Journal articles: 'Pathogenicity genes'

1

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 102 ffu and 106 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 102 ffu of any of the RABV mutants, including GX074, died; at 106 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 LD50 values of the chimeric RABV mutants were measured, with the results showing that the LD50 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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Champoiseau, P., J. H. Daugrois, I. Pieretti, S. Cociancich, M. Royer, and P. Rott. "High Variation in Pathogenicity of Genetically Closely Related Strains of Xanthomonas albilineans, the Sugarcane Leaf Scald Pathogen, in Guadeloupe." Phytopathology® 96, no. 10 (October 2006): 1081–91. http://dx.doi.org/10.1094/phyto-96-1081.

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Pathogenicity of 75 strains of Xanthomonas albilineans from Guadeloupe was assessed by inoculation of sugarcane cv. B69566, which is susceptible to leaf scald, and 19 of the strains were selected as representative of the variation in pathogenicity observed based on stalk colonization. In vitro production of albicidin varied among these 19 strains, but the restriction fragment length polymorphism pattern of their albicidin biosynthesis genes was identical. Similarly, no genomic variation was found among strains by pulsed-field gel electrophoresis. Some variation among strains was found by amplified fragment length polymorphism, but no relationship between this genetic variation and variation in pathogenicity was found. Only 3 (pilB, rpfA, and xpsE) of 40 genes involved in pathogenicity of bacterial species closely related to X. albilineans could be amplified by polymerase chain reaction from total genomic DNA of all nine strains tested of X. albilineans differing in pathogenicity in Guadeloupe. Nucleotide sequences of these genes were 100% identical among strains, and a phylogenetic study with these genes and housekeeping genes efp and ihfA suggested that X. albilineans is on an evolutionary road between the X. campestris group and Xylella fastidiosa, another vascular plant pathogen. Sequencing of the complete genome of Xanthomonas albilineans could be the next step in deciphering molecular mechanisms involved in pathogenicity of X. albilineans.

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Araki, Hitoshi, Hideki Innan, Martin Kreitman, and Joy Bergelson. "Molecular Evolution of Pathogenicity-Island Genes inPseudomonas viridiflava." Genetics 177, no. 2 (August 24, 2007): 1031–41. http://dx.doi.org/10.1534/genetics.107.077925.

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13

VAN DE WOUW, ANGELA P., and BARBARA J. HOWLETT. "Fungal pathogenicity genes in the age of ‘omics’." Molecular Plant Pathology 12, no. 5 (December 6, 2010): 507–14. http://dx.doi.org/10.1111/j.1364-3703.2010.00680.x.

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14

Taylor, Andrew, Viktória Vágány, Alison C. Jackson, Richard J. Harrison, Alessandro Rainoni, and John P. Clarkson. "Identification of pathogenicity-related genes inFusarium oxysporumf. sp.cepae." Molecular Plant Pathology 17, no. 7 (February 23, 2016): 1032–47. http://dx.doi.org/10.1111/mpp.12346.

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15

Aguirre, Andrés, María Laura Cabeza, Silvana V. Spinelli, Michael McClelland, Eleonora García Véscovi, and Fernando C. Soncini. "PhoP-Induced Genes within Salmonella Pathogenicity Island 1." Journal of Bacteriology 188, no. 19 (October 1, 2006): 6889–98. http://dx.doi.org/10.1128/jb.00804-06.

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ABSTRACT The invasive pathogen Salmonella enterica has evolved a sophisticated device that allows it to enter nonphagocytic host cells. This process requires the expression of Salmonella pathogenicity island 1 (SPI-1), which encodes a specialized type III protein secretion system (TTSS). This TTSS delivers a set of effectors that produce a marked rearrangement of the host cytoskeleton, generating a profuse membrane ruffling at the site of interaction, driving bacterial entry. It has been shown that the PhoP/PhoQ two-component system represses the expression of the SPI-1 machinery by down-regulating the transcription of its master regulator, HilA. In this work, we reveal the presence of a PhoP-activated operon within SPI-1. This operon is composed of the orgB and orgC genes, which encode a protein that interacts with the InvC ATPase and a putative effector protein of the TTSS, respectively. Under PhoP-inducing conditions, expression of this operon is directly activated by the phosphorylated form of the response regulator, which recognizes a PhoP box located at the −35 region relative to the transcription start site. Additionally, under invasion-inducing conditions, orgBC expression is driven both by the prgH promoter, induced by the SPI-1 master regulator HilA, and by the directly controlled PhoP/PhoQ promoter. Together, these results indicate that in contrast to the rest of the genes encompassed in the SPI-1 locus, orgBC is expressed during and after Salmonella entry into its host cell, and they suggest a role for the products of this operon after host cell internalization.

