Готові списки джерел за темами / RNA pathogenesis

Добірка наукової літератури з теми "RNA pathogenesis"

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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Статті в журналах з теми "RNA pathogenesis"

Chatterjee, Biswanath, Che-Kun James Shen, and Pritha Majumder. "RNA Modifications and RNA Metabolism in Neurological Disease Pathogenesis." International Journal of Molecular Sciences 22, no. 21 (November 1, 2021): 11870. http://dx.doi.org/10.3390/ijms222111870.

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The intrinsic cellular heterogeneity and molecular complexity of the mammalian nervous system relies substantially on the dynamic nature and spatiotemporal patterning of gene expression. These features of gene expression are achieved in part through mechanisms involving various epigenetic processes such as DNA methylation, post-translational histone modifications, and non-coding RNA activity, amongst others. In concert, another regulatory layer by which RNA bases and sugar residues are chemically modified enhances neuronal transcriptome complexity. Similar RNA modifications in other systems collectively constitute the cellular epitranscriptome that integrates and impacts various physiological processes. The epitranscriptome is dynamic and is reshaped constantly to regulate vital processes such as development, differentiation and stress responses. Perturbations of the epitranscriptome can lead to various pathogenic conditions, including cancer, cardiovascular abnormalities and neurological diseases. Recent advances in next-generation sequencing technologies have enabled us to identify and locate modified bases/sugars on different RNA species. These RNA modifications modulate the stability, transport and, most importantly, translation of RNA. In this review, we discuss the formation and functions of some frequently observed RNA modifications—including methylations of adenine and cytosine bases, and isomerization of uridine to pseudouridine—at various layers of RNA metabolism, together with their contributions to abnormal physiological conditions that can lead to various neurodevelopmental and neurological disorders.

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Karst, Stephanie M. "Pathogenesis of Noroviruses, Emerging RNA Viruses." Viruses 2, no. 3 (March 23, 2010): 748–81. http://dx.doi.org/10.3390/v2030748.

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Baysal, Bora E., Shraddha Sharma, Seyedsasan Hashemikhabir, and Sarath Chandra Janga. "RNA Editing in Pathogenesis of Cancer." Cancer Research 77, no. 14 (June 30, 2017): 3733–39. http://dx.doi.org/10.1158/0008-5472.can-17-0520.

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Day, John W., and Laura P. W. Ranum. "RNA pathogenesis of the myotonic dystrophies." Neuromuscular Disorders 15, no. 1 (January 2005): 5–16. http://dx.doi.org/10.1016/j.nmd.2004.09.012.

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Pekarsky, Yuri, and Carlo M. Croce. "Noncoding RNA genes in cancer pathogenesis." Advances in Biological Regulation 71 (January 2019): 219–23. http://dx.doi.org/10.1016/j.jbior.2018.12.002.

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Poltronieri, Palmiro, Binlian Sun, and Massimo Mallardo. "RNA Viruses: RNA Roles in Pathogenesis, Coreplication and Viral Load." Current Genomics 16, no. 5 (July 10, 2015): 327–35. http://dx.doi.org/10.2174/1389202916666150707160613.

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Romano, Giulia, Michela Saviana, Patricia Le, Howard Li, Lavender Micalo, Giovanni Nigita, Mario Acunzo, and Patrick Nana-Sinkam. "Non-Coding RNA Editing in Cancer Pathogenesis." Cancers 12, no. 7 (July 8, 2020): 1845. http://dx.doi.org/10.3390/cancers12071845.

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In the last two decades, RNA post-transcriptional modifications, including RNA editing, have been the subject of increasing interest among the scientific community. The efforts of the Human Genome Project combined with the development of new sequencing technologies and dedicated bioinformatic approaches created to detect and profile RNA transcripts have served to further our understanding of RNA editing. Investigators have determined that non-coding RNA (ncRNA) A-to-I editing is often deregulated in cancer. This discovery has led to an increased number of published studies in the field. However, the eventual clinical application for these findings remains a work in progress. In this review, we provide an overview of the ncRNA editing phenomenon in cancer. We discuss the bioinformatic strategies for RNA editing detection as well as the potential roles for ncRNA A to I editing in tumor immunity and as clinical biomarkers.

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Gipson, Theresa A., Andreas Neueder, Nancy S. Wexler, Gillian P. Bates, and David Housman. "Aberrantly splicedHTT,a new player in Huntington’s disease pathogenesis." RNA Biology 10, no. 11 (November 2013): 1647–52. http://dx.doi.org/10.4161/rna.26706.

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Ranum, Laura P. W., and John W. Day. "Myotonic Dystrophy: RNA Pathogenesis Comes into Focus." American Journal of Human Genetics 74, no. 5 (May 2004): 793–804. http://dx.doi.org/10.1086/383590.

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Hu, Wen-Yuan, Christopher P. Myers, Jennifer M. Kilzer, Samuel L. Pfaff, and Frederic D. Bushman. "Inhibition of Retroviral Pathogenesis by RNA Interference." Current Biology 12, no. 15 (August 2002): 1301–11. http://dx.doi.org/10.1016/s0960-9822(02)00975-2.

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Дисертації з теми "RNA pathogenesis"

Frederick, Madeline Rose. "The role of RNA-editing in viral mediated pathogenesis." Kent State University Honors College / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ksuhonors152545654349718.

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Alsomali, Khayria. "Investigating RNA editing in the pathogenesis of amyotrophic lateral sclerosis." Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/9182/.

