Biology subjects

Vieira, P.

Publications and source records attributed to Vieira, P..

10 recordsLinked to original sources

bioRxiv2025

Genome reannotation and effector candidate identification in Meloidogyne chitwoodi through gland-specific transcriptome analysis

The root-knot nematode (RKN) Meloidogyne chitwoodi is a threat for potato production in the western United States, negatively impacting potato yield and product value. Meloidogyne chitwoodi produce proteins, called effectors, in their esophageal glands that are secreted during parasitism and play integral roles in plant-nematode interactions. Because the esophageal glands are the main effector secretory organ, we performed juvenile gland isolation and gland transcriptome analysis. The data allowed us to improve the M. chitwoodi genome annotation. Additionally, the gland-specific transcriptome data gave us an enrichment of gland-localized genes, which was validated by in situ hybridization. The gland transcriptome analysis led to the identification of 111 effector candidates. One of the effectors, Mc15g003960, which was highly expressed in the pre-parasitic J2 gland tissue, was further characterized. Expression of Mc15g003960 in Arabidopsis resulted in increased galling by M. chitwoodi. However, the ectopic expression of Mc15g003960 in planta did not suppress defense-related callose deposition, suggesting that this effector might be involved in processes other than interfering with plant basal defense responses. Our data shows that using the gland transcriptome, good quality genome annotation and stringent criteria, we can increase the efficiency of effector identification, which can be used to develop more sustainable management tools. Authors summaryThe root-knot nematode Meloidogyne chitwoodi is a major problem for potato farmers in the western U.S., reducing crop yield and quality. These nematodes produce special proteins, called effectors, in their esophageal glands, which help them infect plants. Since these glands are the main source of effectors, we isolated them from juvenile nematodes and analyzed their gene expression. This helped us improve the nematodes genome map and identify genes specific to the glands. From this study, we found 111 potential effector genes. One of them, Mc15g003960, was highly active before the nematode started feeding. When we introduced this gene into Arabidopsis plants, the nematodes caused more damage, but it didnt seem to weaken the plants basic defense system. This suggests Mc15g003960 is not suppressing plant defenses and has a different role in helping the nematode with successful infection. Overall, our approach helped us identify key effectors more efficiently, which could lead to better ways to manage nematode infestations in the future.

molecular biology↗

bioRxiv2024

The SUbventral-Gland master Regulator (SUGR) of nematode virulence

All pathogens must tailor their gene expression to their environment. Therefore, targeting host:parasite biology that regulates these changes in gene expression could open up routes to pathogen control. Here, we show that in the plant-parasitic nematode Heterodera schachtii, host signals (termed effectostimulins) within plant roots activate the master regulator sugr1. SUGR1, then, directly binds effector promoters, and orchestrates their production. Effector production, in turn, facilitates host entry, releasing more effectostimulins. These data show that gene expression during the very earliest stages of parasitism is defined by a feed forward loop for host entry. Importantly, we demonstrate that blocking SUGR1 blocks parasitism, underlining the SUGR1 signalling cascade as a valuable target for crop protection. Given that nematodes also parasitise humans and other animals, the potential impact is broad: disrupting effector production could, in principle, be applied to any pathogen that secrets effectors. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=146 SRC="FIGDIR/small/576598v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@cebedaorg.highwire.dtl.DTLVardef@153fe87org.highwire.dtl.DTLVardef@16b6957org.highwire.dtl.DTLVardef@d0e920_HPS_FORMAT_FIGEXP M_FIG C_FIG

