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• The smut fungus Sporisorium scitamineum causes the most prevalent disease on sugarcane. The mechanism of its pathogenesis, especially the functions and host targets of its effector proteins, are unknown. • In order to identify putative effectors involving in S. scitamineum infection, a weighted gene co-expression network analysis was conducted based on the transcriptome profiles of both smut fungus and sugarcane using a customized microarray. A smut effector gene, termed SsPele1, showed strong co-expression with sugarcane PLANT ELICITOR PEPTIDE RECEPTOR1 (ScPEPR1), which encodes a receptor like kinase for perception of plant elicitor peptide1 (ScPep1). The relationship between SsPele1 and ScPEPR1, and the biological function of SsPele1 were characterized in this study. • The SsPele1 C-terminus contains a plant elicitor peptide-like motif, by which SsPele1 interacts strongly with ScPEPR1. Strikingly, the perception of ScPep1 on ScPEPR1 is competed by SsPele1 association, leading to the suppression of ScPEPR1-mediated immune responses. Moreover, the Ustilago maydis effector UmPele1, an ortholog of SsPele1, promotes fungal virulence using the same strategy. • This study reveals a novel strategy by which a fungal effector can mimic the plant elicitor peptide to complete its perception and attenuate receptor-activated immunity.

Background Peanut smut is a disease caused by the fungus Thecaphora frezii Carranza & Lindquist to which most commercial cultivars in South America are highly susceptible. It is responsible for severely decreased yield and no effective chemical treatment is available to date. However, smut resistance has been identified in wild Arachis species and further transferred to peanut elite cultivars. To identify the genome regions conferring smut resistance within a tetraploid genetic background, this study evaluated a RIL population {susceptible Arachis hypogaea subsp. hypogaea (JS17304-7-B) × resistant synthetic amphidiploid (JS1806) [ A. correntina (K 11905) ×  A. cardenasii (KSSc 36015)] ×  A. batizocoi (K 9484) 4× } segregating for the trait. Results A SNP based genetic map arranged into 21 linkage groups belonging to the 20 peanut chromosomes was constructed with 1819 markers, spanning a genetic distance of 2531.81 cM. Two consistent quantitative trait loci (QTLs) were identified qSmIA08 and qSmIA02/B02 , located on chromosome A08 and A02/B02, respectively. The QTL qSmIA08 at 15.20 cM/5.03 Mbp explained 17.53% of the phenotypic variance, while qSmIA02/B02 at 4.0 cM/3.56 Mbp explained 9.06% of the phenotypic variance. The combined genotypic effects of both QTLs reduced smut incidence by 57% and were stable over the 3 years of evaluation. The genome regions containing the QTLs are rich in genes encoding proteins involved in plant defense, providing new insights into the genetic architecture of peanut smut resistance. Conclusions A major QTL and a minor QTL identified in this study provide new insights into the genetic architecture of peanut smut resistance that may aid in breeding new varieties resistant to peanut smut.

Summary Sugarcane smut is a worldwide fungal disease caused by Sporisorium scitamineum, which seriously jeopardizes the healthy and sustainable development of the sugarcane industry. WRKY transcription factors are actively involved in plant responses to pathogen infection; however, the mechanisms by which WRKY mediates resistance to sugarcane smut remain elusive. Here, we obtained a nucleus‐localized transcription factor ScWRKY2, which was down‐regulated in smut‐resistant but up‐regulated in smut‐susceptible sugarcane cultivars. Overexpression of the ScWRKY2 gene in sugarcane enhanced its sensitivity to smut disease. Besides, an immune‐related gene ScLRR‐RLK, directly regulated by ScWRKY2, was identified through a combination of transcriptome and DNA affinity purification sequencing. Interestingly, ScWRKY2 suppressed the expression of the ScLRR‐RLK gene by binding to the W‐box element in its promoter region. Furthermore, protein–protein interaction assays demonstrated that ScWRKY2 interacted with the ScPsbP protein in the nucleus. Notably, co‐overexpression of ScWRKY2 and ScPsbP enhanced the sensitivity of plants to pathogens by inducing the expression of reactive oxygen species (ROS) scavenging‐related genes. Collectively, our study revealed that ScWRKY2 negatively regulated sugarcane resistance to smut disease by repressing the expression of the ScLRR‐RLK gene, followed by interacting with the chloroplast protein ScPsbP, and thus inducing the expression of ROS scavenging‐related genes to maintain ROS homeostasis. These findings provided a theoretical basis and gene resources for sugarcane disease resistance breeding.