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The susceptibility of MNs to injury in amyotrophic lateral sclerosis (ALS) may result from excitotoxicity and subsequent dysregulation of intracellular calcium homeostasis. Post-transcriptional editing of the AMPA and Kainate glutamate receptor (GLUR) subunit(s) may alter the calcium ion permeability of the receptor pore, leading to neurodegeneration. The aims of the study are (i) to investigate GLUR2, GLUR5 and GLUR6 RNA editing at Q/R site and its editing enzyme ADAR2 and ADAR3 in ALS/C9ORF72-positive and ALS/C9OR72-negative compared to non neurological controls, and (ii) to determine the aberrant expression of EAAT2 transcripts in the astrocytes of the spinal cord of ALS cases and controls. (iii) To characterise p-TDP43, p62, GLUR2, ADAR2, ADAR3 and GFAP and EAAT2 proteins in motor neurons of ALS/C9ORF72-postive and ALS/C9ORF72-negative cases and controls. (iv) To develop new methodology to look at different levels of the mRNA expression in GLUR2, GLUR5, GLUR6, ADAR2, ADAR3 and EAAT2 that might exist in ALS. RNA was extracted from MNs and cDNA was prepared followed by amplification of cDNA by PCR that was used to generate amplified GLUR2, GLUR5 and GLUR6. These products were digested to produce cuts in the internal site of GLUR mRNA and differentiate edited from non-edited GLUR by analysis using agarose gel electrophoresis and the Agilent Bioanalyser. Independently the mRNA expression of ADAR2, ADAR3 and EAAT2 alternative transcripts of normal and aberrant exon 4 and 9 were quantified by qPCR. p-TDP-43, p62, GLUR2, ADAR2, ADAR3 and GFAP and EAAT2 protein levels were assessed by immunohistochemistry. The mRNA expression of GLUR2, GLUR5, GLUR6, ADAR2, ADAR3 and EAAT2 was assessed by next generation sequencing It was demonstrated that GLUR2 was fully edited in the MNs of ALS/C9ORF72- positive, ALS/C9ORF72-negative cases and controls. GLUR5 was 39% edited in MNs of ALS/C9ORF72-positive, 57% edited in ALS/C9ORF72-negative cases and 30% edited in controls. GLUR6 editing in MNs was 86% editing in the ALS/C9ORF72- positive and 77% editing in ALS/C9ORF72-negative cases compared to 72% editing in controls. An elevated mRNA expression in EAAT2 aberrant and normal transcripts of exon 4 and exon 9 was shown, but did not reach tatistical significance. ADAR2 immunoreactivity was associated with the nuclei of MNs, in contrast to ADAR3 which was exclusively associated with the neuronal cytoplasm. No significant differences in the pattern or distribution of immunoreactivity was detected across all groups. Phosphorylated TDP-43+ and p62+ skein-like bodies and compact inclusions were significantly elevated in both ALS/C9ORF72-positive cases and ALS/C9ORF72- negative cases, compared to control subjects which exhibited neither p-TDP-43 nor p62 expression. No significant difference in the pattern of immunoreactivity of EAAT2 in ALS groups and controls. In conclusion, full editing of GLUR2 in dissected motor neurons isolated by LCM was confirmed in ALS/C9ORF72-positive and ALS/C9ORF72-negative and control individuals. Whereas partial editing has been identified in GLUR5 and GLUR6 receptors. The mRNA and protein expression of ADAR2 and ADAR3 on spinal cord have shown similar levels between tested groups. No significant difference in the mRNA and protein expression of EAAT2. MNs in ALS cases, both with and without C9ORF72 expansion expressed pathogenic inclusions of phosphorylated TDP-43 and p62, which are a hallmark for ALS. ADAR2 and ADAR3 have shown no differences in ALS groups compared to controls.

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Talbot, Kevin. "The molecular pathogenesis of autosomal recessive spinal muscular atrophy." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300137.

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Fris, Elizabeth Megan. "Small RNA Sibling Pairs RyfA and RyfB in Shigella dysenteriae and their Impact on Pathogenesis." Ohio University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1531480621100282.

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Fahl, Willian de Oliveira. "Marcadores moleculares para a patogenia de vírus da raiva: relação entre períodos de incubação, carga viral e os genes codificadores das proteínas virais P e L." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/10/10134/tde-24072014-103209/.

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A raiva é uma doença aguda, progressiva e infecciosa do sistema nervoso central de mamíferos, causada pelo vírus da raiva (RABV). Embora possa ser prevenida por vacina, continua sendo um grave problema de saúde pública, além de ser responsável pela morte de seres humanos e muitos outros animais, incluindo os de interesse econômico. Este estudo teve como objetivo avaliar a relação entre polimorfismos dos genes que codificam as proteínas P e L de amostras de RABV pertencentes a variantes antigênicas 2 e 3 e períodos de incubação e títulos em camundongos. Para isso, foram selecionadas amostras isoladas de diferentes reservatórios de raiva de mamíferos das Ordens Carnivora e Chiroptera e amostras de bovinos, de áreas endêmicas para o vírus da raiva. As sequências obtidas foram utilizadas para a construção de árvores filogenéticas para procurar os padrões de segregação de linhagens. Os resultados mostraram que não houve marcadores ou polimorfismos que explicam as variações nos períodos de incubação e de letalidade entre cepas pertencentes a variantes antigênicas 2 e 3. Esta informação pode ser usada para discussões sobre a importância de reservatórios de raiva, a dinâmica do vírus da manutenção e evolução das diferentes formas desta zoonose entre os animais infectados, contribuindo para um estudo mais aprofundado sobre a busca de marcadores moleculares para patogênese.
Rabies is an acute, progressive and infectious disease of the central nervous system of mammals, caused by Rabies virus (RABV). Although preventable by vaccine, it remains a serious public health problem, and is responsible for the death of humans and many other animals, including those of economic interest. This study aimed to assess the relationship between polymorphisms in genes encoding the P and L proteins of RABV samples belonging to antigenic variants 2 and 3 and incubation periods and titers in mice. For this, samples isolated from different mammalian rabies reservoirs of the Orders Carnivora and Chiroptera and samples of cattle from endemic areas for rabies virus were selected. The sequences obtained were used to construct phylogenetic trees to search for the segregation patterns of strains. The results showed that there were no markers or polymorphisms that explain variations in incubation periods and lethality amongst strains belonging to antigenic variants 2 and 3. This information might be used for discussions about the importance of rabies reservoirs, the dynamics of the virus maintenance and evolution of the different forms of this zoonotic disease among infected animals, contributing to further study about the search for molecular markers for pathogenesis.

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Zentner, Gabriel Etienne. "Genomic analysis of ribosomal DNA and its application to the investigation of disease pathogenesis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1321478238.

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Santana, Estevan Alexis. "Identification of a Fur-regulated small regulatory RNA in nontypeable Haemophilus influenzae." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1410472201.

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Cunyat, Viaplana Francesc. "Changes in the HIV-1 env gene: Implications at the RNA and protein structure levels." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/96233.

