Relevant bibliographies by topics / Pathogenicity genes

Academic literature on the topic 'Pathogenicity genes'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Pathogenicity genes"

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Wei, X. K., Y. Z. Zhong, Y. Pan, X. N. Li, J. J. Liang, and T. R. Luo. "The N and P genes facilitate pathogenicity of the rabies virus G gene." Veterinární Medicína 63, No. 12 (December 3, 2018): 561–70. http://dx.doi.org/10.17221/63/2018-vetmed.

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To explore the effects of different gene combinations on the pathogenicity of the rabies virus (RABV), six chimeric RABV mutants, rRC-HL(G), rRC-HL(NG), rRC-HL(PG), rRC-HL(NP), rRC-HL(NM) and rRC-HL(NPG), were constructed using a reverse genetic technique based on an avirulent parental rRC-HL strain and a virulent parental GX074 isolate. These mutants were intracerebrally inoculated into adult mice. The results indicated that 10<sup>2</sup> ffu and 10<sup>6</sup> ffu of rRC-HL(G), rRC-HL(NG), rRC-HL(PG) and rRC-HL(NPG) were 100% lethal. In the case of intramuscular viral infection, none of the mice inoculated with 10<sup>2 </sup>ffu of any of the RABV mutants, including GX074, died; at 10<sup>6 </sup>ffu, rRC-HL(G) was lethal in 2/5 cases, rRC-HL(NG) was lethal in 1/5 cases and rRC-HL(PG) was lethal for 2/5 mice. The rRC-HL(NPG) mutant was fatal for 3/5 mice, as was the parental GX074. Furthermore, the LD<sub>50</sub> values of the chimeric RABV mutants were measured, with the results showing that the LD<sub>50</sub> values of both rRC-HL(NG) and rRC-HL(PG) were lower than that of rRC-HL(G), but higher than that of rRC-HL(NPG). Thus, the action of N + G, or P + G, or N + P + G gene combinations may be more pronounced than that of the G gene alone. Body weight changes and the clinical symptoms of the tested mice were consistent with pathogenicity. These data indicate that the N and P genes are involved in and facilitate the pathogenicity of the RABV G gene. These experiments provide further evidence that multi-gene cooperation is responsible for the virulence of RABV.
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Idnurm, Alexander, and Barbara J. Howlett. "Pathogenicity genes of phytopathogenic fungi." Molecular Plant Pathology 2, no. 4 (July 2001): 241–55. http://dx.doi.org/10.1046/j.1464-6722.2001.00070.x.

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Czislowski, E., S. Fraser-Smith, M. Zander, and E. A. B. Aitken. "Identifying pathogenicity genes inFusarium oxysporumf. sp.cubense." Acta Horticulturae, no. 1114 (March 2016): 101–6. http://dx.doi.org/10.17660/actahortic.2016.1114.14.

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Leal, Gildemberg A., Luiz H. Gomes, Paulo S. B. Albuquerque, Flávio C. A. Tavares, and Antonio Figueira. "Searching for Moniliophthora perniciosa pathogenicity genes." Fungal Biology 114, no. 10 (October 2010): 842–54. http://dx.doi.org/10.1016/j.funbio.2010.07.009.

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Tsuge, Takashi. "Studies on pathogenicity genes of Alternaria alternata." Journal of General Plant Pathology 69, no. 6 (December 1, 2003): 418–20. http://dx.doi.org/10.1007/s10327-003-0065-8.

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Koszinowski, Ulrich. "MHC class I regulatory genes of CMV. Are they pathogenicity genes?" Journal of Clinical Virology 12, no. 2 (April 1999): 89. http://dx.doi.org/10.1016/s1386-6532(99)90393-1.

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Baldwin, Thomas K., Rainer Winnenburg, Martin Urban, Chris Rawlings, Jacob Koehler, and Kim E. Hammond-Kosack. "The Pathogen-Host Interactions Database (PHI-base) Provides Insights into Generic and Novel Themes of Pathogenicity." Molecular Plant-Microbe Interactions® 19, no. 12 (December 2006): 1451–62. http://dx.doi.org/10.1094/mpmi-19-1451.

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Fungal and oomycete pathogens of plants and animals are a major global problem. In the last 15 years, many genes required for pathogenesis have been determined for over 50 different species. Other studies have characterized effector genes (previously termed avirulence genes) required to activate host responses. By studying these types of pathogen genes, novel targets for control can be revealed. In this report, we describe the Pathogen-Host Interactions database (PHI-base), which systematically compiles such pathogenicity genes involved in pathogen-host interactions. Here, we focus on the biology that underlies this computational resource: the nature of pathogen-host interactions, the experimental methods that exist for the characterization of such pathogen-host interactions as well as the available computational resources. Based on the data, we review and analyze the specific functions of pathogenicity genes, the host-specific nature of pathogenicity and virulence genes, and the generic mechanisms of effectors that trigger plant responses. We further discuss the utilization of PHI-base for the computational identification of pathogenicity genes through comparative genomics. In this context, the importance of standardizing pathogenicity assays as well as integrating databases to aid comparative genomics is discussed.
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Sawczyc, Maria K. "The Role in Pathogenicity of Some Related Genes inXanthomonas campestrisPathovarscampestrisandtranslucens: A Shuttle Strategy for Cloning Genes Required for Pathogenicity." Molecular Plant-Microbe Interactions 2, no. 5 (1989): 249. http://dx.doi.org/10.1094/mpmi-2-249.

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Wang, Ying, Ying Wáng, Qi Tan, Ying Nv Gao, Yan Li, and Da Peng Bao. "Comparison and Validation of Putative Pathogenicity-Related Genes Identified by T-DNA Insertional Mutagenesis and Microarray Expression Profiling inMagnaporthe oryzae." BioMed Research International 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/7198614.

