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The control of powdery mildew disease is one of the main objectives in Mango production. Mango production with superior quality is becoming increasingly challenging due to climate change, which may negatively affect all stages of their development. Recently, Nanotechnology is a promising and rapidly evolving field that could be a very useful tool to raise the efficiency of fungicides. The aim of this study was to evaluate the role of sulfur nanoparticles (SNPs) and reducing the incidence of powdery mildew, improving growth performance and productivity of mango cv. Keitt ( Mangifera indica L.). Four concentrations of SNPs (0, 100, 300, and 500 ppm) were compared to sulfur microform (bulk) at a concentration of 500 ppm. At a private farm on Cairo Alex Desert Road K78, Egypt, foliar spray treatments were administered to an eight-year-old mango cv. Keitt grafted on Sukari rootstock. The experiment was conducted using a randomized complete block design, with each tree receiving a five-liter spray of the solution. The results suggested that the use of 500 ppm concentration of SNPs led to reducing powdery mildew disease incidence by 8.8% but it negatively affected productivity, as it decreased by 27% compared to the control treatment. Whereas 100 ppm concentration of SNPs led to increasing the productivity by 342% compared to the control treatment, reducing powdery mildew disease incidence in mango was recorded at 14.6%. Furthermore, the TSS and vitamin C increased significantly by 16 Brix and 46.3 mg, respectively, in association with decreasing titratable acidity in fruits. In aggregate, our data demonstrated that 100 ppm and 300 ppm of sulfur nanoparticles was more efficient than 500 ppm of sulfur bulk in improving POD and PPO enzyme activity. It is recommended to add SNPs of 100 ppm as foliar spraying three times at 15-day intervals for alleviating the harmful impact of disease on mango trees by improving the enzyme activity, thereby yield, and fruit quality of mango trees exposed to powdery mildew disease.

Background Parasites are able to alter numerous aspects of their hosts’ life history, behaviour and distribution. One central question in parasitology is to determine the degree of impact that parasites have on their hosts. Laboulbeniales (Fungi: Ascomycota) are ectoparasitic fungi of arthropods. Even though these fungi are widely distributed, little is known about their ecology and their possible physiological effects on their hosts. We used a highly specific bat fly-fungi association to assess the effect of these fungal parasites on their dipteran hosts. Methods We collected bat flies (Diptera: Nycteribiidae) belonging to two species, Nycteribia schmidlii and Penicillidia conspicua from their bat host Miniopterus schreibersii (Chiroptera: Miniopteridae). We experimentally tested the effect of infection on the lifespan of bat flies. Results The prevalence of Laboulbeniales fungi was 17.9% in N. schmidlii and 64.8% in P. conspicua . Two fungi species were identified, Arthrorhynchus eucampsipodae and A. nycteribiae , both showing strict host specificity with N. schmidlii and P. conspicua , respectively. We found that fungal infection reduced by half the survival rate of P. conspicua regardless of sex, whereas N. schmidlii was not affected by the infection. Moreover, the intensity of infection showed negative correlation with the lifespan of P. conspicua . Conclusions To our knowledge, this is the first indication that fungal infection can alter bat fly survival and thus may play a significant role in the population dynamics of these bat ectoparasites.

Pathogens utilize multiple types of effectors to modulate plant immunity. Although many apoplastic and cytoplasmic effectors have been reported, nuclear effectors have not been well characterized in fungal pathogens. Here, we characterize two nuclear effectors of the rice blast pathogen Magnaporthe oryzae . Both nuclear effectors are secreted via the biotrophic interfacial complex, translocated into the nuclei of initially penetrated and surrounding cells, and reprogram the expression of immunity-associated genes by binding on effector binding elements in rice. Their expression in transgenic rice causes ambivalent immunity: increased susceptibility to M . oryzae and Xanthomonas oryzae pv. oryzae , hemibiotrophic pathogens, but enhanced resistance to Cochliobolus miyabeanus , a necrotrophic pathogen. Our findings help remedy a significant knowledge deficiency in the mechanism of M . oryzae –rice interactions and underscore how effector-mediated manipulation of plant immunity by one pathogen may also affect the disease severity by other pathogens. Plant pathogens secrete various effectors to manipulate host immunity. Here, Kim et al. describe two Magnaporthe oryzae effectors that translocate into the nuclei of infected rice cells and reprogram expression of immunity-associated genes, increasing susceptibility to hemibiotrophic pathogens.