pathology↗

bioRxiv2024

The origin, deployment, and evolution of a plant-parasitic nematode effectorome

Plant-parasitic nematodes constrain global food security. During parasitism, they secrete effectors into the host plant from two types of pharyngeal gland cells. These effectors elicit profound changes in host biology to suppress immunity and establish a unique feeding organ from which the nematode draws nutrition. Despite the importance of effectors in nematode parasitism, there has been no comprehensive identification and characterisation of the effector repertoire of any plant-parasitic nematode. To address this, we advance techniques for gland cell isolation and transcriptional analysis to define a stringent annotation of putative effectors for the cyst nematode Heterodera schachtii at three key life-stages. We define 659 effector gene loci: 293 "known" high-confidence homologs of plant-parasitic nematode effectors, and 366 "novel" effectors with high gland cell expression. In doing so we define a comprehensive "effectorome" of a plant-parasitic nematode. Using this effector definition, we provide the first systems-level understanding of the origin, deployment and evolution of a plant-parasitic nematode effectorome. The robust identification of the comprehensive effector repertoire of a plant-parasitic nematode will underpin our understanding of nematode pathology, and hence, inform strategies for crop protection.

plant biology↗

bioRxiv2023

Cellular insights of beech leaf disease reveal abnormal ectopic cell division of symptomatic interveinal leaf areas

The beech leaf disease nematode, Litylenchus crenatae subsp. mccannii, is recognized as a newly emergent nematode species that causes beech leaf disease (BLD) in beech trees (Fagus spp.) in North America. Changes of leaf morphology induced by BLD can provoke dramatic effects into the leaf architecture and consequently to tree performance and development. The initial symptoms of BLD appear as dark green interveinal banding patterns of the leaf. Despite the fast progression of this disease, the cellular mechanisms leading to the formation of such type of aberrant leaf phenotype remains totally unknown. To understand the cellular basis of BLD, we employed several microscopy approaches to provide an exhaustive characterization of nematode-infected buds and leaves. Histological sections revealed a dramatic cell change composition of these nematode-infected tissues. Diseased bud scale cells were typically hypertrophied and showed a high variability of size. Moreover, while altered cell division had no influence on leaf organogenesis, induction of cell proliferation on young leaf primordia led to a dramatic change in cell layer architecture. Hyperplasia and hypertrophy of the different leaf cell layers, coupled with an abnormal proliferation of chloroplasts specially in the spongy mesophyll cells, resulted in the typical interveinal leaf banding. These discrepancies in leaf cell structure were depicted by an abnormal rate of cellular division of the leaf interveinal areas infected by the nematode, promoting significant increase of cell size and leaf thickness. The formation of symptomatic BLD leaves is therefore orchestrated by distinct cellular processes, to enhance the value of these feeding sites and to improve their nutrition status to the nematode. These results revealed a high specialized mode of parasitism of L. crenatae subsp. mccannii.

cell biology↗

bioRxiv2022

Root-knot nematodes produce functional mimics of tyrosine-sulfated plant peptides

Root-knot nematodes (Meloidogyne spp.) are highly evolved obligate parasites that threaten global food security. These parasites have a remarkable ability to establish elaborate feeding sites in roots, which are their only source of nutrients throughout their life cycle. A wide range of nematode effectors have been implicated in modulation of host pathways for feeding site development. Plants produce a diverse array of peptide hormones including plant peptides containing sulfated tyrosine (PSYs), which promote root growth via cell expansion and proliferation. A sulfated PSY-like peptide RaxX (required for activation of XA21 mediated immunity X) produced by the biotrophic bacterial pathogen (Xanthomonas oryzae pv. oryzae), has been previously shown to contribute to bacterial virulence. Here, we report the identification of genes from root-knot nematodes predicted to encode PSY-like peptides (MigPSYs) with high sequence similarity to both bacterial RaxX and plant PSYs. Sulfated synthetic peptides corresponding to predicted MigPSYs stimulate root growth in Arabidopsis. MigPSY transcript levels are highest early in the infection cycle. Down-regulation of MigPSY gene expression reduces root galling and egg production, suggesting that the MigPSYs serve as nematode virulence factors. Together these results indicate that nematodes and bacteria utilize similar sulfated peptides to hijack plant developmental signaling pathways to facilitate parasitism.