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High-throughput technologies of functional genomics such as T-DNA insertional mutagenesis and microarray expression profiling have been employed to identify genes related to pathogenicity inMagnaporthe oryzae. However, validation of the functions of individual genes identified by these high-throughput approaches is laborious. In this study, we compared two published lists of genes putatively related to pathogenicity inM. oryzaeidentified by T-DNA insertional mutagenesis (comprising 1024 genes) and microarray expression profiling (comprising 236 genes), respectively, and then validated the functions of some overlapped genes between the two lists by knocking them out using the method of target gene replacement. Surprisingly, only 13 genes were overlapped between the two lists, and none of the four genes selected from the overlapped genes exhibited visible phenotypic changes on vegetative growth, asexual reproduction, and infection ability in their knockout mutants. Our results suggest that both of the lists might contain large proportions of unrelated genes to pathogenicity and therefore comparing the two gene lists is hardly helpful for the identification of genes that are more likely to be involved in pathogenicity as we initially expected.
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Sweigard, James A., Anne M. Carroll, Leonard Farrall, Forrest G. Chumley, and Barbara Valent. "Magnaporthe grisea Pathogenicity Genes Obtained Through Insertional Mutagenesis." Molecular Plant-Microbe Interactions® 11, no. 5 (May 1998): 404–12. http://dx.doi.org/10.1094/mpmi.1998.11.5.404.

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We have initiated a mutational analysis of pathogenicity in the rice blast fungus, Magnaporthe grisea, in which hygromycin-resistant transformants, most generated by restriction enzyme-mediated integration (REMI), were screened for the ability to infect plants. A rapid primary infection assay facilitated screening of 5,538 transformants. Twenty-seven mutants were obtained that showed a reproducible pathogenicity defect, and 18 of these contained mutations that cosegregated with the hygromycin resistance marker. Analysis of eight mutants has resulted in the cloning of seven PTH genes that play a role in pathogenicity on barley, weeping lovegrass, and rice. Two independent mutants identified the same gene, PTH2, suggesting nonrandom insertion of the transforming DNA. These first 7 cloned PTH genes are described.
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Dissertations / Theses on the topic "Pathogenicity genes"

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Reitmann, Anandi. "Identification of pathogenicity genes in Phytophthora cinnamomi." Diss., University of Pretoria, 2014. http://hdl.handle.net/2263/79179.

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Nishiyama, Yukihiro. "Herpesvirus Genes: Molecular Basis of Viral Replication and Pathogenicity." 名古屋大学医学部, 1996. http://hdl.handle.net/2237/6180.

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Holman, Holly A. "Investigation of ICP34.5 and its role in HSV pathogenicity." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321914.

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Fulton, Ciaran Eugene. "The isolation of virulence genes from the ubiquitous plant pathogen, Colletotrichum gloeosporioides." Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337296.

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Jackson, Robert Wilson. "Plasmids and virulence in Pseudomonas syringae pv. phaseolicola." Thesis, University of the West of England, Bristol, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389510.

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Liddle, Shona. "Strategies for studying pathogenicity genes of Xanthomanas campestris pv. campestris." Thesis, University of East Anglia, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306113.

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Besi, Maria. "Identification of novel pathogenicity-related genes in the rice blast fungus, Magnaporthe oryzae." Thesis, University of East Anglia, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539361.

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Couchman, Edward C., Hilary P. Browne, Matt Dunn, Trevor D. Lawley, J. Glenn Songer, Val Hall, Liljana Petrovska, et al. "Clostridium sordellii genome analysis reveals plasmid localized toxin genes encoded within pathogenicity loci." BioMed Central Ltd, 2015. http://hdl.handle.net/10150/610282.

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BACKGROUND: Clostridium sordellii can cause severe infections in animals and humans, the latter associated with trauma, toxic shock and often-fatal gynaecological infections. Strains can produce two large clostridial cytotoxins (LCCs), TcsL and TcsH, related to those produced by Clostridium difficile, Clostridium novyi and Clostridium perfringens, but the genetic basis of toxin production remains uncharacterised. RESULTS: Phylogenetic analysis of the genome sequences of 44 strains isolated from human and animal infections in the UK, US and Australia placed the species into four clades. Although all strains originated from animal or clinical disease, only 5 strains contained LCC genes: 4 strains contain tcsL alone and one strain contains tcsL and tcsH. Four toxin-positive strains were found within one clade. Where present, tcsL and tcsH were localised in a pathogenicity locus, similar to but distinct from that present in C. difficile. In contrast to C. difficile, where the LCCs are chromosomally localised, the C. sordellii tcsL and tcsH genes are localised on plasmids. Our data suggest gain and loss of entire toxigenic plasmids in addition to horizontal transfer of the pathogenicity locus. A high quality, annotated sequence of ATCC9714 reveals many putative virulence factors including neuraminidase, phospholipase C and the cholesterol-dependent cytolysin sordellilysin that are highly conserved between all strains studied. CONCLUSIONS: Genome analysis of C. sordellii reveals that the LCCs, the major virulence factors, are localised on plasmids. Many strains do not contain the LCC genes; it is probable that in several of these cases the plasmid has been lost upon laboratory subculture. Our data are consistent with LCCs being the primary virulence factors in the majority of infections, but LCC-negative strains may precipitate certain categories of infection. A high quality genome sequence reveals putative virulence factors whose role in virulence can be investigated.
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Ammouneh, Hassan. "Molecular characterisation of virulence genes on a pathogenicity island in Pseudomonas savastanoi pv. phaseolicola." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405032.

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Gamieldien, Junaid. "Novel genomic approaches for the identification of virulence genes and drug targets in pathogenic bacteria." Thesis, University of the Western Cape, 2001. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_4400_1185438906.

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While the many completely sequenced genomes of bacterial pathogens contain all the determinants of the host-pathogen interaction, and also every possible drug target and recombinant vaccine candidate, computational tools for selecting suitable candidates for further experimental analyses are limited to date. The overall objective of my PhD project was to attempt to design reusable systems that employ the two most important features of bacterial evolution, horizontal gene transfer and adaptive mutation, for the identification of potentially novel virulence-associated factors and possible drug targets. In this dissertation, I report the development of two novel technologies that uncover novel virulence-associated factors and mechanisms employed by bacterial pathogens to effectively inhabit the host niche. More importantly, I illustrate that these technologies may present a reliable starting point for the development of screens for novel drug targets and vaccine candidates, significantly reducing the time for the development of novel therapeutic strategies. Our initial analyses of proteins predicted from the preliminary genomic sequences released by the Sanger Center indicated that a significant number appeared to be more similar to eukaryotic proteins than to their bacterial orthologs. In order determine whether acquisition of genetic material from eukaryotes has played a role in the evolution of pathogenic bacteria, we developed a system that detects genes in a bacterial genome that have been acquired by interkingdom horizontal gene transfer.. Initially, 19 eukaryotic genes were identified in the genome of Mycobacterium tuberculosis of which 2 were later found in the genome of Pseudomonas aeruginosa, along with two novel eukaryotic genes.