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La glicoproteïna de l’envolta (Env) és una de les proteïnes claus del VIH-1 en patogènesi. La seqüència del gen env és important per a codificar l’Env però també per les estructures secundàries dels RREs que contenen els seus trànscrits. La rellevància dels dos elements s’ha comprovat extensament, tot i que assajos funcionals són requerits en ambdós casos per estudiar l’impacte de canvis específics. El tractament amb l’inhibidor de fusió T-20 selecciona virus resistents després d’adquirir canvis al gen env. Per estudiar variants funcionalment rellevants d’env que es trobessin in vivo vam decidir utilitzar mutacions associades a T-20. Les prediccions de les estructures secundàries dels RRE van resultar alterades en els canvis que codificaven per G36V/D, V38A, Q40H i L45M, però no per N43D o Q40H-L45M. Funcionalment vam demostrar que només els mutants que presenten el canvi L45M a la seva seqüència pateixen un impacte en la capacitat d’unir-se a la proteïna viral Rev quan aquesta es troba en baixes concentracions, suggerint que els canvis nucleotídics que afecten a la formació de l’aminoàcid 45 de gp41 juguen un paper en la unió a Rev. De totes maneres, ninguna variant d’RRE va ser afectada en la seva capacitat per a ser transportada al citoplasma. Per tant, alteracions en les prediccions d’estructures secundàries a partir de seqüències nucleotídiques no necessàriament impliquen impactes funcionals i la mutació L45M no s’incorpora com a mutació secundària degut a un restaurament de les funcions del RRE. Com que és important caracteritzar funcionalment Envs derivades de pacients per a estudiar la seva patogenicitat, vam establir una metodologia completa per a estudiar-les basant-nos en el paper principal que hi juga la subunitat gp41. Els resultats demostren que la selecció de la línia cel·lular efectora és essencial per optimitzar la sensibilitat dels assajos. La línia cel·lular 293T hauria de ser utilitzada per experiments fusogènics i la HeLa per analitzar paràmetres relacionats amb la mort. Estudis clínics havien suggerit que virus que contenien la mutació V38A i que havien aparegut sota un context que tinguessin el polimorfisme viral N140I eren menys patogènics degut a que estaven associats amb fallada virològica i beneficis immunològics. Per tal d’entendre aquestes dades discordants vam basar-nos en la nostra metodologia per a analitzar Envs derivades de pacients que tinguessin aquests canvis. Aquestes Envs V38A-N140I van resultar tenir menys capacitat per induir la mort per cèl·lula individual tot i no veure’s alterada la seva capacitat fusogènica, remarcant la importància del context de l’Env i el paper central de gp41 a la patogènesi del VIH-1.
La glicoproteína de la envuelta (Env) es una de les proteínas claves del VIH-1 en patogénesis. La secuencia del gen env es importante para codificar la Env pero también para las estructuras secundarias de los RREs presentes en sus tránscritos. La relevancia de estos dos elementos ha sido comprobada extensamente, pese a que ensayos funcionales aún son requeridos en ambos casos para estudiar el impacto de cambios específicos. El tratamiento con el inhibidor de fusión T-20 selecciona virus resistentes después de adquirir cambios en el gen env. Para estudiar variantes funcionalmente relevantes de env que se encontraran in vivo decidimos utilizar mutaciones asociadas a T-20. Las predicciones de las estructuras secundarias de los RRE resultaron alteradas en los cambios que codificaban para G36V/D, V38A, Q40H y L45M, pero no para N43D o Q40H-L45M. Funcionalmente demostramos que sólo los mutantes que presentan el cambio L45M en su secuencia sufren un impacto de unión a la proteína viral Rev cuando ésta se encuentra en bajas concentraciones, sugiriendo que los cambios nucleotídicos que afectan a la formación del aminoácido 45 de gp41 juegan un papel en la unión a Rev. No obstante, la capacidad de transporte al citoplasma de estos RRE no está afectada. Por lo tanto, alteraciones en las estructuras secundarias predictivas a partir de secuencias nucleotídicas no necesariamente implican impactos funcionales y la mutación L45M tampoco se incorpora como mutación secundaria debido a la restauración de las funciones del RRE. Como es importante caracterizar funcionalmente Envs derivadas de pacientes para estudiar su patogenicidad, establecimos una metodología completa basándonos en el papel principal de la subunidad gp41. Los resultados demostraron que la línea celular efectora es esencial para optimizar la sensibilidad de los ensayos. La línea celular 293T debería utilizarse para experimentos de fusión y la HeLa per analizar parámetros de citopaticidad. Estudios clínicos habían sugerido que virus que contenían la mutación V38A y el polimorfismo viral N140I estaban asociados a una fallo virológico y beneficios inmunológicos del paciente debido a que eran menos patogénicos. Para entender estos datos discordantes analizamos Envs derivadas de pacientes y vimos que cuando éstas tenían los cambios V38A-N140I tenían menos capacidad para matar células diana de forma individual pese a no tener alterada su capacidad fusogénica. Estos datos remarcan la importancia del contexto de la Env y el papel central de gp41 en la patogénesis del VIH-1.
The Env glycoprotein is one of the key proteins used by HIV-1 to mediate its pathogenicity. The sequence of the env gene is important to encode the Env glycoprotein but also for the secondary structure of the RRE that harbor its transcripts. The relevance of both elements has been extensively proved, although functional assays were needed in both cases to study the impact of specific changes. Treatment with the fusion inhibitor T-20 in patients infected with HIV-1 select resistant viruses to this drug after acquiring changes in their env gene. Therefore, we decided to use T-20-associated changes in order to functionally study relevant in vivo env variants. Predictions of the RRE secondary structures showed alterations when they were encoding for the changes G36V/D, V38A, Q40H and L45M, but not when harboring N43D and Q40H-L45M. Functional data showed that only the mutants harboring the L45M mutation had impairments in their binding capacity to Rev when this protein was at low concentrations, suggesting that the nucleotide changes affecting the encoding of the amino acid 45 in gp41 plays a role in Rev binding. However, none of the RRE variants were affected in their ability to being transported to the cytoplasm. Thus, it was found that alterations in RRE secondary structures predicted from nucleotide sequences might not necessary imply functional impairments and that the L45M change was not incorporated as a secondary mutation due to a restoration of the RRE functions. As it is important to functionally characterize patient-derived Envs to understand their in vivo pathogenesis, we established a complete methodology to study them by focusing on the main role of the subunit gp41. Based on our results, the correct selection of the effector cell line is essential to optimize the sensitivity of the assays. The 293T cell line might be used for fusogenic experiments and the HeLa for analyzing death parameters. Clinical trials had suggested that V38A viral mutants arising in an Env context containing the N140I polymorphism, were low pathogenic due to they were associated with virological failure and immunologic benefits. In order to understand these in vivo discordant data, we used our complete methodology to analyze patient-derived Envs that harbored these changes. We found that the V38A mutant Envs that were arisen in a N140I context were less able to induce single-cell death to target cells despite not having an altered fusogenic capacity. Thus, these data supports the importance of the Env context and the main role of gp41 in HIV-1 pathogenesis.

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Wilf, Nabil M. "The role of post-transcriptional regulators in pathogenesis and secondary metabolite production in Serratia sp. ATCC 39006." Thesis, University of Cambridge, 2011. https://www.repository.cam.ac.uk/handle/1810/245284.

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Serratia sp. ATCC 39006 (S39006) is a Gram-negative bacterium that is virulent in plant (potato) and animal (Caenorhabditis elegans) models. It produces two secondary metabolite antibiotics, prodigiosin and a carbapenem, and the plant cell wall degrading exoenzymes, pectate lyase and cellulase. A complex regulatory network controls production of prodigiosin, including a quorum sensing (QS) system, and the role of post-transcriptional regulation was investigated. It was hypothesized that Hfq-dependent small regulatory RNAs (sRNAs) might also play a role. Hfq is an RNA chaperone involved in post-transcriptional regulation that plays a key role in stress response and virulence in other bacterial species. An S39006 ∆hfq mutant was constructed and in the mutants production of prodigiosin and carbapenem was abolished, while production of the QS molecule, butanoyl homoserine lactone (BHL), was unaffected. Using transcriptional fusions, it was found that Hfq regulated the QS response regulators, SmaR and CarR. Additionally, exoenzyme production and swimming motility were decreased in the ∆hfq mutant, and virulence was attenuated in potato and C. elegans. It was also shown that the phenotype of an hfq mutant is independent of its role in regulating the stationary phase sigma factor, rpoS. In order to define the complete regulon of Hfq and identify relevant potential sRNAs, deep sequencing of strand-specific cDNAs (RNA-seq) was used to analyse the whole transcriptome of S39006 WT and the ∆hfq mutant. The regulon of another post-transcriptional regulator, RsmA, also involved in regulating prodigiosin production, was investigated by performing RNA-seq on an rsmA mutant. Moreover, global changes in the proteome of the hfq mutant was analysed using an LC-MS/MS approach with isobaric tags for relative and absolute quantification (iTRAQ). This study confirms a role for Hfq in pathogenesis and the regulation of antibiotic production in S39006, and begins to provide a systems-level understanding of Hfq and RsmA regulation using a combination of transcriptomics and proteomics.

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Delbianco, Alice. "Molecular mechanisms involved in the pathogenesis of beet soil-borne viruses." Phd thesis, Université de Strasbourg, 2013. http://tel.archives-ouvertes.fr/tel-01017177.