Main ConclusionThe Ustilaginoidea virens –rice pathosystem has been used as a model for flower-infecting fungal pathogens. The molecular biology of the interactions between U. virens and rice, with an emphasis on the attempt to get a deeper comprehension of the false smut fungus's genomes, proteome, host range, and pathogen biology, has been investigated. Meta-QTL analysis was performed to identify potential QTL hotspots for use in marker-assisted breeding.The Rice False Smut (RFS) caused by the fungus Ustilaginoidea virens currently threatens rice cultivators across the globe. RFS infects rice panicles, causing a significant reduction in grain yield. U. virens can also parasitize other hosts though they play only a minor role in its life cycle. Furthermore, because it produces mycotoxins in edible rice grains, it puts both humans and animals at risk of health problems. Although fungicides are used to control the disease, some fungicides have enabled the pathogen to develop resistance, making its management challenging. Several QTLs have been reported but stable gene(s) that confer RFS resistance have not been discovered yet. This review offers a comprehensive overview of the pathogen, its virulence mechanisms, the genome and proteome of U. virens, and its molecular interactions with rice. In addition, information has been compiled on reported resistance QTLs, facilitating the development of a consensus genetic map using meta-QTL analysis for identifying potential QTL hotspots. Finally, this review highlights current developments and trends in U. virens–rice pathosystem research while identifying opportunities for future investigations.

Sugarcane smut caused by Sporisorium scitamineum is one of the most severe fungal diseases worldwide. In this study, a cross was made between a smut-resistant variety YT93-159 and a smut-susceptible variety ROC22, and 312 progenies were obtained. Two bulks of progenies were then constructed, one consisted of 27 highly smut resistant progenies and the other 24 smut susceptible progenies. Total RNAs of the progenies of each bulk, were pooled and subject to bulked segregant RNA-sequence analysis (BSR-Seq). A total of 164.44 Gb clean data containing 2,341,449 SNPs and 64,999 genes were obtained, 7,295 of which were differentially expressed genes (DEGs). These DEGs were mainly enriched in stress-related metabolic pathways, including carbon metabolism, phenylalanine metabolism, plant hormone signal transduction, glutathione metabolism, and plant-pathogen interactions. Besides, 45,946 high-quality, credible SNPs, a 1.27 Mb region at Saccharum spontaneum chromosome Chr5B (68,904,827 to 70,172,982), and 129 candidate genes were identified to be associated with smut resistance. Among them, twenty-four genes, either encoding key enzymes involved in signaling pathways or being transcription factors, were found to be very closely associated with stress resistance. RT-qPCR analysis demonstrated that they played a positive role in smut resistance. Finally, a potential molecular mechanism of sugarcane and S. scitamineum interaction is depicted that activations of MAPK cascade signaling, ROS signaling, Ca 2+ signaling, and PAL metabolic pathway and initiation of the glyoxalase system jointly promote the resistance to S. scitamineum in sugarcane. This study provides potential SNP markers and candidate gene resources for smut resistance breeding in sugarcane.

Ustilago maydis is the causal agent of maize smut disease. During the colonization process, the fungus secretes effector proteins that suppress immune responses and redirect the host metabolism in favor of the pathogen. As effectors play a critical role during plant colonization, their identification and functional characterization are essential to understanding biotrophy and disease.Using biochemical, molecular, and transcriptomic techniques, we performed a functional characterization of the U. maydis effector Jasmonate/Ethylene signaling inducer 1 (Jsi1).Jsi1 interacts with several members of the plant corepressor family Topless/Topless related (TPL/TPR). Jsi1 expression in Zea mays and Arabidopsis thaliana leads to transcriptional induction of the ethylene response factor (ERF) branch of the jasmonate/ethylene (JA/ET) signaling pathway. In A. thaliana, activation of the ERF branch leads to biotrophic susceptibility. Jsi1 likely activates the ERF branch via an EAR (ET-responsive element binding-factor-associated amphiphilic repression) motif, which resembles EAR motifs from plant ERF transcription factors, that interacts with TPL/TPR proteins.EAR-motif-containing effector candidates were identified from different fungal species, including Magnaporthe oryzae, Sporisorium scitamineum, and Sporisorium reilianum. Interaction between plant TPL proteins and these effector candidates from biotrophic and hemibiotrophic fungi indicates the convergent evolution of effectors modulating the TPL/TPR corepressor hub.