Surprisingly, six of the M. tuberculosis genes and all four eukaryotic genes in P. aeruginosa may be involved in modulating the host immune response through altering the steroid balance and the production of pro-inflammatory lipids. We also compared the genome of the H37Rv M. tuberculosis strain to that of the CDC- 1551 strain that was sequenced by TIGR and found that the organisms were virtually identical with respect to their gene content, and hypothesized that the differences in virulence may be due to evolved differences in shared genes, rather than the absence/presence of unique genes. Using this observation as rationale, we developed a system that compares the orthologous gene complements of two strains of a bacterial species and mines for genes that have undergone adaptive evolution as a means to identify possibly novel virulence &ndash
associated genes. By applying this system to the genome sequences of two strains of Helicobacter pylori and Neisseria meningitidis, we identified 41 and 44 genes that are under positive selection in these organisms, respectively. As approximately 50% of the genes encode known or potential virulence factors, the remaining genes may also be implicated in virulence or pathoadaptation. Furthermore, 21 H. pylori genes, none of which are classic virulence factors or associated with a pathogenicity island, were tested for a role in colonization by gene knockout experiments. Of these, 61% were found to be either essential, or involved in effective stomach colonization in a mouse infection model. A significant amount of strong circumstantial and empirical evidence is thus presented that finding genes under positive selection is a reliable method of identifying novel virulence-associated genes and promising leads for drug targets.

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Books on the topic "Pathogenicity genes"

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Becker, Yechiel, and Gholamreza Darai, eds. Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85004-2.

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Liddle, Shona. Strategies for studying pathogenicity genes of Xanthomonas campestris pv. campestris. Norwich: Universityof East Anglia, 1992.

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Gupta, Vijai Kumar. Biotechnology of fungal genes. Boca Raton, FL: CRC Press, 2012.

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Levente, Emödy, and FEMS Symposium on Genes and Proteins Underlying Microbial Urinary Tract Virulence: Basic Aspects and Applications (1999 : Pécs, Hungary), eds. Genes and proteins underlying microbial urinary tract virulence: Basic aspects and applications. New York: Kluwer Academic/Plenum Publishers, 2000.

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Jörg, Hacker, and Dobrindt Ulrich, eds. Pathogenomics: Genome analysis of pathogenic microbes. Weinheim: Wiley-VCH, 2006.

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Becker, Yechiel. Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes. Springer, 2011.

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Yechiel, Becker, and Darai Gholamreza, eds. Pathogenicity of human herpesviruses due to specific pathogenicity genes. Berlin: Springer-Verlag, 1994.

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Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes. Springer, 2011.

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Becker, Yechiel, and Gholamreza Darai. Pathogenicity of Human Herpesviruses Due to Specific Pathogenicity Genes. Springer London, Limited, 2012.

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Swarup, Sanjay. Isolation of pathogenicity genes from xanthomonas species and a study of their regulation. 1991.

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Book chapters on the topic "Pathogenicity genes"

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Sarwar, Muhammad Kaleem, Imran Ul Haq, Siddra Ijaz, Iqrar Ahmad Khan, and Aşkim Hediye Sekmen Çetinel. "Pathogenicity Genes." In Phytomycology and Molecular Biology of Plant–Pathogen Interactions, 75–86. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003162742-4.

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Van Etten, Hans, Scott Soby, Catherine Wasmann, and Kevin McCluskey. "Pathogenicity Genes in Fungi." In Advances in Molecular Genetics of Plant-Microbe Interactions, 163–70. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0177-6_25.

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Daniels, M. J., P. C. Turner, C. E. Barber, M. K. Sawczyc, and F. Dums. "Pathogenicity Genes of Xanthomonas Campestris." In Plant Pathogenic Bacteria, 394–403. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3555-6_79.

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Becker, Yechiel, Eynat Tabor, Yael Asher, Mirta Grifman, Yosef Kleinman, and Avner Yayon. "Entry of Herpes Simplex Virus Type 1 into Cells — Early Steps in Virus Pathogenicity." In Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes, 3–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85004-2_1.

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Rösen-Wolff, Angela, Roland Kehm, Eva Lorentzen, Wolfram Lamade, and Gholamreza Darai. "Pathogenicity and Latency of Herpes Simplex Virus in the Animal Model System Tree Shrew." In Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes, 177–202. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85004-2_10.

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Grifman, Mirta, and Yechiel Becker. "Computer Analysis of the Protein Coded by Herpes Simplex Virus Type 1 UL56 Gene." In Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes, 203–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85004-2_11.

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Wagner, Edward K. "The Herpes Simplex Type 1 Virus Latency Gene." In Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes, 210–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85004-2_12.

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Levine, Myron, David J. Fink, Ramesh Ramakrishnan, Prashant Desai, William F. Goins, and Joseph C. Glorioso. "Neurovirulence of Herpes Simplex Virus Type 1 Accessory Gene Mutants." In Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes, 222–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85004-2_13.

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Latchman, David S. "Herpes Simplex Virus Latency and Immediate Early Gene Repression by the Cellular Octamer-Binding Protein Oct-2." In Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes, 238–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85004-2_14.

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Moyal, Michal, and Yechiel Becker. "The Cell Fusion Protein Gene (UL53) of Herpes Simplex Virus Type 1 — A Pathogenicity Gene." In Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes, 253–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85004-2_15.

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Conference papers on the topic "Pathogenicity genes"

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Slukin, P. V., L. V. Kolupaeva, and N. K. Fursova. "PATHOGENICITY ISLAND SAND VIRULENCE GENES OF UROPATHOGENIC ESCHERICHIA COLI." In Molecular Diagnostics and Biosafety. Federal Budget Institute of Science 'Central Research Institute for Epidemiology', 2020. http://dx.doi.org/10.36233/978-5-9900432-9-9-71.