plant biology↗

bioRxiv2021

The spatial network structure of intertidal meiofaunal communities derived from environmental DNA metabarcoding surveys in Northwest Iberia

The identification of the patterns and mechanisms behind species distribution is one of the major challenges in ecology, having also important outcomes for the conservation and management of ecosystems. This is especially true for those components of biodiversity providing essential ecosystem functions and for which standard surveys may underestimate their real taxonomic diversity due to their high degree of cryptic diversity and inherent diagnosis difficulties, such as meiofaunal communities. Environmental DNA (eDNA) metabarcoding may provide a fast and reliable way to refine and scale-up the characterization of biological diversity in complex environmental samples, allowing to bypass such drawbacks and increase the resolution of biodiversity estimates. Moreover, the possibility of integrating eDNA metabarcoding-derived data with tools and methods rooted in network theory would deepen the knowledge of the structuring processes of ecological communities in ways that cannot be predicted from studying individual species/communities in isolation. Here, a sediment eDNA metabarcoding of mitochondrial cytochrome c oxidase I (COI) and the nuclear hypervariable V4 region of the 18S rDNA (18S) was used to reconstruct the spatial networks of intertidal meiofaunal OTUs from three estuaries of North-Western Iberian Peninsula. Null models were used to identify the role of environmental and spatial constraints on the structure of COI- and 18S-derived spatial networks and to characterize the macroecological features of surveyed phyla. Our results show the feasibility of eDNA metabarcoding, not only to capture a fair amount of diversity hard to detect with standard surveys procedures, but also to identify hierarchical spatial structures in intertidal meiofaunal assemblages. This suggests that exclusivity of occurrence rather than pervasiveness appears to be the norm in meiofaunal organisms and that niche-based processes predominantly drive the spatial aggregation and contemporary distribution of meiofaunal phyla within the system.

ecology↗

bioRxiv2019

A wave of hematopoietic stem cell-derived T/ILC-restricted progenitors initiates thymopoiesis and shapes the embryonic thymus architecture.

Multiple waves of hematopoietic progenitors with distinct lineage potentials are differentially regulated in time and space. We show that the first thymic seeding progenitors comprise a unique population of bipotent cells that generate lymphoid tissue inducer and invariant V{gamma}5+ T cells. Both populations are of embryonic origin and induce the maturation of medullary thymic epithelial cells. Indeed, temporal depletion of the first wave of thymocytes results in a five-fold reduction of mature medullary thymic epithelial cells, after birth. We further show that these progenitors are of hematopoietic stem cell, and not, of yolk sac origin, despite the temporal overlap between the onset of lymphopoiesis and the transient expression of lymphoid transcripts in yolk sac precursors, that does not impact their strict erythro-myeloid potential. Our work highlights the relevance of the developmental timing on the emergence of different lymphoid subsets required for the establishment of a functionally diverse immune system.

immunology↗

bioRxiv2019

Evaluation of Trichoderma harzianum mutant lines in the resistance induction against white mold and growth promotion of common bean

Genetic engineering has brought improvements of Trichoderma species for biotechnological processes such as agriculture. It has previously been reported that sm1 and aquaglyceroporin genes from Trichoderma harzianum are strongly expressed during pathogens biocontrol. We have previously shown that Sm1 plays a significant role in plant disease resistance and aquaporin (AQP) regulate physiological processes and responses related to water stress. Here, we report the evaluation of mutant lines with sm1 (deleated) and aqp (overexpressed) in Phaseoulus vulgaris growth promotion and disease resistance induction. It was investigated plants physiological and biochemical responses, plant growth promotion and biocontrol of Sclerotinia sclerotiorum, the causal agent of white mold. Treatments included Trichoderma harzianum wyld type, mutant line overexpressing aquaporin (Aqua), and deleted{Delta} Epl1mutant line. Our results demonstrated that Aqua mutant line increased leaf area in 25%, in comparison to non-treated plants. It also differed from other treatments, in comparison to plants with treatments ALL-42 and{Delta} Epl1, which increased 28% and 91%, respectively (Isso e abstract, ta confuse e extensor. Specific activity of {beta}-1.3 glucanase was higher in plants treated with T. harzianum {Delta}Epl1 mutant isolate, in leaves and roots respectively with 2.07 Umg-1 and 2.57 Umg-1. Plants inoculated or not with S. sclerotiorum presented with 2.27 Umg-1 and 2.34 Umg-1 of {beta}-1.3 glucanase on average, respectively, but enzymatic activity was higher on leaves when compared to the roots. The Aqua mutant demonstrated excellent growth promoting properties. Both mutants of T. harzianum do not induce resistance to white mold on common bean plants.

