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The association of MAPT (Tau) with various tauopathies and other neurological disorders has long been established. However, the role of microtubule-associated protein Tau (MAPT) expression in brain cancer is largely unknown. To determine whether MAPT expression is related to low-grade glioma (LGG) survival rates, RNASeq data representing samples from the Cancer Genome Atlas (TCGA) were assessed. Results revealed that high expression of the MAPT gene is very strongly associated with increased overall and disease-free survival in LGG but not in breast cancer or melanoma. No such association was apparent for either amyloid precursor protein or α-synuclein gene expression. The expression levels of particular apoptosis- and pro-proliferative-effector genes were consistent with the Tau-associated increased survival rates. It has been well established that the Tau protein plays a neurodegenerative role, and in this study we identified, for the first time, a potential cell apoptosis function that Tau may play in cancers of the central nervous system.

Background Many plant-pathogenic fungi have a tendency towards genome size expansion, mostly driven by increasing content of transposable elements (TEs). Through comparative and evolutionary genomics, five members of the Leptosphaeria maculans - Leptosphaeria biglobosa species complex (class Dothideomycetes , order Pleosporales ), having different host ranges and pathogenic abilities towards cruciferous plants, were studied to infer the role of TEs on genome shaping, speciation, and on the rise of better adapted pathogens. Results L. maculans ‘brassicae’, the most damaging species on oilseed rape, is the only member of the species complex to have a TE-invaded genome (32.5%) compared to the other members genomes (<4%). These TEs had an impact at the structural level by creating large TE-rich regions and are suspected to have been instrumental in chromosomal rearrangements possibly leading to speciation. TEs, associated with species-specific genes involved in disease process, also possibly had an incidence on evolution of pathogenicity by promoting translocations of effector genes to highly dynamic regions and thus tuning the regulation of effector gene expression in planta . Conclusions Invasion of L. maculans ‘brassicae’ genome by TEs followed by bursts of TE activity allowed this species to evolve and to better adapt to its host, making this genome species a peculiarity within its own species complex as well as in the Pleosporales lineage.

Main conclusionMi-msp10 and Mi-msp23 effector genes play a significant role during Meloidogyne incognita parasitism on Arabidopsis roots. The role of these genes was confirmed by demonstrating the decrease of the level of susceptibility of Arabidopsis by the silencing of Mi-msp10 and Mi-msp23 genes using HD-RNAi technology.Root-knot nematodes (RKNs) are the most damaging pathogens severely affecting global food production. The sustainable options to minimize menace of nematode populations through economically feasible measures are limited. Thus, the development of innovative and target-specific strategies that aid in their management is imperative. RNAi technology has emerged as a sustainable and target-specific alternative to control phytonematodes. Here, we characterized two novel subventral gland and dorsal gland-specific effectors, Mi-msp10 and Mi-msp23, to determine their potential effectiveness in controlling M. incognita. Comparative developmental profiling using qRT-PCR revealed higher expression of both effectors in the adult nematode female. Furthermore, functional evaluation of Mi-msp10 and Mi-msp23 dsRNA cassettes was performed using host-delivered RNAi (HD-RNAi) in Arabidopsis. The transgenic lines were examined against M. incognita, and the phenotypic effect of HD-RNAi was evident with a 61% and 51% reduction in gall formation in the Mi-msp10 and Mi-msp23 RNAi lines, respectively. A significant drop in the nematode adult females by 59% for Mi-msp10 and 49% for Mi-msp23-RNAi lines was observed. Similarly, production in egg masses decreased significantly by 76% (Mi-msp10) and 60% (Mi-msp23) for the RNAi lines, which eventually decreased the reproductive factor by 92% and 75%, respectively. The gene expression analysis showed a significant decrease in the transcript level by up to 72% (Mi-msp10) and 66% (Mi-msp23) in M. incognita females feeding on RNAi lines, providing further evidence of effective gene silencing. Overall, our findings provide useful information and support further development of RNAi-based strategies to control M. incognita.