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The genus Benyvirus includes the most important and widespread sugar beet viruses transmitted through the soil by the plasmodiophorid Polymyxa betae. In particular Beet necrotic yellow vein virus (BNYVV), the leading infectious agent that affects sugar beet, causes an abnormal rootlet proliferation known as rhizomania. Beet soil-borne mosaic virus (BSBMV) is widely distributed in the United States and, up to date has not been reported in others countries. My PhD project aims to investigate molecular interactions between BNYVV and BSBMV and the mechanisms involved in the pathogenesis of these viruses.BNYVV full-length infectious cDNA clones were available as well as full-length cDNA clones of BSBMV RNA-1, -2, -3 and -4. Handling of these cDNA clones in order to produce in vitro infectious transcripts need sensitive and expensive steps, so Ideveloped agroclones of BNYVV and BSBMV RNAs, as well as viral replicons allowing the expression of different proteins.Chenopodium quinoa and Nicotiana benthamiana plants have been infected with in vitro transcripts and agroclones to investigate the interaction between BNYVV and BSBMV RNA-1 and -2 and the behavior of artificial viral chimeras. Simultaneously I characterized BSBMV p14 and demonstrated that it is a suppressor of posttranscriptional gene silencing sharing common features with BNYVV p14.

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Книги з теми "RNA pathogenesis"

Chistyakova, Guzel, Lyudmila Ustyantseva, Irina Remizova, Vladislav Ryumin, and Svetlana Bychkova. CHILDREN WITH EXTREMELY LOW BODY WEIGHT: CLINICAL CHARACTERISTICS, FUNCTIONAL STATE OF THE IMMUNE SYSTEM, PATHOGENETIC MECHANISMS OF THE FORMATION OF NEONATAL PATHOLOGY. au: AUS PUBLISHERS, 2022. http://dx.doi.org/10.26526/monography_62061e70cc4ed1.46611016.

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The purpose of the monograph, which contains a modern view of the problem of adaptation of children with extremely low body weight, is to provide a wide range of doctors with basic information about the clinical picture, functional activity of innate and adaptive immunity, prognostic criteria of postnatal pathology, based on their own research. The specific features of the immunological reactivity of premature infants of various gestational ages who have developed bronchopulmonary dysplasia (BPD) and retinopathy of newborns (RN) from the moment of birth and after reaching postconceptional age (37-40 weeks) are described separately. The mechanisms of their implementation with the participation of factors of innate and adaptive immunity are considered in detail. Methods for early prediction of BPD and RN with the determination of an integral indicator and an algorithm for the management of premature infants with a high risk of postnatal complications at the stage of early rehabilitation are proposed. The information provided makes it possible to personify the treatment, preventive and rehabilitation measures in premature babies. The monograph is intended for obstetricians-gynecologists, neonatologists, pediatricians, allergists-immunologists, doctors of other specialties, residents, students of the system of continuing medical education. This work was done with financial support from the Ministry of Education and Science, grant of the President of the Russian Federation No. MK-1140.2020.7.

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Selvarajan, Ramasamy, Rajarshi Kumar Gaur, and Basavaprabhu L. Patil. Plant RNA Viruses: Molecular Pathogenesis and Management. Elsevier Science & Technology, 2023.

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Selvarajan, Ramasamy, Rajarshi Kumar Gaur, and Basavaprabhu L. Patil. Plant RNA Viruses: Molecular Pathogenesis and Management. Elsevier Science & Technology Books, 2023.

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Vaheri, Antti, James N. Mills, Christina F. Spiropoulou, and Brian Hjelle. Hantaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0035.

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Hantaviruses (genus Hantavirus, family Bunyaviridae) are rodent- and insectivore-borne zoonotic viruses. Several hantaviruses are human pathogens, some with 10-35% mortality, and cause two diseases: hemorrhagic fever with renal syndrome (HFRS) in Eurasia, and hantavirus cardiopulmonary syndrome (HCPS) in the Americas. Hantaviruses are enveloped and have a three-segmented, single-stranded, negative-sense RNA genome. The L gene encodes an RNA-dependent RNA polymerase, the M gene encodes two glycoproteins (Gn and Gc), and the S gene encodes a nucleocapsid protein. In addition, the S genes of some hantaviruses have an NSs open reading frame that can act as an interferon antagonist. Similarities between phylogenies have suggested ancient codivergence of the viruses and their hosts to many authors, but increasing evidence for frequent, recent host switching and local adaptation has led to questioning of this model. Infected rodents establish persistent infections with little or no effect on the host. Humans are infected from aerosols of rodent excreta, direct contact of broken skin or mucous membranes with infectious virus, or rodent bite. One hantavirus, Andes virus, is unique in that it is known to be transmitted from person-to-person. HFRS and HCPS, although primarily affecting kidneys and lungs, respectively, share a number of clinical features, such as capillary leakage, TNF-, and thrombocytopenia; notably, hemorrhages and alterations in renal function also occur in HCPS and cardiac and pulmonary involvement are not rare in HFRS. Of the four structural proteins, both in humoral and cellular immunity, the nucleocapsid protein appears to be the principal immunogen. Cytotoxic T-lymphocyte responses are seen in both HFRS and HCPS and may be important for both protective immunity and pathogenesis. Diagnosis is mainly based on detection of IgM antibodies although viral RNA (vRNA) may be readily, although not invariably, detected in blood, urine and saliva. For sero/genotyping neutralization tests/RNA sequencing are required. Formalin-inactivated vaccines have been widely used in China and Korea but not outside Asia. Hantaviruses are prime examples of emerging and re-emerging infections and, given the limited number of rodents and insectivores thus far studied, it is likely that many new hantaviruses will be detected in the near future.

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Hughes, Alis, and Lesley Jones. Pathogenic Mechanisms. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0013.

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Huntington’s disease (HD) pathogenesis is complex. In the two decades since the gene and its mutation were discovered, there has been extensive exploration of how the expanded CAG repeat in HTT leads to neurodegeneration in HD. This chapter focuses on the mechanisms that potentially contribute to the dysfunction and death of cells in HD. These include repeat instability and RNA toxicity and the production, processing, modification, and degradation of mutant huntingtin. The effects of mutant HTT on cellular processes such as transcription, transport, neurotransmission, and protein clearance are also described. The interdependence and individual importance of these mechanisms in disease etiology remains to be clarified; however, consideration of each could be important for the development of therapeutic interventions in HD.

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Denton, Christopher P., and Pia Moinzadeh. Systemic sclerosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0121.