microbiology↗

bioRxiv2018

Influenza A(H1N1)pdm09 M and HA segments sequences from Rio Grande do Sul, Brazil

The influenza virus is one of the most critical viruses in epidemiology. The 2009 pandemic was caused by a reassortment of the human-avian-swine virus with eight RNA segments responsible for all virus proteins. Segment 7 codifies for matrix proteins M1 and M2. These proteins exhibited low mutation rate because the matrix is fundamental for virion encapsidation and ion channel formation. However, hemagglutinin (HA) segment 4 is one of the most important segments for virulence and hence, is more studied. Brazil had many influenza virus infection cases just before 2009 and from 2011 to 2015, particularly in the Rio Grande do Sul (RS) State. Two hundred samples obtained during the pandemic were used for amplification and sequencing of the viral genome; a total of 19 M and 17 HA amplified segments were sequenced. Sequencing of the M fragment showed that RS has a virus origin different from that in Eastern Asia, Western Europe, USA, and Central America (Mexico and Nicaragua). All the sequences showed amantadine resistance (S31N) and one was out of the phylogenetic tree (Brazil/RS-3335/2009) due to high mutation rate. RS-3335 was the only sample obtained from a patient who died. Many migratory birds that flock to RS are from Europe, Asia, and USA, which could explain this rate of mutation. Insertions and deletions were found in the M1 protein in these samples. The HA sequences showed worldwide spread and less diversity than the M sequences in this study. The most divergent sample was Brazil/RS-3093/2009 that showed mutations in the sialic acid ligation site.

microbiology↗

bioRxiv2018

Contribution of rare and common variants to intellectual disability in a high-risk population sub-isolate of Northern Finland

The contribution of de novo and ultra-rare genetic variants in severe and moderate intellectual disability (ID) has been extensively studied whereas the genetic architecture of mild ID has been less well characterized. To elucidate the genetic background of milder ID we studied a regional cohort of 442 ID patients enriched for mild ID (>50%) from a population isolate of Finland. We analyzed rare variants using exome sequencing and CNV genotyping and common variants using common variant polygenic risk scores. As controls we used a Finnish collection of exome sequenced (n=11311) and GWAS chip genotyped (n=11699) individuals.\n\nWe show that rare damaging variants in genes known to be associated with cognitive defects are observed more often in severe (27%) than in mild ID (13%) patients (p-value: 7.0e-4). We further observed a significant enrichment of protein truncating variants in loss-of-function intolerant genes, as well as damaging missense variants in genes not yet associated with cognitive defects (OR: 2.1, p-value: 3e-8). For the first time to our knowledge, we show that a common variant polygenic load significantly contributes to all severity forms of ID. The heritability explained was the highest for educational attainment (EDU) in mild ID explaining 2.2% of the heritability on liability scale. For more severe ID it was lower at 0.6%. Finally, we identified a homozygote variant in the CRADD gene to be a cause of a specific syndrome with ID and pachygyria. The frequency of this variant is 50x higher in the Finnish population than in non-Finnish Europeans, demonstrating the benefits of utilizing population isolates in rare variant analysis of diseases under negative selection.

genetics↗