Background Fungal pathogens are major contributors to global losses of crop yields. Despite large-scale efforts to develop fungicides and resistant plant genotypes, disease outbreaks still pose severe risks to food security due to fungicide resistance and high adaptability of fungal pathogens. Genetic mechanisms behind the acquisition of resistance and renewed virulence have been uncovered by genome sequencing, especially of pathogens of main crops targeted by major control programs. Here, we investigate the use of comparative genomics of historical isolates to investigate how the wider community of fungal plant pathogens evolved during agricultural intensification. Results We analysed historical cryopreserved fungal isolates from three species that were collected in the UK between 1950 and 2000. Comparative genomics of 32 genomes was used to identify variable genome regions that represent putative targets of strong selection during this period, focusing especially on targets of fungicides and putative effector genes that might underpin changes in virulence. Using methods suitable for isolate rather than population sampling, we found evidence of rapid changes in single nucleotide polymorphism frequency in a suite of genes involved in pathogenesis, which overlapped partly between two of the species. We also found turnover in effector gene content in the UK during the period, but generally conserved evolution of fungicide target genes. Sample time and host explained similar amounts of variation in both single nucleotide polymorphism (SNP) changes and variation in effector gene content. Conclusions The described approach could be scaled up in the future to reconstruct the evolution of hundreds of species and samples held in historical fungal collections worldwide throughout the course of the Green Revolution.

Leptosphaeria maculans is a phytopathogenic fungus responsible for stem canker on Brassica napus. Its infectious cycle goes through an early phase of leaf infection and a late phase of colonisation and infection of the stem. The disease is mainly controlled by plant genetic resistances targeting a limited set of early fungal effector genes overexpressed during leaf infection and located in dynamic repeat‐rich genomic regions. Thus, these resistances can be rapidly overcome by the pathogen. To find new sources of resistance, we focused on late effector genes, expressed during stem infection and located in gene‐rich regions. A previous study revealed a quantitative resistance in the stem, partly relying on a gene‐for‐gene interaction with a late effector gene. In this study, we deciphered whether all late effector genes shared the same genomic and evolutionary characteristics and if they could be more stable than early effector genes, rendering the resistance they trigger more durable. In addition, as previous studies highlighted new criteria for selecting late effectors and suggested B. napus semi‐winter genotypes as an interesting genetic pool for uncovering resistance sources, we selected six new late effector gene candidates and screened an enlarged panel of semi‐winter genotypes. We revealed that early and late effector genes diverged for most of their genomic characteristics, supporting the hypothesis of late effector genes being more conserved. Moreover, we revealed new resistance sources to late effector genes, almost all belonging to the semi‐winter genetic pool, validating their importance to uncover new resistance sources. To uncover new durable resistance sources to Leptosphaeria maculans in Brassica napus, we targeted late effector genes, located in conserved genomic regions and overexpressed during stem infection.

Core promoter types differ in the extent to which RNA polymerase II (Pol II) pauses after initiation, but how this affects their tissue‐specific gene expression characteristics is not well understood. While promoters with Pol II pausing elements are active throughout development, TATA promoters are highly active in differentiated tissues. We therefore used a genomics approach on late‐stage Drosophila embryos to analyze the properties of promoter types. Using tissue‐specific Pol II ChIP‐seq, we found that paused promoters have high levels of paused Pol II throughout the embryo, even in tissues where the gene is not expressed, while TATA promoters only show Pol II occupancy when the gene is active. The promoter types are associated with different chromatin accessibility in ATAC‐seq data and have different expression characteristics in single‐cell RNA‐seq data. The two promoter types may therefore be optimized for different properties: paused promoters show more consistent expression when active, while TATA promoters have lower background expression when inactive. We propose that tissue‐specific genes have evolved to use two different strategies for their differential expression across tissues. SYNOPSIS This study characterizes expression properties of different promoter types of effector genes in late‐stage Drosophila embryos, using scRNA‐seq combined with profiles of Pol II occupancy, chromatin accessibility and nucleosome occupancy. Paused promoters with high levels of Pol II pausing throughout the embryo have low expression variability but high background expression. TATA promoters with tissue‐specific Pol II recruitment and low chromatin accessibility have low background expression but high expression variability. No promoter type shows both low background expression and low expression variability, suggesting a tradeoff between these characteristics. Graphical Abstract This study characterizes expression properties of different promoter types of effector genes in late‐stage Drosophila embryos, using scRNA‐seq combined with profiles of Pol II occupancy, chromatin accessibility and nucleosome occupancy.

Many bacterial diseases of plants depend on the interaction of type III effector genes of the pathogen and disease-susceptibility genes of the host. The host susceptibility genes are largely unknown. Here, we show that expression of the rice gene Os8N3, a member of the MtN3 gene family from plants and animals, is elevated upon infection by Xanthomonas oryzae pv. oryzae strain PXO99A and depends on the type III effector gene pthXo1. Os8N3 resides near xa13, and PXO99A failed to induce Os8N3 in rice lines with xa13. Silencing of Os8N3 by inhibitory RNA produced plants that were resistant to infection by strain PXO99A yet remained susceptible to other strains of the pathogen. The effector gene avrXa7 from strain PXO86 enabled PXO99A compatibility on either xa13- or Os8N3-silenced plants. The findings indicate that Os8N3 is a host susceptibility gene for bacterial blight targeted by the type III effector PthXo1. The results support the hypothesis that X. oryzae pv. oryzae commandeers the regulation of otherwise developmentally regulated host genes to induce a state of disease susceptibility. Furthermore, the results support a model in which the pathogen induces disease susceptibility in a gene-for-gene manner.