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The term 'scleroderma' describes a group of conditions in which the development of thickened, fibrotic skin is a cardinal feature. This includes localized forms of scleroderma (e.g. morphoea) and also systemic forms of the disease that are more correctly termed systemic sclerosis. Systemic sclerosis (SSc) is a multiorgan, autoimmune disease that has a high clinical burden and mortality, due to affecting the skin as well as internal organs. As with other related diseases there is a female predominance and marked clinical diversity. The pathogenesis of SSc is not fully elucidated; it includes endothelial cell injury fibroblast activation and autoimmunity that lead to skin and internal organ manifestations. The majority of cases exhibit characteristic serum autoantibodies. Some of these antibodies are scleroderma-specific reactivities including anti-centromere (ACA), anti-topoisomerase-1 (ATA or Scl 70) or anti-RNA polymerase III antibodies. These anti-nuclear antibody (ANA) patterns are generally mutually exclusive and serve as useful clinical markers of disease subgroups. Additional subsetting of scleroderma cases, based on the extent of skin sclerosis, permits classification into limited and diffuse subsets. Because of the heterogeneity of the disease patients may suffer from different organ manifestations, such as lung fibrosis, hypertensive renal crisis, severe cardiac disease, gastrointestinal involvement, and pulmonary arterial hypertension. Although outcomes have improved recently, systemic sclerosis still has the highest case-specific mortality of any of the autoimmune rheumatic diseases and requires careful and systematic investigation, management and follow-up. Treatment includes symptomatic strategies with attention to each involved organ system; it is still an area where therapeutic progress and better understanding of pathogenesis is increasingly anticipated.

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Meng, X. J. Hepatitis E virus. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0048.

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Hepatitis E virus (HEV) is a small, non-enveloped, single-strand, positive-sense RNA virus of approximately 7.2 kb in size. HEV is classified in the family Hepeviridae consisting of four recognized major genotypes that infect humans and other animals. Genotypes 1 and 2 HEV are restricted to humans and often associated with large outbreaks and epidemics in developing countries with poor sanitation conditions, whereas genotypes 3 and 4 HEV infect humans, pigs and other animal species and are responsible for sporadic cases of hepatitis E in both developing and industrialized countries. The avian HEV associated with Hepatitis-Splenomegaly syndrome in chickens is genetically and antigenically related to mammalian HEV, and likely represents a new genus in the family. There exist three open reading frames in HEV genome: ORF1 encodes non-structural proteins, ORF2 encodes the capsid protein, and the ORF3 encodes a small phosphoprotein. ORF2 and ORF3 are translated from a single bicistronic mRNA, and overlap each other but neither overlaps ORF1. Due to the lack of an efficient cell culture system and a practical animal model for HEV, the mechanisms of HEV replication and pathogenesis are poorly understood. The recent identification and characterization of animal strains of HEV from pigs and chickens and the demonstrated ability of cross-species infection by these animal strains raise potential public health concerns for zoonotic HEV transmission. It has been shown that the genotypes 3 and 4 HEV strains from pigs can infect humans, and vice versa. Accumulating evidence indicated that hepatitis E is a zoonotic disease, and swine and perhaps other animal species are reservoirs for HEV. A vaccine against HEV is not yet available.

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Walters, Douglas B., and Lawrence H. Keith. Compendium of Safety Data Sheets for Research and Industrial Chemicals: Flavor and Fragrance Substances (Compendium of Safety Data Sheets for Research). Vch Pub, 1989.

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Gaston, J. S. Hill. Reactive arthritis and enteropathic arthropathy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0115.

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Reactive arthritis (ReA), and enteropathic arthritis secondary to inflammatory bowel disease, are forms of spondyloarthritis, all of which share an association with HLA B27 and can involve both axial and peripheral joints. Genetic studies strongly implicate the cytokines IL-17 and IL-23 in their pathogenesis, and evidence for autoimmunity is lacking. ReA is triggered by particular bacteria, mainly affecting the gut and genitourinary tract, though infections are sometimes asymptomatic. Classically an acute oligo- or monoarthritis with enthesitis occurs, often with inflammatory back pain, though mild polyarthritis can also occur. Septic and crystal-induced arthritis are the principal differential diagnoses. Extra-articular features may aid diagnosis, which otherwise requires laboratory evidence of preceding infection. Bacterial components traffic to the joint (which is nevertheless sterile), and elicit local proinflammatory immune responses. Most ReA is self-limiting, but persistent cases may require disease-modifying anti-rheumatic drugs or even biologics.

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Gaston, J. S. Hill. Reactive arthritis and enteropathic arthropathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0115_update_002.

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Reactive arthritis (ReA), and enteropathic arthritis secondary to inflammatory bowel disease, are forms of spondyloarthritis, all of which share an association with HLA B27 and can involve both axial and peripheral joints. Genetic studies strongly implicate the cytokines IL-17 and IL-23 in their pathogenesis, and evidence for autoimmunity is lacking. ReA is triggered by particular bacteria, mainly affecting the gut and genitourinary tract, though infections are sometimes asymptomatic. Classically an acute oligo- or monoarthritis with enthesitis occurs, often with inflammatory back pain, though mild polyarthritis can also occur. Septic and crystal-induced arthritis are the principal differential diagnoses. Extra-articular features may aid diagnosis, which otherwise requires laboratory evidence of preceding infection. Bacterial components traffic to the joint (which is nevertheless sterile), and elicit local pro-inflammatory immune responses. Most ReA is self-limiting, but persistent cases may require disease-modifying anti-rheumatic drugs or even biologics.

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Частини книг з теми "RNA pathogenesis"

Guha, Shalini, Priyanka Barman, Aruniti Manawa, and Sukesh R. Bhaumik. "Nuclear Export of mRNAs with Disease Pathogenesis and Therapeutic Implications." In RNA Technologies, 371–95. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08415-7_17.

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Bishop, David H. L. "Viruses with Ambisense RNA Genomes." In Concepts in Viral Pathogenesis II, 32–39. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4958-0_4.

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Palmenberg, A. C., and J. E. Osorio. "Cardioviral poly(C) tracts and viral pathogenesis." In Positive-Strand RNA Viruses, 67–77. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9326-6_8.

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Racaniello, V. R., and R. Ren. "Transgenic mice and the pathogenesis of poliomyelitis." In Positive-Strand RNA Viruses, 79–86. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9326-6_9.

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Okada, Yoshimi, Tetsuo Meshi, and Yuichiro Watanabe. "Structure and Functions of Tobacco Mosaic Virus RNA." In Viral Genes and Plant Pathogenesis, 23–38. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3424-1_3.

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Rennick, Linda J., and Paul Duprex. "Modification of Measles Virus and Application to Pathogenesis Studies." In Reverse Genetics of RNA Viruses, 150–99. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118405338.ch6.

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Harrison, Stephen C. "Common Features in the Design of Small RNA Viruses." In Concepts in Viral Pathogenesis III, 3–19. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4613-8890-6_1.

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Davis, N. L., F. B. Grieder, J. F. Smith, G. F. Greenwald, M. L. Valenski, D. C. Sellon, P. C. Charles, and R. E. Johnston. "A molecular genetic approach to the study of Venezuelan equine encephalitis virus pathogenesis." In Positive-Strand RNA Viruses, 99–109. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9326-6_11.

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Napierala, D., and M. Napierala. "Toxic RNA in Pathogenesis of Human Neuromuscular Disorders." In RNA Technologies in Cardiovascular Medicine and Research, 325–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-78709-9_17.

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Gerlach, W. L., J. P. Haseloff, M. J. Young, and G. Bruening. "Use of Plant Virus Satellite RNA Sequences to Control Gene Expression." In Viral Genes and Plant Pathogenesis, 177–86. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3424-1_18.

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Тези доповідей конференцій з теми "RNA pathogenesis"

Arnold, Lisa, Shashi Chillappagari, Martina Korfei, Andreas Guenther, and Poornima Mahavadi. "Regulation of RNA Binding Proteins in the Pathogenesis of Lung Fibrosis." In Herbsttagung der Sektion Zellbiologie in der Deutschen Gesellschaft für Pneumologie und Beatmungsmedizin e. V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678406.