Oryza sativa (Rice) is one of the most cultivated staple food crops in India. The crop is affected by Rice False Smut (RFS) caused by Ustilaginoidea virens (UV), which leads to a substantial reduction in the crop yield, and the mycotoxins released pose a health risk. In the present study, bacterial strains were isolated from rhizosphere soil samples collected from the eastern regions of Uttar Pradesh, India. A total of 105 isolates were screened for their antagonistic activity against U. virens and the best four among them were selected and identified using 16S rRNA sequencing. Three isolates were identified as Bacillus subtilis, and one as Bacillus amyloliquefaciens. Additionally, plant growth promoting (PGP) traits such as siderophore production, IAA production, phosphate solubilization, HCN production etc. were assessed. To assess the biocontrol activity and PGP properties in rice a talc-based bioformulation was prepared using bacterial isolates. The control of UV infection was tested on rice variety HKR-126 involving 10 treatments with screened isolates. Enhanced germination was recorded in all bacterial treatments of UV infected seeds. Greenhouse experiments were also carried out to evaluate the biocontrol efficiency until the harvest stage, as well as plant growth in different stages. Collectively, the results suggested that biopriming with talc-based formulations consisting of B. subtilis and B. amyloliquefaciens can serve as an alternative to fungicides to control the severity of UV disease in susceptible rice varieties, along with improving overall plant growth and fitness.

In previous work, we have shown that the transcription factor Nit2 plays a major role in the utilisation of non‐favoured nitrogen sources like nitrate, minor amino acids or nucleobases in saprotrophic sporidia of the basidiomycete corn smut fungus Ustilago maydis. Addressing the knowledge gap regarding how filamentous phytopathogens adapt to nitrogen limitation in the host plant, we employed Δnit2 mutants in the natural FB1 × FB2 background to identify Nit2‐regulated genes during biotrophy. We further investigated the impact of Nit2 on the physiology of leaf galls in nitrogen‐replete versus nitrogen‐limited host plants by comparative RNA‐Seq and metabolic steady state analysis. About one third of the fungal genes affected by Nit2 during biotrophy were involved in nitrogen metabolism and transport, only showing minor overlap to saprotrophic sporidia. Induction of the nitrate assimilation cluster was completely dependent on Nit2 during biotrophy. In nitrogen‐limited host plants, Δnit2 leaf galls accumulated nitrate and showed reduced accumulation of the nitrogen‐rich phloem transport amino acids asparagine and glutamine compared to wild‐type galls. However, total protein content in galls and pathogenicity were comparable between fungal genotypes in both nitrogen regimes. The findings of our physiological and transcriptomic analysis demonstrate that nitrate utilisation is dispensable for U. maydis during biotrophy and can likely be actively compensated by increased utilisation of abundant organic nitrogen sources, like asparagine, GABA and glutamine in a partially Nit2‐dependent fashion. The transcription factor Nit2 of the smut Ustilago maydis controls nitrate utilisation during biotrophy and affects steady state nitrate and amino acid contents in maize leaf galls under nitrogen depletion.

Background The architecture of inflorescence in crops is a key agronomic feature determining grain yield and thus has been a major target trait of cereal domestication. Results In this study, we show that a simple spreading panicle change in rice panicle shape, controlled by the Spreading Panicle 9 ( SPR9) locus, also has a significant impact on the resistance to rice false smut (RFS). Meanwhile, we mapped a novel spr9 mutant gene between markers Indel5-18 and Indel5-22 encompassing a genomic region of 43-kb with six candidate genes. Through gene prediction and cDNA sequencing, we confirmed that LOC_Os05g38520 is the target gene in the spr9 mutant, which encodes 60 S ribosomal protein L36-2. Further analysis showed that the spr9 mutant is caused by a 1 bp deletion in the first exon that resulted in premature termination. Knockout experiments showed that the SPR9 gene is responsible for the spreading panicle phenotype of the spr9 mutant. Interestingly, the spr9 mutant was found to improve resistance to RFS without affecting major agronomic traits. Taken together, our results revealed that the spr9 allele has good application prospects in rice breeding for disease resistance and panicle improvement. Conclusions We report the map-based cloning and functional characterization of SPR9 , which encodes a 60 S ribosomal protein that regulates spreading panicles and affects the resistance to false smut in rice.