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Kim, Mansuck, Huan Zhang, Charles Woloshuk, Won-Bo Shim, and Byung-Jun Yoon. "Computational identification of key functional genes associated with fusarium verticillioides pathogenicity." In BCB '15: ACM International Conference on Bioinformatics, Computational Biology and Biomedicine. New York, NY, USA: ACM, 2015. http://dx.doi.org/10.1145/2808719.2814831.

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Webb, Kimberly M., Paul Covey, Brett Kuwitzky, and Mia Hanson. "CHARACTERIZATION OF A POPULATION OF FUSARIUM OXYSPORUM, FROM SUGAR BEET, USING THE POPULATION STRUCTURE OF PUTATIVE PATHOGENICITY GENES." In 37th Biennial Meeting of American Society of Sugarbeet Technologist. ASSBT, 2013. http://dx.doi.org/10.5274/assbt.2013.52.

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Azmi, Muhammad Bilal. "In Silico Basis to Understand the Molecular Interaction of Human NNATGene With Therapeutic Compounds of Anorexia Nervosa." In INTERNATIONAL CONFERENCE ON BIOLOGICAL RESEARCH AND APPLIED SCIENCE. Jinnah University for Women, Karachi,Pakistan, 2022. http://dx.doi.org/10.37962/ibras/2022/1-2.

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Introduction: Anorexia nervosa (AN)– a perplexing heritable, psychiatric eating disorder condition characterized by low body weight. The prevalence of AN is found to be high in younger age adults with a raised mortality rate. Genetic studies have been insufficient in identifying the role of specific genes that predispose an individual to AN. Objectives: The objective was to explore the role of NNAT (neuronatin) gene variants and its structure based molecular interactions with therapeutic compounds of AN. To investigate the role of structural missense pathogenic variants (SNPs: single nucleotide polymorphism) or change in the expression of NNAT with possibility of AN. Methodology: NNAT gene protein coding sequence, SNPs were extracted and validated from public databases. Gene to gene interactions, protein localization and human tissue-specific expression analysis of NNAT gene showed highest tissue-specific expression in the brain. Estimates of functional impact of SNPs using transcript sequence and machine learning based approaches (in silico algorithms) were computed to investigate the pathogenicity and protein stability of NNAT variants. Sequence alignment, ab initio 3D structure-modeling of wild-type, validation and recognition of binding cavities of NNAT through in silico web based tools were performed. Alternate model prediction for NNAT variants through residue specific mutation approach and structural validation were also done through Chimera tool. The 3D compounds involved in the management of AN were extracted from the Drug Bank database, afterwards energy minimization and rule of drug-likeness were performed. The eligible 3D compounds were docked with identified variants, to evaluate the drugs binding molecular mechanics. Results & Conclusion: Overall, 10 NNAT missense variants were extracted on the basis of minor allele frequency (MAF < 0.001) and other consequence types. Further three variants were selected among ten according to the transcript sequence, which includesrs542858994 (F26L), rs539681368 (C30Y) and rs542858994 (F53L). Structures for these variants’ protein were generated, validated and docked with AN drugs. The functional impact analyses of selected missense SNPs of NNAT showed high risk pathogenicity and can cause changes in the physical and chemical properties of amino acids, thus affecting the function of protein. The computation of binding energies of variants of NNAT with AN compounds strengthen the hypothesis that these variants strongly interact with the AN drugs, hence reducing the level of free NNAT as well as target drugs, for neuronal functioning. Therefore, constitutionally reduced level of NNAT and binding of NNAT variants with AN drugs may serve as the basis to increases the susceptibility towards AN.
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Ferreira, Shirley Cristina Reis, Luísa Neiva Araújo, Sérgio Rubens Lacerda Morais, Maria Fernanda Soares Batista, and Silvia Fernandes Ribeiro da Silva. "MÉTODOS DIAGNÓSTICOS DE INFECÇÃO POR H. PYLORI: UMA REVISÃO LITERÁRIA." In I Congresso Brasileiro de Doenças Infectocontagiosas On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/2226.

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Introdução: A infecção pela bactéria Helicobacter pylori (H. pylori) é mundialmente frequente e relaciona-se a doenças, como dispepsia, úlcera péptica e neoplasias gástricas. É um bastonete espiralado, multiflagelado e gram negativo, que provoca a destruição gradativa das camadas gástricas e duodenais. Objetivo: Revisar os principais métodos que identificam a presença da bactéria H. pylori no TGI. Material e métodos: Este resumo foi realizado com base em uma pesquisa bibliográfica qualitativa exploratória feita nas bases de dados PubMed e SciELO utilizando H. pylori, pathogenicity e diagnosis como descritores. Foram incluídos 10 artigos dos últimos 5 anos. Resultados: A histologia e/ou cultura e exame direto da amostra de biópsia gástrica é padrão ouro para o diagnóstico da infecção pelo H. pylori, com sensibilidade e especificidade de até 95% e 98%, respectivamente. Porém, devido a necessidade de endoscopia para obtenção da amostra, são considerados métodos invasivos, mas fundamentais para o diagnóstico e avaliação do(a): a) grau da inflamação; b) presença de úlceras; e c) gravidade da gastrite. Além disso, pode identificar linfoma MALT e câncer. O teste rápido da urease (RUT), que também necessita da endoscopia para a sua realização, a análise da amostra do patógeno em fezes ou teste do antígeno fecal, a detecção de anticorpos anti-H. pylori e os testes baseados em reação em cadeia da polimerase (PCR), que detecta os genes de virulência, também são opções utilizadas. Alguns autores relatam que há uma relação direta dos genes de virulência com as possíveis manifestações clínicas. Conforme consenso internacional, um único teste não invasivo positivo é fundamental para indicação de endoscopia com avaliação histológica. Embora, o teste respiratório de uréia, possa apresentar resultados falso-positivos, é utilizado, bem como o teste de antígeno fecal, para detectar a erradicação da bactéria durante o tratamento. Conclusão: Os principais métodos diagnósticos utilizados para a confirmação da presença da bactéria H. pylori são testes invasivos, com endoscopia associada à biópsia, sendo a amostra obtida analisada por histologia, cultura, RUT e PCR. Os testes não invasivos sinalizam o uso de testes invasivos para confirmar patologias associadas à infecção e avaliam a erradicação da bactéria durante o tratamento.
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Lincoln, S., K. Nykamp, Y. Kobayashi, S. Yang, M. Powers, M. Anderson, F. Monzon, and S. Topper. "Abstract P2-09-11: Consistency of pathogenicity determinations for hereditary cancer gene mutations." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p2-09-11.

