analysis revealing changes associated with the observed phenotypes. To further investigate the functional interplay between FsBmh1 and FsBmh2, we constructed and analyzed mutants with combined deletion and silencing (ΔFsBmh/siFsBmh) as well as overexpression (O-FsBmh). The combinations of ΔFsBmh1/siFsBmh2 or ΔFsBmh2/siFsBmh1 displayed more severe phenotypes than those with single allele deletions, suggesting a functional redundancy between the two 14-3-3 proteins. Yeast two-hybrid (Y2H) assays identified 20 proteins with pivotal roles in primary metabolism or diverse biological functions, 12 of which interacted with both FsBmh1 and FsBmh2. Three proteins were specifically associated with FsBmh1, while five interacted exclusively with FsBmh2. In summary, this research provides novel insights into the roles of FsBmh1 and FsBmh2 in F. sacchari and highlights potential targets for PBD management through the modulation of FsBmh functions.

The body is the very basis of children’s self-growth and their understanding of the world. However, children’s body experiences of growing up have rarely been studied. This paper uses a hermeneutic phenomenological approach to study the body experience of 35 kindergarten children aged 5–6 from Nanjing, China. We found that children’s body experiences can be grouped into two themes: the experience of body through physical changes, that is, children’s experience of their physical changes; and the experience of body through actions, that is, children’s experience of using their bodies to learn different skills and knowledge. Children’s body experiences are multi-dimensional, ambivalent, and socially interactive throughout different events growing up. Even the same event involves multiple and contradictory experiences, which are influenced by both internal and external sources. Suggestions are discussed to address the problem of children’s body experiences being neglected by adults.

In a survey of mycoviruses in Fusarium species that cause sugarcane Pokkah boeng disease, twelve Fusarium strains from three Fusarium species (F. sacchari, F. andiyazi, and F. solani) were found to contain Fusarium sacchari hypovirus 1 (FsHV1), which we reported previously. The genomes of these variants range from 13,966 to 13,983 nucleotides, with 98.6% to 99.9% nucleotide sequence identity and 98.70% to 99.9% protein sequence similarity. Phylogenetic analysis placed these FsHV1 variants within the Alphahypovirus cluster of Hypoviridae. Intriguingly, no clear correlation was found between the geographic origin and host specificity of these viral variants. Additionally, six out of the twelve variants displayed segmental deletions of 1.5 to 1.8 kilobases, suggesting the existence of defective viral dsRNA. The presence of defective viral dsRNA led to a two-thirds reduction in the dsRNA of the wild-type viral genome, yet a tenfold increase in the total viral dsRNA content. To standardize virulence across natural strains, all FsHV1 strains were transferred into a single, virus-free Fusarium recipient strain, FZ06-VF, via mycelial fusion. Strains of Fusarium carrying FsHV1 exhibited suppressed pigment synthesis, diminished microspore production, and a marked decrease in virulence. Inoculation tests revealed varying capacities among different FsHV1 variants to modulate fungal virulence, with the strain harboring the FsHV1-FSA1 showing the lowest virulence, with a disease severity index (DSI) of 3.33, and the FsHV1-FS1 the highest (DSI = 17.66). The identification of highly virulent FsHV1 variants holds promise for the development of biocontrol agents for Pokkah boeng management.

Fusarium sacchari , the causal agent of pokkah boeng disease (PBD), is a globally devastating pathogen of sugarcane that causes substantial economic losses. During infection, the fungus employs elicitors to induce necrosis in plant tissues, thereby enhancing pathogen fitness. However, the key elicitors in F. sacchari and the mechanism by which plants recognize them remain unclear. Here, we identified a predicted glycosylated phosphatidylinositol (GPI)‐anchored protein FsEcm33 as an elicitor that activates plant immunity. FsEcm33 is perceived in the apoplast of Nicotiana benthamiana by the receptor‐like protein NbRE02 and induces cell death in a manner that requires the co‐receptors NbBAK1 and NbSOBIR1. Purified FsEcm33 triggers basal immune responses in N. benthamiana and enhances disease resistance in multiple plant species, including sugarcane, rice, wheat, and star anise. In F. sacchari , FsEcm33 localizes to the cell surface, where its recognition by the host limits pathogen colonization. Notably, FsEcm33 specifically interacts with a 14‐3‐3 protein, FsBmh1, which reduces its accumulation at the fungal cell surface, suggesting a spatial sequestration mechanism that helps F. sacchari evade host immunity. Together, these findings establish FsEcm33 as a cell‐surface elicitor perceived by NbRE02 and reveal an evolutionary strategy in which FsBmh1 sequesters FsEcm33 to evade host recognition and facilitate infection in F. sacchari .

Fusarium sacchari causes devastating Sugarcane Pokkah Boeng Disease by infecting tissues through conidia that enter via micro-wounds or stomata on the leaf surface, making conidial germination a critical step in its pathogenicity. Here, we identified a trehalase, FsTreA, which contains not only the essential trehalase structural domain characteristic of neutral trehalases but also features an N-terminal signal peptide. FsTreA exhibits the highest transcriptional level among all trehalases during conidial germination. Disruption of FsTreA significantly elevated intracellular trehalose accumulation in conidia, confirming its role in intracellular mobilization. However, ΔFsTreA showed accelerated trehalose mobilization rates during germination, coinciding with enhanced conidial germination, and increased conidial yield. This was attributed to functional compensation by two other trehalases, FsNth1 and FsAth1. Furthermore, we found that FsTreA predominantly localizes to the cell surface and possesses the ability to mobilize extracellular trehalose. Moreover, the virulence of FsTreA mutant strain was positively correlated with the capability for extracellular trehalose mobilization. In conclusion, our results demonstrate that the bifunctional trehalase FsTreA coordinates intracellular and extracellular trehalose utilization to modulate virulence in F. sacchari . IMPORTANCE: Sugarcane Pokkah Boeng Disease, caused by Fusarium sacchari , poses a severe threat to global sugarcane production. This study represents the first identification of the bifunctional trehalase FsTreA in F. sacchari , which breaks the traditional dichotomous classification framework of traditional fungal trehalases. FsTreA harbors both the GH37 catalytic domain characteristic of neutral trehalases and an N-terminal signal peptide conferring the secretory trait of acid trehalases. This enzyme participates in intracellular trehalose mobilization and is simultaneously secreted extracellularly to hijack host-derived trehalose as a carbon source, constituting a distinctive infection strategy that provides new insights into host-pathogen interaction mechanisms. These findings advance the theoretical understanding of fungal metabolic regulation, holding significant scientific and practical value for safeguarding the security of the global sugarcane industry.