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Tsers, I., V. Gorshkov, N. Gogoleva, and Y. Gogolev. "Revealing the potential “master regulators” of pathogenesis in plants based on RNA-Seq data." In 2nd International Scientific Conference "Plants and Microbes: the Future of Biotechnology". PLAMIC2020 Organizing committee, 2020. http://dx.doi.org/10.28983/plamic2020.254.

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We propose an algorithm for RNA-Seq data analysis useful for revealing the “master regulators” of gene expression in experimental condition, as well as of cis-elements regulating transcript level of genes from certain groups.

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Omura, Junichi, Sandra Breuils-Bonnet, Olivier Boucherat, Steeve Provencher, and Sébastien Bonnet. "Long noncoding RNA H19 in the pathogenesis of right ventricular failure with pulmonary arterial hypertension." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa3933.

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Al-Kershi, S., S. Emmrich, C. Reimer, D. Heckl, and JH Klusmann. "Stem cell-enriched long non-coding RNA HOXA10-AS contributes to the pathogenesis of MLL-rearranged AML." In 30. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch-onkologische Forschung. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1602195.

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Mumby, S., V. Elyasigomari, C. K. Hui, F. Perros, A. Hautefort, M. Humbert, J. Wort, and I. M. Adcock. "Evidence for Endothelial Barrier Dysfunction, Vascular Permeability and Altered Matrix Degradation in PAH Pathogenesis Using RNA-Sequence Analysis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7194.

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Chatterji, Priya, Kathryn Hamilton, Sarah Andres, Rei Mizuno, Philip Hicks, Arjun Jeganathan, Monte M. Winslow, et al. "Abstract 1136: Cooperative functional roles of RNA binding proteins LIN28B and IMP1 in the pathogenesis of colorectal cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1136.

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Camilleri, Emily T., Pauli J. Beckmann, Jon D. Larson, Morito Kurata, Jingmin Shu, Emily Pope, Wendy A. Hudson, et al. "Abstract 2264: RNA sequencing based analysis of transposon-induced tumors reveals novel insights into cancer pathogenesis and progression." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2264.

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Omura, J., K. Habbout, S. Martineau, S. Breuils-Bonnet, V. Nadeau, F. Potus, S. L. Archer, et al. "Long Non-Coding RNA H19 in the Pathogenesis of Right Ventricular Failure Associated with Pulmonary Arterial Hypertension -A Putative Novel Biomarker and Therapeutic Target-." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2403.

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Guggenbiller, Matthew, Md Sazzad Hassan, Min Yan, Jun Li, Victoria Makuru, and Urs von Holzen. "Abstract 3604: Identification of genes involved in pathogenesis of esophageal adenocarcinoma using RNA sequencing from laser capture micro-dissected formalin-fixed paraffin-embedded tissue specimens." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3604.

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Ramos, Jairo, and Deodutta Roy. "Abstract 1552: Integrative bioinformatics analyses of ChIP seq and RNA seq data reveals a complex regulatory landscape of NRF1 network involved in the pathogenesis of breast cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1552.

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Звіти організацій з теми "RNA pathogenesis"

Mawassi, Munir, and Valerian Dolja. Role of RNA Silencing Suppression in the Pathogenicity and Host Specificity of the Grapevine Virus A. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7592114.bard.

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RNA silencing is a defense mechanism that functions against virus infection and involves sequence-specific degradation of viral RNA. Diverse RNA and DNA viruses of plants encode RNA silencing suppressors (RSSs), which, in addition to their role in viral counterdefense, were implicated in the efficient accumulation of viral RNAs, virus transport, pathogenesis, and determination of the virus host range. Despite rapidly growing understanding of the mechanisms of RNA silencing suppression, systematic analysis of the roles played by diverse RSSs in virus biology and pathology is yet to be completed. Our research was aimed at conducting such analysis for two grapevine viruses, Grapevine virus A (GVA) and Grapevine leafroll-associated virus-2 (GLRaV- 2). Our major achievements on the previous cycle of BARD funding are as follows. 1. GVA and GLRaV-2 were engineered into efficient gene expression and silencing vectors for grapevine. The efficient techniques for grapevine infection resulting in systemic expression or silencing of the recombinant genes were developed. Therefore, GVA and GLRaV-2 were rendered into powerful tools of grapevine virology and functional genomics. 2. The GVA and GLRaV-2 RSSs, p10 and p24, respectively, were identified, and their roles in viral pathogenesis were determined. In particular, we found that p10 functions in suppression and pathogenesis are genetically separable. 3. We revealed that p10 is a self-interactive protein that is targeted to the nucleus. In contrast, p24 mechanism involves binding small interfering RNAs in the cytoplasm. We have also demonstrated that p10 is relatively weak, whereas p24 is extremely strong enhancer of the viral agroinfection. 4. We found that, in addition to the dedicated RSSs, GVA and GLRaV-2 counterdefenses involve ORF1 product and leader proteases, respectively. 5. We have teamed up with Dr. Koonin and Dr. Falnes groups to study the evolution and function of the AlkB domain presents in GVA and many other plant viruses. It was demonstrated that viral AlkBs are RNA-specific demethylases thus providing critical support for the biological relevance of the novel process of AlkB-mediated RNA repair.

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Dawson, William O., Moshe Bar-Joseph, Charles L. Niblett, Ron Gafny, Richard F. Lee, and Munir Mawassi. Citrus Tristeza Virus: Molecular Approaches to Cross Protection. United States Department of Agriculture, January 1994. http://dx.doi.org/10.32747/1994.7570551.bard.

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Citrus tristeza virus (CTV) has the largest genomes among RNA viruses of plants. The 19,296-nt CTV genome codes for eleven open reading frames (ORFs) and can produce at least 19 protein products ranging in size from 6 to 401 kDa. The complex biology of CTV results in an unusual composition of CTV-specific RNAs in infected plants which includes multiple defective RNAs and mixed infections. The complex structure of CTV populations poses special problems for diagnosis, strain differentiation, and studies of pathogenesis. A manipulatable genetic system with the full-length cDNA copy of the CTV genome has been created which allows direct studies of various aspects of the CTV biology and pathology. This genetic system is being used to identify determinants of the decline and stem-pitting disease syndromes, as well as determinants responsible for aphid transmission.

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Tianzi, Zhang. The Emerging Roles of Long Non-coding RNAs in the Pathogenesis of Breast Cancer. Envirarxiv, November 2022. http://dx.doi.org/10.55800/envirarxiv488.

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Sionov, Edward, Nancy Keller, and Shiri Barad-Kotler. Mechanisms governing the global regulation of mycotoxin production and pathogenicity by Penicillium expansum in postharvest fruits. United States Department of Agriculture, January 2017. http://dx.doi.org/10.32747/2017.7604292.bard.