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Saputra, Indra Kurniawan, I. Made Artika, and Tasliah. "The blight-resistance gene response to bacterial leaf blight disease in isogenic varieties through pathogenicity test." In PROCEEDINGS OF THE 3RD INTERNATIONAL SEMINAR ON METALLURGY AND MATERIALS (ISMM2019): Exploring New Innovation in Metallurgy and Materials. AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0002644.

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Ghasemi, Farzaneh, Mohammad Mehdi Heidari, Yuriy L. Orlov, Mehri Khatami, and Ludmila E. Tabikhanova. "Consideration of pathogenicity of nsSNVs in CDKN2A gene, as a new tumor marker for leukemia, using bioinformatics methods." In 2020 Cognitive Sciences, Genomics and Bioinformatics (CSGB). IEEE, 2020. http://dx.doi.org/10.1109/csgb51356.2020.9214605.

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Reports on the topic "Pathogenicity genes"

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Prusky, Dov, and Jeffrey Rollins. Modulation of pathogenicity of postharvest pathogens by environmental pH. United States Department of Agriculture, December 2006. http://dx.doi.org/10.32747/2006.7587237.bard.

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Until recently, environmental pH was not considered a factor in determining pathogen compatibility. Our hypothesis was that the environmental pH at the infection site, which is dynamically controlled by activities of both the host and the pathogen, regulates the expression of genes necessary for disease development in Colletotrichum gloeosporioides and Sclerotinia sclerotiorum. This form of regulation ensures that genes are expressed at optimal conditions for their encoded activities.Pectate lyase encoded by pelB, has been demonstrated to play a key role in virulence of C. gloeosporioides in avocado fruit. Polyglacturonase synergism with oxalic acid production is considered to be an essential pathogenicity determinant in the interactions of S. sclerotiorum with its numerous hosts. A common regulatory feature of these virulence and pathogenicity factors is their dependence upon environmental pH conditions within the host niche to create optimal conditions for expression and secretion. In this proposal we have examined, 1) the mechanisms employed by these fungi to establish a suitable pH environment, 2) the molecular levels at which genes and gene products are regulated in response to environmental pH, and 3) the molecular basis and functional importance of pH-responsive gene regulation during pathogenicity. The specific objectives of the proposal were: 1. Characterize the mechanism of local pH modulation and the effect of ambient pH on the expression and secretion of virulence factors. 2. Provide evidence that a conserved molecular pathway for pH-responsive gene expression exists in C. gloeosporioides by cloning a pacC gene homologue. 3. Determine the role of pacC in pathogenicity by gene disruption and activating mutations. Major conclusions 1. We determined the importance of nitrogen source and external pH in the secretion of the virulence factor pectate lyase with respect to the ambient pH transcriptional regulator pacC. It was concluded that nitrogen source availability and ambient pH are two independent signals for the transcriptional regulation of genes required for the disease process of C. gloeosporioides and possibly of other pathogens. 2. We also determined that availability of ammonia regulate independently the alkalinization process and pelB expression, pecate lyase secretion and virulence of C. gloeosporioides. 3. Gene disruption of pacC reduced virulence of C. gloeosporioides however did not reduced fully pelB expression. It was concluded that pelB expression is regulated by several factors including pH, nitrogen and carbon sources. 4. Gene disruption of pacC reduced virulence of S. slcerotiourum Creation of a dominant activating
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Shaw, John, Arieh Rosner, Thomas Pirone, Benjamin Raccah, and Yehezkiel Antignus. The Role of Specific Viral Genes and Gene Products in Potyviral Pathogenicity, Host Range and Aphid Transmission. United States Department of Agriculture, August 1992. http://dx.doi.org/10.32747/1992.7561070.bard.

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In this research we have studied the molecular biology of carotenoid biosynthesis in tomato. The investigations focused on the genes Pds and Psy, encoding desaturase and phytoene synthase, respectively, which are key enzymes in the biosynthetic pathway of lycopene and b-carotene. In addition, we have investigated the genes for lycopene cyclase. We have cloned from tomato and characterized the cDNA of CrtL-e, which encodes the lycopene e-cyclase, and analyzed its expression during fruit development. The results establish a paradigm for the regulation of carotenoid pigment biosynthesis during the ripening process of fruits. It is concluded that transcriptional regulation of genes that encode carotenoid-biosynthesis enzymes is the major mechanism that governs specific pigment accumulation. During the ripening of tomato fruits transcription of the genes encoding the enzymes phytoene synthase and phytoene desaturase is up-regulated, while the transcription of the genes for both lycopene cyclases decreases and thus the conversion of lycopene to subsequent carotenoids is inhibited. These findings support the working hypothesis of the molecular approach to manipulating carotenogenesis by altering gene expression in transgenic plants, and offer obvious strategies to future application in agriculture. The molecular and physiological knowledge on carotenogenesis gained in this project, suggest a concept for manipulating gene expression that will alter carotenoid composition in fruits and flowers.
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Prusky, Dov, Nancy P. Keller, and Amir Sherman. global regulation of mycotoxin accumulation during pathogenicity of Penicillium expansum in postharvest fruits. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7600012.bard.