Disruption of susceptibility ( S ) genes in crops is an attractive breeding strategy for conferring disease resistance 1 , 2 . However, S genes are implicated in many essential biological functions and deletion of these genes typically results in undesired pleiotropic effects 1 . Loss-of-function mutations in one such S gene, Mildew resistance locus O ( MLO ), confers durable and broad-spectrum resistance to powdery mildew in various plant species 2 , 3 . However, mlo- associated resistance is also accompanied by growth penalties and yield losses 3 , 4 , thereby limiting its widespread use in agriculture. Here we describe Tamlo-R32 , a mutant with a 304-kilobase pair targeted deletion in the MLO-B1 locus of wheat that retains crop growth and yields while conferring robust powdery mildew resistance. We show that this deletion results in an altered local chromatin landscape, leading to the ectopic activation of Tonoplast monosaccharide transporter 3 ( TaTMT3B ), and that this activation alleviates growth and yield penalties associated with MLO disruption. Notably, the function of TMT3 is conserved in other plant species such as Arabidopsis thaliana . Moreover, precision genome editing facilitates the rapid introduction of this mlo resistance allele ( Tamlo-R32) into elite wheat varieties. This work demonstrates the ability to stack genetic changes to rescue growth defects caused by recessive alleles, which is critical for developing high-yielding crop varieties with robust and durable disease resistance. Tamlo-R32 , an engineered wheat mutant allele of the Mildew resistance locus O ( MLO ) gene, confers resistance to powdery mildew, retains robust wheat growth, and can be transferred to other agriculturally important wheat varieties.

Microbes typically secrete a plethora of molecules to promote niche colonization. Soil-dwelling microbes are well-known producers of antimicrobials that are exploited to outcompete microbial coinhabitants. Also, plant pathogenic microbes secrete a diversity of molecules into their environment for niche establishment. Upon plant colonization, microbial pathogens secrete so-called effector proteins that promote disease development. While such effectors are typically considered to exclusively act through direct host manipulation, we recently reported that the soil-borne, fungal, xylem-colonizing vascular wilt pathogen Verticillium dahliae exploits effector proteins with antibacterial properties to promote host colonization through the manipulation of beneficial host microbiota. Since fungal evolution preceded land plant evolution, we now speculate that a subset of the pathogen effectors involved in host microbiota manipulation evolved from ancient antimicrobial proteins of terrestrial fungal ancestors that served in microbial competition prior to the evolution of plant pathogenicity. Here, we show that V. dahliae has co-opted an ancient antimicrobial protein as effector, named VdAMP3, for mycobiome manipulation in planta. We show that VdAMP3 is specifically expressed to ward off fungal niche competitors during resting structure formation in senescing mesophyll tissues. Our findings indicate that effector-mediated microbiome manipulation by plant pathogenic microbes extends beyond bacteria and also concerns eukaryotic members of the plant microbiome. Finally, we demonstrate that fungal pathogens can exploit plant microbiome-manipulating effectors in a life stage–specific manner and that a subset of these effectors has evolved from ancient antimicrobial proteins of fungal ancestors that likely originally functioned in manipulation of terrestrial biota.

TALEN-induced mutation of all homologous copies of a gene that represses resistance to an important wheat pathogen confers a trait that has eluded plant breeders for decades. Sequence-specific nucleases have been applied to engineer targeted modifications in polyploid genomes 1 , but simultaneous modification of multiple homoeoalleles has not been reported. Here we use transcription activator–like effector nuclease (TALEN) 2 , 3 and clustered, regularly interspaced, short palindromic repeats (CRISPR)-Cas9 (refs. 4 , 5 ) technologies in hexaploid bread wheat to introduce targeted mutations in the three homoeoalleles that encode MILDEW-RESISTANCE LOCUS (MLO) proteins 6 . Genetic redundancy has prevented evaluation of whether mutation of all three MLO alleles in bread wheat might confer resistance to powdery mildew, a trait not found in natural populations 7 . We show that TALEN-induced mutation of all three TaMLO homoeologs in the same plant confers heritable broad-spectrum resistance to powdery mildew. We further use CRISPR-Cas9 technology to generate transgenic wheat plants that carry mutations in the TaMLO-A1 allele. We also demonstrate the feasibility of engineering targeted DNA insertion in bread wheat through nonhomologous end joining of the double-strand breaks caused by TALENs. Our findings provide a methodological framework to improve polyploid crops.