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The original objectives of the study, as defined in the approved proposal, are: To characterize the relationship of CreA and LaeA in regulation of P T production To understand how PacC modulates P. expansumpathogenicity on apples To examine if other secondary metabolites are involved in virulence or P. expansumfitness To identify the signaling pathways leading to PAT synthesis Penicilliumexpansum, the causal agent of blue mould rot, is a critical health concern because of the production of the mycotoxinpatulin (PAT) in colonized apple fruit tissue. Although PAT is produced by many Penicilliumspecies, the factors activating its biosynthesis were not clear. This research focused on host and fungal mechanisms of activation of LaeA (the global regulator of secondary metabolism), PacC (the global pH modulator) and CreA (the global carbon catabolite regulator) on PAT synthesis with intention to establish P. expansumas the model system for understanding mycotoxin synthesis in fruits. The overall goal of this proposal is to identify critical host and pathogen factors that mechanistically modulate P. expansumgenes and pathways to control activation of PAT production and virulence in host. Several fungal factors have been correlated with disease development in apples, including the production of PAT, acidification of apple tissue by the fungus, sugar content and the global regulator of secondary metabolism and development, LaeA. An increase in sucrose molarity in the culture medium from 15 to 175 mM negatively regulated laeAexpression and PAT accumulation, but, conversely, increased creAexpression, leading to the hypothesis that CreA could be involved in P. expansumPAT biosynthesis and virulence, possibly through the negative regulation of LaeA. We found evidence for CreAtranscriptional regulation of laeA, but this was not correlated with PAT production either in vitro or in vivo, thus suggesting that CreA regulation of PAT is independent of LaeA. Our finding that sucrose, a key ingredient of apple fruit, regulates PAT synthesis, probably through suppression of laeAexpression, suggests a potential interaction between CreA and LaeA, which may offer control therapies for future study. We have also identified that in addition to PAT gene cluster, CreA regulates other secondary metabolite clusters, including citrinin, andrastin, roquefortine and communesins, during pathogenesis or during normal fungal growth. Following creation of P. expansumpacCknockout strain, we investigated the involvement of the global pH regulator PacC in fungal pathogenicity. We demonstrated that disruption of the pH signaling transcription factor PacC significantly decreased the virulence of P. expansumon deciduous fruits. This phenotype is associated with an impairment in fungal growth, decreased accumulation of gluconic acid and reduced synthesis of pectolytic enzymes. We showed that glucose oxidase- encoding gene, which is essential for gluconic acid production and acidification during fruit colonization, was significantly down regulated in the ΔPepacCmutant, suggesting that gox is PacC- responsive gene. We have provided evidence that deletion of goxgene in P. expansumled to a reduction in virulence toward apple fruits, further indicating that GOX is a virulence factor of P. expansum, and its expression is regulated by PacC. It is also clear from the present data that PacC in P. expansumis a key factor for the biosynthesis of secondary metabolites, such as PAT. On the basis of RNA-sequencing (RNA-seq) analysis and physiological experimentation, the P. expansumΔlaeA, ΔcreAand ΔpacCmutants were unable to successfully colonize apples for a multitude of potential mechanisms including, on the pathogen side, a decreased ability to produce proteolytic enzymes and to acidify the environment and impaired carbon/nitrogen metabolism and, on the host side, an increase in the oxidative defence pathways. Our study defines these global regulatory factors and their downstream signalling pathways as promising targets for the development of strategies to fight against this post-harvest pathogen.

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Xu, Jin-Rong, and Amir Sharon. Comparative studies of fungal pathogeneses in two hemibiotrophs: Magnaporthe grisea and Colletotrichum gloeosporioides. United States Department of Agriculture, May 2008. http://dx.doi.org/10.32747/2008.7695585.bard.

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Plant pathogenic fungi have various life styles and different plant infection strategies. Hemibiotrophs like Magnaporthe grisea and Colletotrichum species develop specialized structures during plant infection. The goal of this study was to identify, characterize, and compare genes required for plant infection in M. grisea and C. gloeosporioides. Specific objectives are to: 1) further characterize genes identified in the preliminary studies of C. gloeosporioides and M. grisea;2) identify and characterize additional fungal genes tagged by GFP; and 3) identify in planta growth and appressorium-specific genes by subtractive hybridization and transcript profiling by the LongSAGE method. In this study, the PI and Co-PI collaborated closely on studies in M. grisea and C. gloeosporioides. In M. grisea, REMI and ATMT were used to transform the wildtype with promoter-less EGFP constructs. A total of 28 mutants defective in different plant infection processes or expressing EGFP during plant infection were identified. Genes disrupted in five selected mutants have been identified, including MG03295 that encodes a putative Rho GTPase. In transformant L1320, the transforming vector was inserted in the MIRI gene that encodes a nuclear protein. The expression of MIRI was highly induced during infection. Deletion and site-directed mutagenesis analyses were used to identify the promoter regions and elements that were essential for induced in planta expression of MIRI. This was the first detailed characterization of the promoter of an in planta gene in M. grisea and the MIRI promoter can be used to monitor infectious growth. In addition, the Agilent whole-genome array of M. grisea was used for microarray analyses with RNA samples from appressoria formed by the wild-type shain and the pmkl and mstl2 mutants. Over 200 genes were downregulated in the mst I 2 and pmkl mutants. Some of them are putative transcription factors that may regulate appressorium formation and infectious hyphal growth. In C. gloeosporioides, various REMI mutants showing different pathogenic behavior were identified and characterized. Mutants N3736 had a single insertion and was hyper-virulent. The gene disrupted in mutant3736 (named CgFMOI) encodes a FAD-dependent monooxygenase. Expression analyses linked the expression of the CgFMOI gene with the necrotrophic phase of fungal infection, and also suggest that expression of CgFMOl is unnecessary for the first stages of infection and for biotrophy establishment. All CgFMOl-silenced mutants had reduced virulence. In REMI mutant N159, the tagged gene encodes a putative copper transporter that is homologue of S. cerevisiae CTR2. In yeast, Ctr2 is a vacuolar transporter for moving copper from the vacuole to the cytoplasm. The gene was therefore termed CgCTR2. In addition to characterization of CgCTR2, we also conducted comparative analyses in M. grisea. The M. grisea CgCTR-2 homolog was isolated, knockout strains were generated and characterized and the M. grisea was used to complement the Nl 59 C. gloeosporioides mutant. Overall, we have accomplished most of proposed experiments and are in the process of organizing and publishing other data generated in this project. For objective 3, we used the microarray analysis approach. Several genes identified in this study are novel fungal virulence factors. They have the potential to be used as targets for developing more specific or effective fungicides. In the long run, comparative studies of fungal genes, such as our CgCTR2 work, may lead to better disease control strategies.

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Harman, Gary E., and Ilan Chet. Enhancement of plant disease resistance and productivity through use of root symbiotic fungi. United States Department of Agriculture, July 2008. http://dx.doi.org/10.32747/2008.7695588.bard.