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Background to the topic- Penicilliumas a postharvest pathogen and producer of the mycotoxin PAT. Penicilliumspp. are destructive phytopathogens, capable of causing decay in many deciduous fruits, during postharvest handling and storage; and the resulting losses can amount to 10% of the stored produce and the accumulation of large amounts of the mycotoxinpatulin. The overall goal of this proposal is to identify critical host and pathogen factors that modulate P. expansummycotoxin genes and pathways which are required for PAT production and virulence. Our preliminary results indicated that gluconic acid are strongly affecting patulin accumulation during colonization. P. expansumacidifies apple fruit tissue during colonization in part through secretion of gluconic acid (GLA). Several publications suggested that GLA accumulation is an essential factor in P. expansumpathogenicity. Furthermore, down regulation of GOX2 significantly reduced PAT accumulation and pathogenicity. PAT is a polyketide and its biosynthesis pathway includes a 15-gene cluster. LaeA is a global regulator of mycotoxin synthesis. It is now known that patulin synthesis might be subjected to LaeA and sometimes by environmental sensing global regulatory factors including the carbon catabolite repressor CreA as well as the pH regulator factor PacC and nitrogen regulator AreA. The mechanisms by which LaeA regulates patulin synthesis was not fully known and was part of our work. Furthermore, the regulatory system that controls gene expression in accordance with ambient pH was also included in our work. PacC protein is in an inactive conformation and is unable to bind to the promoter sites of the target genes; however, under alkaline growth conditions activated PacC acts as both an activator of alkaline-expressed genes and a repressor of acid-expressed genes. The aims of the project- This project aims to provide new insights on the roles of LaeA and PacC and their signaling pathways that lead to GLA and PAT biosynthesis and pathogenicity on the host. Specifically, our specific aims were: i) To elucidate the mechanism of pH-controlled regulation of GLA and PAT, and their contribution to pathogenesis of P. expansum. We are interested to understanding how pH and/or GLA impact/s under PacC regulation affect PAT production and pathogenesis. ii) To characterize the role of LaeA, the global regulator of mycotoxin production, and its effect on PAT and PacC activity. iii) To identify the signaling pathways leading to GLA and PAT synthesis. Using state- of-the-art RNAseq technologies, we will interrogate the transcriptomes of laeAand pacCmutants, to identify the common signaling pathways regulating synthesis of both GLA and PAT. Major conclusions, solutions, achievements- In our first Aim our results demonstrated that ammonia secreted at the leading edge of the fungal colony induced transcript activation of the global pH modulator PacC and PAT accumulation in the presence of GLA. We assessed these parameters by: (i) direct exogenous treatment of P. expansumgrowing on solid medium; (ii) direct exogenous treatment on colonized apple tissue; (iii) growth under self-ammonia production conditions with limited carbon; and (iv) analysis of the transcriptional response to ammonia of the PAT biosynthesis cluster. Ammonia induced PAT accumulation concurrently with the transcript activation of pacCand PAT biosynthesis cluster genes, indicating the regulatory effect of ammonia on pacCtranscript expression under acidic conditions. Transcriptomic analysis of pH regulated processes showed that important genes and BARD Report - Project 4773 Page 2 of 10 functionalities of P. expansumwere controlled by environmental pH. The differential expression patterns of genes belonging to the same gene family suggest that genes were selectively activated according to their optimal environmental conditions to enable the fungus to cope with varying conditions and to make optimal use of available enzymes. Concerning the second and third Aims, we demonstrated that LaeA regulates several secondary metabolite genes, including the PAT gene cluster and concomitant PAT synthesis invitro. Virulence studies of ΔlaeAmutants of two geographically distant P. expansumisolates (Pe-21 from Israel and Pe-T01 from China) showed differential reduction in disease severity in freshly harvested fruit ranging from no reduction for Ch-Pe-T01 strains in immature fruit to 15–25% reduction for both strains in mature fruit, with the ΔlaeAstrains of Is-Pe-21 always showing a greater loss in virulence. Results suggest the importance of LaeA regulation of PAT and other secondary metabolites on pathogenicity. Our work also characterized for the first time the role of sucrose, a key nutritional factor present in apple fruit, as a negative regulator of laeAexpression and consequent PAT production in vitro. This is the first report of sugar regulation of laeAexpression, suggesting that its expression may be subject to catabolite repression by CreA. Some, but not all of the 54 secondary metabolite backbone genes in the P. expansumgenome, including the PAT polyketide backbone gene, were found to be regulated by LaeA. Together, these findings enable for the first time a straight analysis of a host factor that potentially activates laeAand subsequent PAT synthesis.
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VanEtten, H. Phytoalexin detoxification genes and gene products: Implication for the evolution of host specific traits for pathogenicity. Final report. Office of Scientific and Technical Information (OSTI), June 1997. http://dx.doi.org/10.2172/491534.

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Lichter, Amnon, Gopi K. Podila, and Maria R. Davis. Identification of Genetic Determinants that Facilitate Development of B. cinerea at Low Temperature and its Postharvest Pathogenicity. United States Department of Agriculture, March 2011. http://dx.doi.org/10.32747/2011.7592641.bard.

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Botrytis cinerea is the postharvest pathogen of many agricultural produce with table grapes, strawberries and tomatoes as major targets. The high efficiency with which B. cinerea causes disease on these produce during storage is attributed in part due to its exceptional ability to develop at very low temperature. Our major goal was to understand the genetic determinants which enable it to develop at low temperature. The specific research objectives were: 1. Identify expression pattern of genes in a coldenriched cDNA library. 2. Identify B. cinerea orthologs of cold-induced genes 3. Profile protein expression and secretion at low temperature on strawberry and grape supplemented media. 4. Test novel methods for the functional analysis of coldresponsive genes. Objective 1 was modified during the research because a microarray platform became available and it allowed us to probe the whole set of candidate genes according to the sequence of 2 strains of the fungus, BO5.10 and T4. The results of this experiment allowed us to validate some of our earlier observations which referred to genes which were the product of a SSH suppression-subtraction library. Before the microarray became available during 2008 we also analyzed the expression of 15 orthologs of cold-induced genes and some of these results were also validated by the microarray experiment. One of our goals was also to perform functional analysis of cold-induced genes. This goal was hampered for 3 years because current methodology for transformation with ‘protoplasts’ failed to deliver knockouts of bacteriordopsin-like (bR) gene which was our primary target for functional analysis. Consequently, we developed 2 alternative transformation platforms, one which involves an air-gun based technique and another which involves DNA injection into sclerotia. Both techniques show great promise and have been validated using different constructs. This contribution is likely to serve the scientific community in the near future. Using these technologies we generated gene knockout constructs of 2 genes and have tested there effect on survival of the fungus at low temperature. With reference to the bR genes our results show that it has a significant effect on mycelial growth of the B. cinerea and the mutants have retarded development at extreme conditions of ionic stress, osmotic stress and low temperature. Another gene of unknown function, HP1 is still under analysis. An ortholog of the yeast cold-induced gene, CCH1 which encodes a calcium tunnel and was shown to be cold-induced in B. cinerea was recently cloned and used to complement yeast mutants and rescue them from cold-sensitivity. One of the significant findings of the microarray study involves a T2 ribonuclease which was validated to be cold-induced by qPCR analysis. This and other genes will serve for future studies. In the frame of the study we also screened a population of 631 natural B. cinerea isolates for development at low temperature and have identified several strains with much higher and lower capacity to develop at low temperature. These strains are likely to be used in the future as candidates for further functional analysis. The major conclusions from the above research point to specific targets of cold-induced genes which are likely to play a role in cold tolerance. One of the most significant observations from the microarray study is that low temperature does not induce ‘general stress response in B. cinerea, which is in agreement to its exceptional capacity to develop at low temperature. Due to the tragic murder of the Co-PI Maria R. Davis and GopiPodila on Feb. 2010 it is impossible to deliver their contribution to the research. The information of the PI is that they failed to deliver objective 4 and none of the information which relates to objective 3 has been delivered to the PI before the murder or in a visit to U. Alabama during June, 2010. Therefore, this report is based solely on the IS data.
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Karpeeva, E. A. Frequency of Occurrence of Pathogenicity Genes in Case of Coculture of Escherichia Coli With Protozoans Blastocystis Hominis. Prof. Dr Kuznetsov Alexandre Semenovich, March 2015. http://dx.doi.org/10.14526/25_2015_25.