Transposable elements (TEs) are drivers of genome evolution and affect the expression landscape of the host genome. Stress is a major factor inducing TE activity; however, the regulatory mechanisms underlying de-repression are poorly understood. Plant pathogens are excellent models to dissect the impact of stress on TEs. The process of plant infection induces stress for the pathogen, and virulence factors (i.e., effectors) located in TE-rich regions become expressed. To dissect TE de-repression dynamics and contributions to virulence, we analyzed the TE expression landscape of four strains of the major wheat pathogen Zymoseptoria tritici. We experimentally exposed strains to nutrient starvation and host infection stress. Contrary to expectations, we show that the two distinct conditions induce the expression of different sets of TEs. In particular, the most highly expressed TEs, including miniature inverted-repeat transposable element and long terminal repeat-Gypsy element, show highly distinct de-repression across stress conditions. Both the genomic context of TEs and the genetic background stress (i.e., different strains harboring the same TEs) were major predictors of de-repression under stress. Gene expression profiles under stress varied significantly depending on the proximity to the closest TEs and genomic defenses against TEs were largely ineffective to prevent de-repression. Next, we analyzed the locus encoding the Avr3D1 effector. We show that the insertion and subsequent silencing of TEs in close proximity likely contributed to reduced expression and virulence on a specific wheat cultivar. The complexity of TE responsiveness to stress across genetic backgrounds and genomic locations demonstrates substantial intraspecific genetic variation to control TEs with consequences for virulence.

Powdery mildews are phytopathogens whose growth and reproduction are entirely dependent on living plant cells. The molecular basis of this life-style, obligate biotrophy, remains unknown. We present the genome analysis of barley powdery mildew, Blumeria graminis f.sp. hordei (Blumeria), as well as a comparison with the analysis of two powdery mildews pathogenic on dicotyledonous plants. These genomes display massive retrotransposon proliferation, genome-size expansion, and gene losses. The missing genes encode enzymes of primary and secondary metabolism, carbohydrate-active enzymes, and transporters, probably reflecting their redundancy in an exclusively biotrophic life-style. Among the 248 candidate effectors of pathogenesis identified in the Blumeria genome, very few (less than 10) define a core set conserved in all three mildews, suggesting that most effectors represent species-specific adaptations.

Yield losses caused by fungal pathogens represent a major threat to global food production. One of the most devastating fungal wheat pathogens is Zymoseptoria tritici . Despite the importance of this fungus, the underlying mechanisms of plant–pathogen interactions are poorly understood. Here we present a conceptual framework based on coinfection assays, comparative metabolomics, and microbiome profiling to study the interaction of Z. tritici in susceptible and resistant wheat. We demonstrate that Z. tritici suppresses the production of immune-related metabolites in a susceptible cultivar. Remarkably, this fungus-induced immune suppression spreads within the leaf and even to other leaves, a phenomenon that we term “systemic induced susceptibility”. Using a comparative metabolomics approach, we identify defense-related biosynthetic pathways that are suppressed and induced in susceptible and resistant cultivars, respectively. We show that these fungus-induced changes correlate with changes in the wheat leaf microbiome. Our findings suggest that immune suppression by this hemibiotrophic pathogen impacts specialized plant metabolism, alters its associated microbial communities, and renders wheat vulnerable to further infections. The fungal plant pathogen Zymoseptoria tritici is a major threat to wheat yield. Here Seybold et al. show that Z. tritici can suppress immune responses not only in infected tissue but also on other leaves, a phenomenon termed “systemic induced susceptibility” that is correlated with systemic changes in metabolite accumulation.

Canker caused by ascomycetous Valsa species are among the most destructive diseases of woody plants worldwide. These pathogens are distinct from other pathogens because they only effectively attack tree bark in the field. To unravel the potential adaptation mechanism of bark colonization, we examined the genomes of Valsa mali and Valsa pyri that preferentially infect apple and pear, respectively. We reported the 44.7 and 35.7 Mb genomes of V. mali and V. pyri, respectively. We also identified the potential genomic determinants of wood colonization by comparing them with related cereal pathogens. Both genomes encode a plethora of pathogenicity‐related genes involved in plant cell wall degradation and secondary metabolite biosynthesis. In order to adapt to the nutrient limitation and low pH environment in bark, they seem to employ membrane transporters associated with nitrogen uptake and secrete proteases predominantly with acidic pH optima. Remarkably, both Valsa genomes are especially suited for pectin decomposition, but are limited in lignocellulose and cutin degradation. Besides many similarities, the two genomes show distinct variations in many secondary metabolism gene clusters. Our results show a potential adaptation of Valsa canker pathogens to colonize woody bark. Secondary metabolism gene clusters are probably responsible for this host specificity.