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The objectives of the project were to (a) compare effects ofT22 and T-203 on growth promotion and induced resistance of maize inbred line Mol7; (b) follow induced resistance of pathogenesis-related proteins through changes in gene expression with a root and foliar pathogen in the presence or absence of T22 or T-203 and (c) to follow changes in the proteome of Mol? over time in roots and leaves in the presence or absence of T22 or T-203. The research built changes in our concepts regarding the effects of Trichoderma on plants; we hypothesized that there would be major changes in the physiology of plants and these would be reflected in changes in the plant proteome as a consequence of root infection by Trichoderma spp. Further, Trichoderma spp. differ in their effects on plants and these changes are largely a consequence of the production of different elicitors of elicitor mixtures that are produced in the zone of communication that is established by root infection by Trichoderma spp. In this work, we demonstrated that both T22 and T-203 increase growth and induce resistance to pathogens in maize. In Israel, it was shown that a hydrophobin is critical for root colonization by Trichoderma strains, and that peptaibols and an expansin-like protein from Ttrichoderma probably act as elicitors of induced resistance in plants. Further, this fungus induces the jasmonate/ethylene pathway of disease resistance and a specific cucumber MAPK is required for transduction of the resistance signal. This is the first such gene known to be induced by fungal systems. In the USA, extensive proteomic analyses of maize demonstrated a number of proteins are differentially regulated by T. harzianum strain T22. The pattern of up-regulation strongly supports the contention that this fungus induces increases in plant disease resistance, respiratory rates and photosynthesis. These are all very consistent with the observations of effects of the fungus on plants in the greenhouse and field. In addition, the chitinolytic complex of maize was examined. The numbers of maize genes encoding these enzymes was increased about 3-fold and their locations on maize chromosomes determined by sequence identification in specific BAC libraries on the web. One of the chitinolytic enzymes was determined to be a heterodimer between a specific exochitinase and different endochitinases dependent upon tissue differences (shoot or root) and the presence or absence of T. harzianum. These heterodimers, which were discovered in this work, are very strongly antifungal, especially the one from shoots in the presence of the biocontrol fungus. Finally, RNA was isolated from plants at Cornell and sent to Israel for transcriptome assessment using Affymetrix chips (the chips became available for maize at the end of the project). The data was sent back to Cornell for bioinformatic analyses and found, in large sense, to be consistent with the proteomic data. The final assessment of this data is just now possible since the full annotation of the sequences in the maize Affy chips is just now available. This work is already being used to discover more effective strains of Trichoderma. It also is expected to elucidate how we may be able to manipulate and breed plants for greater disease resistance, enhanced growth and yield and similar goals. This will be possible since the changes in gene and protein expression that lead to better plant performance can be elucidated by following changes induced by Trichoderma strains. The work was in, some parts, collaborative but in others, most specifically transcriptome analyses, fully synergistic.

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Sharon, Amir, and Maor Bar-Peled. Identification of new glycan metabolic pathways in the fungal pathogen Botrytis cinerea and their role in fungus-plant interactions. United States Department of Agriculture, 2012. http://dx.doi.org/10.32747/2012.7597916.bard.

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The involvement of glycans in microbial adherence, recognition and signaling is often a critical determinant of pathogenesis. Although the major glycan components of fungal cell walls have been identified there is limited information available on its ‘minor sugar components’ and how these change during different stages of fungal development. Our aim was to define the role of Rhacontaining-glycans in the gray mold disease caused by the necrotrophic fungus B. cinerea. The research was built on the discovery of two genes, Bcdhand bcer, that are involved in formation of UDP-KDG and UDP-Rha, two UDP- sugars that may serve as donors for the synthesis of cell surface glycans. Objectives of the proposed research included: 1) To determine the function of B. cinereaBcDh and BcEr in glycan biosynthesis and in pathogenesis, 2) To determine the expression pattern of BcDH and BcERand cellular localization of their encoded proteins, 3) Characterize the structure and distribution of Rha- containing glycans, 4) Characterization of the UDP-sugar enzymes and potential of GTs involved in glycanrhamnosylation. To address these objectives we generated a series of B. cinereamutants with modifications in the bchdhand bcergenes and the phenotype and sugar metabolism in the resulting strains were characterized. Analysis of sugar metabolites showed that changes in the genes caused changes in primary and secondary sugars, including abolishment of rhamnose, however abolishment of rhamnose synthesis did not cause changes in the fungal phenotype. In contrast, we found that deletion of the second gene, bcer, leads to accumulation of the intermediate sugar – UDP- KDG, and that such mutants suffer from a range of defects including reduced virulence. Further analyses confirmed that UDP-KDG is toxic to the fungus. Studies on mode of action suggested that UDP-KDG might affect integrity of the fungal cell wall, possibly by inhibiting UDP-sugars metabolic enzymes. Our results confirm that bcdhand bcerrepresent a single pathway of rhamnose synthesis in B. cinerea, that rhamnose does not affect in vitro development or virulence of the fungus. We also concluded that UDP-KDG is toxic to B. cinereaand hence UDP-KDG or compounds that inhibit Er enzymes and lead to accumulation of UDP-KDG might have antifungal activity. This toxicity is likely the case with other fungi, this became apparent in a collaborative work with Prof. Bart Thomma of Wageningen University, NETHERLANDS . We have shown the deletion of ER mutant in Verticillium dahlia gave plants resistance to the fungal infection.

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Levisohn, Sharon, Mark Jackwood, and Stanley Kleven. New Approaches for Detection of Mycoplasma iowae Infection in Turkeys. United States Department of Agriculture, February 1995. http://dx.doi.org/10.32747/1995.7612834.bard.

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Mycoplasma iowae (Mi) is a pathogenic avian mycoplasma which causes mortality in turkey embryos and as such has clinical and economic significance for the turkey breeder industry. Control of Mi infection is severely hampered by lack of adequate diagnostic tests, together with resistance to most antibiotics and resilience to environment. A markedly high degree of intra-species antigenic variation also contributes to difficulties in detection and control of infection. In this project we have designed an innovative gene-based diagnostic test based on specific amplification of the 16S rRNA gene of Mi. This reaction, designed Multi-species PCR-RFLP test, also amplifies the DNA of the pathogenic avian mycoplasmas M. gallisepticum (Mg) and M. synoviae (Ms). This test detects DNA equivalent to about 300 cfu Mi or either of the other two target mycoplasmas, individually or in mixed infection. It is a quick test, applicable to a wide variety of clinical samples, such as allantoic fluid or tracheal or cloacal swab suspensions. Differential diagnosis is carried out by gel electro-phoresis of the PCR amplicon digested with selected restriction enzymes (Restriction Fragment Length Polymorphism). This can also be readily accomplished by using a simple Dot-Blot hybridization assay with digoxigenin-labeled oligonucleotide probes reacting specifically with unique Mi, Mg or Ms sequences in the PCR amplicon. The PCR/OLIGO test increased sensitivity by at least 10-fold with a capacity for rapid testing of large numbers of samples. Experimental infection trials were carried out to evaluate the diagnostic tools and to study pathogenesis of Mi infection. Field studies and experimental infection of embryonated eggs indicated both synergistic and competitive interaction of mycoplasma pathogens in mixed infection. The value of the PCR diagnostic tests for following the time course of egg transmission was shown. A workable serological test (Dot Immunobinding Assay) was also developed but there was no clear-cut evidence that infected turkeys develop an immune response. Typing of a wide spectrum of Mi field isolates by a variety of gene-based molecular techniques indicated a higher degree of genetic homogeneity than predicted on the basis of the phenotypic variability. All known strains of Mi were detected by the method developed. Together with an M. meleagridis-PCR test based on the same gene, the Multi-species PCR test is a highly valuable tool for diagnosis of pathogenic mycoplasmas in single or mixed infection. The further application of this rapid and specific test as a part of Mi and overall mycoplasma control programs will be dependent on developments in the turkey industry.

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