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Dickman, Martin B., and Oded Yarden. Phosphorylative Transduction of Developmental and Pathogenicity-Related Cues in Sclerotinia Sclerotiorum. United States Department of Agriculture, April 2004. http://dx.doi.org/10.32747/2004.7586472.bard.

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Sclerotinia sclerotiorum (Lib.) de Bary is among the world's most successful and omnivorous fungal plant pathogens. Included in the more than 400 species of plants reported as hosts to this fungus are canola, alfalfa, soybean, sunflower, dry bean, and potato. The general inability to develop resistant germplasm with these economically important crops to this pathogen has focused attention on the need for a more detailed examination of the pathogenic determinants involved in disease development. This proposal involved experiments that examined the involvement of protein phosphorylation during morphogenesis (hyphal elongation and sclerotia formation) and pathogenesis (oxalic acid). Data obtained from our laboratories during the course of this project substantiates the fact that kinases and phosphatases are involved and important for these processes. A mechanistic understanding of the successful strategy(ies) used by S . sclerotiorum in infecting and proliferating in host plants and this linkage to fungal development will provide targets and/or novel approaches with which to design resistant crop plants including interference with fungal pathogenic development. The original objectives of this grant included: I. Clone the cyclic AMP-dependent protein kinase A (PKA) catalytic subunit gene from S.sclerotiorum and determine its role in fungal pathogenicity, OA production (OA) and/or morphogenesis (sclerotia formation). II. Clone and characterize the catalytic and regulatory subunits of the protein phosphatase PP2A holoenzyme complex and determine their role in fungal pathogenicity and/or morphogenesis as well as linkage with PKA-regulation of OA production and sclerotia formation. III. Clone and characterize the adenylate cyclase-encoding gene from S . sclerotiorum and detennine its relationship to the PKA/PP2A-regulated pathway. IV. Analyze the expression patterns of the above-mentioned genes and their products during pathogenesis and determine their linkage with infection and fungal growth.
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Wisniewski, Michael E., Samir Droby, John L. Norelli, Noa Sela, and Elena Levin. Genetic and transcriptomic analysis of postharvest decay resistance in Malus sieversii and the characterization of pathogenicity effectors in Penicillium expansum. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7600013.bard.

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Blue mold of apple caused by Penicilliumexpansumis a major postharvest disease. Selection for postharvest disease resistance in breeding programs has been ignored in favor of fruit quality traits such as size, color, taste, etc. The identification of postharvest disease resistance as a heritable trait would represent a significant accomplishment and has not been attempted in apple. Furthermore, insight into the biology of the pathogenicity of P. expansumin apple could provide new approaches to postharvest decay management. Hypothesis: Postharvest resistance of apple to P. expansumcan be mapped to specific genetic loci and significant quantitative-trait-loci (QTLs) can be identified that account for a major portion of the population variance. Susceptibility of apple fruit to P. expansumis dependent on the ability of the pathogen to produce LysM effectors that actively suppress primary and/or secondary resistance mechanisms in the fruit. Objectives: 1) Identify QTL(s) and molecular markers for blue mold resistance in GMAL4593 mapping population (‘Royal Gala’ X MalussieversiiPI613981), 2) Characterize the transcriptome of the host and pathogen (P. expansum) during the infection process 3) Determine the function of LysM genes in pathogenicity of P. expansum. Methods: A phenotypic evaluation of blue mold resistance in the GMAL4593 mapping population, conducted in several different years, will be used for QTL analysis (using MapQTL 6.0) to identify loci associated with blue mold resistance. Molecular markers will be developed for the resistance loci. Transcriptomic analysis by RNA-seq will be used to conduct a time course study of gene expression in resistant and susceptible apple GMAL4593 genotypes in response to P. expansum, as well as fungal responses to both genotypes. Candidate resistance genes identified in the transcriptomic study and or bioinformatic analysis will be positioned in the ‘Golden Delicious’ genome to identify markers that co-locate with the identified QTL(s). A functional analysis of LysM genes on pathogenicity will be conducted by eliminating or reducing the expression of individual effectors by heterologous recombination and silencing technologies. LysMeffector genes will also be expressed in a yeast expression system to study protein function. Expected Results: Identification of postharvest disease resistance QTLs and tightly-linked genetic markers. Increased knowledge of the role of effectors in blue mold pathogenic
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Lindow, Steven, Isaac Barash, and Shulamit Manulis. Relationship of Genes Conferring Epiphytic Fitness and Internal Multiplication in Plants in Erwinia herbicola. United States Department of Agriculture, July 2000. http://dx.doi.org/10.32747/2000.7573065.bard.