Summary The ascomycete fungus Magnaporthe oryzae is a hemibiotrophic pathogen that causes rice blast disease. Magnaporthe oryzae infects rice leaves, stems and panicles, and induces severe reductions in yield. Effector proteins secreted by M. oryzae in planta are thought to be involved its virulence activity. Here, using RNA‐sequencing (RNA‐Seq), we generated transcriptome data for M. oryzae isolate Ina168 during the initial stages of infection. We prepared samples from conidia (the inoculum) and from peeled epidermal cotyledon tissue of susceptible barley Hordeum vulgare ‘Nigrate’ at 12, 24, 36 and 48 hours post‐inoculation (hpi). We also generated a draft genome sequence of M. oryzae isolate Ina168 and used it as a reference for mapping the RNA‐Seq reads. Gene expression profiling across all stages of M. oryzae infection revealed 1728 putative secreted effector protein genes. We selected seven such genes that were strongly up‐regulated at 12 hpi and down‐regulated at 24 or 36 hpi and performed gene knockout analysis to determine their roles in pathogenicity. Knockout of MoSVP, encoding a small putative secreted protein with a hydrophobic surface binding protein A domain, resulted in a reduction in pathogenicity, suggesting that MoSVP is a novel virulence effector of M. oryzae.

Effectors are secreted by plant-associated microorganisms to modify the host cell physiology. As effectors, the Necrosis- and Ethylene-inducing peptide 1-like proteins (NLPs) are involded in the early phases of plant infection and may trigger host immune responses. Corynespora cassiicola is a polyphagous plant pathogen that causes target spot on many agriculturally important crops. Using genome assembly, gene prediction, and proteome annotation tools, we retrieved 135 NLP-encoding genes from proteomes of 44 isolates. We explored the evolutionary history of NLPs using Bayesian phylogeny, gene genealogies, and selection analyses. We accessed the expression profiles of the NLP genes during the early phase of C. cassiicola –soybean interaction. Three NLP putative-effector genes (Cc_NLP1.1, Cc_NLP1.2A, and Cc_NLP1.2B) were maintained in the genomes of all isolates tested. An NLP putative-non-effector gene (Cc_NLP1.3) was found in three isolates that had been originally obtained from soybean. Putative-effector NLPs were under different selective constraints: Cc_NLP1.1 was under stronger selective pressure, while Cc_NLP1.2A was under a more relaxed constraint. Meanwhile, Cc_NLP1.2B likely evolved under either positive or balancing selection. Despite highly divergent, the putative-effector NLPs maintain conserved the residues necessary to trigger plant immune responses, suggesting they are potentially functional. Only the Cc_NLP1.1 putative-effector gene was significantly expressed at the early hours of soybean colonization, while Cc_NLP1.2A and Cc_NLP1.2B showed much lower levels of gene expression.

The importance of segmental duplications and copy number variants as a source of genetic and phenotypic variation is gaining greater appreciation, in a variety of organisms. Now, we have identified the Phytophthora sojae avirulence genes Avr1a and Avr3a and demonstrate how each of these Avr genes display copy number variation in different strains of P. sojae. The Avr1a locus is a tandem array of four near-identical copies of a 5.2 kb DNA segment. Two copies encoding Avr1a are deleted in some P. sojae strains, causing changes in virulence. In other P. sojae strains, differences in transcription of Avr1a result in gain of virulence. For Avr3a, there are four copies or one copy of this gene, depending on the P. sojae strain. In P. sojae strains with multiple copies of Avr3a, this gene occurs within a 10.8 kb segmental duplication that includes four other genes. Transcriptional differences of the Avr3a gene among P. sojae strains cause changes in virulence. To determine the extent of duplication within the superfamily of secreted proteins that includes Avr1a and Avr3a, predicted RXLR effector genes from the P. sojae and the P. ramorum genomes were compared by counting trace file matches from whole genome shotgun sequences. The results indicate that multiple, near-identical copies of RXLR effector genes are prevalent in oomycete genomes. We propose that multiple copies of particular RXLR effectors may contribute to pathogen fitness. However, recognition of these effectors by plant immune systems results in selection for pathogen strains with deleted or transcriptionally silenced gene copies.