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Most bacterial plant pathogens colonize the surface of healthy plants as epiphytes before colonizing internally and initiating disease. The epiphytic phase of these pathogens is thus an important aspect of their epidemiology and a stage at which chemical and biological control is aimed. However, little is known of the genes and phenotypes that contribute to the ability of bacteria to grow on leaves and survive the variable physical environment in this habitat. In addition, while genes such as hrp awr and others which confer pathogenicity and in planta growth ability have been described, their contribution to other aspects of bacterial epidemiology such as epiphytic fitness have not been addressed. We hypothesized that bacterial genes conferring virulence or pathogenicity to plants also contribute to the epiphytic fitness of these bacteria and that many of these genes are preferentially located on plasmids. We addressed these hypotheses by independently identifying genes that contribute to epiphytic fitness, in planta growth, virulence and pathogenicity in the phytopathogenic bacterium Erwinia herbicola pv gypsophilae which causes gall formation on gypsophila. This species is highly epiphytically fit and has acquired a plasmid (pPATH) that contains numerous pathogenicity and virulence determinants, which we have found to also contribute to epiphytic fitness. We performed saturation transposon mutagenesis on pPATH as well as of the chromosome of E.h. gypsophilae, and identified mutants with reduced ability to grow in plants and/or cause disease symptoms, and through a novel competition assay, identified mutants less able to grow or survive on leaves. The number and identity of plasmid-borne hrp genes required for virulence was determined from an analysis of pPATH mutants, and the functional role of these genes in virulence was demonstrated. Likewise, other pPATH-encoded genes involved in IAA and cytokinin biosynthesis were characterized and their pattern of transcriptional activity was determined in planta. In both cases these genes involved in virulence were found to be induced in plant apoplasts. About half of avirulent mutants in pPATH were also epiphytically unfit whereas only about 10% of chromosomal mutants that were avirulent also had reduced epiphytic fitness. About 18% of random mutants in pPATH were avirulent in contrast to only 2.5% of random chromosomal mutants. Importantly, as many as 28% of pPATH mutants had lower epiphytic fitness while only about 10% of random chromosomal mutants had lower epiphytic fitness. These results support both of our original hypotheses, and indicate that genes important in a variety of interactions with plant have been enriched on mobile plasmids such as pPATH. The results also suggest that the ability of bacteria to colonize the surface of plants and to initiate infections in the interior of plants involves many of the same traits. These traits also appear to be under strong regulatory control, being expressed in response to the plant environment in many cases. It may be possible to alter the pattern of expression of such genes by altering the chemical environment of plants either by genetic means or by additional or chemical antagonists of the plant signals. The many novel bacterial genes identified in this study that are involved in plant interactions should be useful in further understanding of bacterial plant interactions.
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Coplin, David L., Shulamit Manulis, and Isaac Barash. roles Hrp-dependent effector proteins and hrp gene regulation as determinants of virulence and host-specificity in Erwinia stewartii and E. herbicola pvs. gypsophilae and betae. United States Department of Agriculture, June 2005. http://dx.doi.org/10.32747/2005.7587216.bard.

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Gram-negative plant pathogenic bacteria employ specialized type-III secretion systems (TTSS) to deliver an arsenal of pathogenicity proteins directly into host cells. These secretion systems are encoded by hrp genes (for hypersensitive response and pathogenicity) and the effector proteins by so-called dsp or avr genes. The functions of effectors are to enable bacterial multiplication by damaging host cells and/or by blocking host defenses. We characterized essential hrp gene clusters in the Stewart's Wilt of maize pathogen, Pantoea stewartii subsp. stewartii (Pnss; formerly Erwinia stewartii) and the gall-forming bacterium, Pantoea agglomerans (formerly Erwinia herbicola) pvs. gypsophilae (Pag) and betae (Pab). We proposed that the virulence and host specificity of these pathogens is a function of a) the perception of specific host signals resulting in bacterial hrp gene expression and b) the action of specialized signal proteins (i.e. Hrp effectors) delivered into the plant cell. The specific objectives of the proposal were: 1) How is the expression of the hrp and effector genes regulated in response to host cell contact and the apoplastic environment? 2) What additional effector proteins are involved in pathogenicity? 3) Do the presently known Pantoea effector proteins enter host cells? 4) What host proteins interact with these effectors? We characterized the components of the hrp regulatory cascade (HrpXY ->7 HrpS ->7 HrpL ->7 hrp promoters), showed that they are conserved in both Pnss and Fag, and discovered that the regulation of the hrpS promoter (hrpSp) may be a key point in integrating apoplastic signals. We also analyzed the promoters recognized by HrpL and demonstrated the relationship between their composition and efficiency. Moreover, we showed that promoter strength can influence disease expression. In Pnss, we found that the HrpXY two-component signal system may sense the metabolic status of the bacterium and is required for full hrp gene expression in planta. In both species, acyl-homoserine lactone-mediated quorum sensing may also regulate epiphytic fitness and/or pathogenicity. A common Hrp effector protein, DspE/WtsE, is conserved and required for virulence of both species. When introduced into corn cells, Pnss WtsE protein caused water-soaked lesions. In other plants, it either caused cell death or acted as an Avr determinant. Using a yeast- two-hybrid system, WtsE was shown to interact with a number of maize signal transduction proteins that are likely to have roles in either programmed cell death or disease resistance. In Pag and Pab, we have characterized the effector proteins HsvG, HsvB and PthG. HsvG and HsvB are homologous proteins that determine host specificity of Pag and Pab on gypsophila and beet, respectively. Both possess a transcriptional activation domain that functions in yeast. PthG was found to act as an Avr determinant on multiple beet species, but was required for virulence on gypsophila. In addition, we demonstrated that PthG acts within the host cell. Additional effector genes have been characterized on the pathogenicity plasmid, pPATHₚₐg, in Pag. A screen for HrpL- regulated genes in Pnsspointed up 18 candidate effector proteins and four of these were required for full virulence. It is now well established that the virulence of Gram-negative plant pathogenic bacteria is governed by Hrp-dependent effector proteins. However; the mode of action of many effectors is still unresolved. This BARD supported research will significantly contribute to the understanding of how Hrp effectors operate in Pantoea spp. and how they control host specificity and affect symptom production. This may lead to novel approaches for genetically engineering plants resistant to a wide range of bacterial pathogens by inactivating the Hrp effectors with "plantabodies" or modifying their receptors, thereby blocking the induction of the susceptible response. Alternatively, innovative technologies could be used to interfere with the Hrp regulatory cascade by blocking a critical step or mimicking plant or quorum sensing signals.
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