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Haq, Imran Ul, Siddra Ijaz, Nabeeha Aslam Khan, Iqrar Ahmad Khan, Hayssam M. Ali, and Ernesto A. Moya-Elizondo. "Integrative Pathogenicity Assay and Operational Taxonomy-Based Detection of New Forma Specialis of Fusarium oxysporum Causing Datepalm Wilt." Plants 11, no. 19 (October 8, 2022): 2643. http://dx.doi.org/10.3390/plants11192643.

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Pathogenicity-associated genes are highly host-specific and contribute to host-specific virulence. We tailored the traditional Koch’s postulates with integrative omics by hypothesizing that the effector genes associated with host-pathogenicity are determinant markers for virulence, and developed Integrative Pathogenicity (IP) postulates for authenticated pathogenicity testing in plants. To set the criteria, we experimented on datepalm (Phoenix dactylifera) for the vascular wilt pathogen and confirmed the pathogen based on secreted in xylem genes (effectors genes) using genomic and transcriptomic approaches, and found it a reliable solution when pathogenicity is in question. The genic regions ITS, TEF1-α, and RPBII of Fusarium isolates were examined by phylogenetic analysis to unveil the validated operational taxonomy at the species level. The hierarchical tree generated through phylogenetic analysis declared the fungal pathogen as Fusarium oxysporum. Moreover, the Fusarium isolates were investigated at the subspecies level by probing the IGS, TEF1-α, and Pgx4 genic regions to detect the forma specialis of F. oxysporum that causes wilt in datepalm. The phylogram revealed a new forma specialis in F. oxysporum that causes vascular wilt in datepalm.

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Gamboa-Becerra, Roberto, Daniel López-Lima, Luc Villain, Jean-Christophe Breitler, Gloria Carrión, and Damaris Desgarennes. "Molecular and Environmental Triggering Factors of Pathogenicity of Fusarium oxysporum and F. solani Isolates Involved in the Coffee Corky-Root Disease." Journal of Fungi 7, no. 4 (March 27, 2021): 253. http://dx.doi.org/10.3390/jof7040253.

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Coffee corky-root disease causes serious damages to coffee crop and is linked to combined infection of Fusarium spp. and root-knot nematodes Meloidogyne spp. In this study, 70 Fusarium isolates were collected from both roots of healthy coffee plants and with corky-root disease symptoms. A phylogenetic analysis, and the detection of pathogenicity SIX genes and toxigenicity Fum genes was performed for 59 F. oxysporum and 11 F. solani isolates. Based on the molecular characterization, seven F. oxysporum and three F. solani isolates were assessed for their pathogenicity on coffee seedlings under optimal watering and water stress miming root-knot nematode effect on plants. Our results revealed that a drastic increment of plant colonization capacity and pathogenicity on coffee plants of some Fusarium isolates was caused by water stress. The pathogenicity on coffee of F. solani linked to coffee corky-root disease and the presence of SIX genes in this species were demonstrated for the first time. Our study provides evidence for understanding the pathogenic basis of F. oxysporum and F. solani isolates on coffee and revealed the presence of SIX and Fum genes as one of their pathogenicity-related mechanisms. We also highlight the relevance of chlorophyll, a fluorescence as an early and high-throughput phenotyping tool in Fusarium pathogenicity studies on coffee.

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Ment, Dana, Noam Alkan, Neta Luria, Fang-Cheng Bi, Eli Reuveni, Robert Fluhr, and Dov Prusky. "A Role of AREB in the Regulation of PACC-Dependent Acid-Expressed-Genes and Pathogenicity of Colletotrichum gloeosporioides." Molecular Plant-Microbe Interactions® 28, no. 2 (February 2015): 154–66. http://dx.doi.org/10.1094/mpmi-09-14-0252-r.

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Gene expression regulation by pH in filamentous fungi and yeasts is controlled by the PACC/RIM101 transcription factor. In Colletotrichum gloeosporioides, PACC is known to act as positive regulator of alkaline-expressed genes, and this regulation was shown to contribute to fungal pathogenicity. PACC is also a negative regulator of acid-expressed genes, however; the mechanism of downregulation of acid-expressed genes by PACC and their contribution to C. gloeosporioides pathogenicity is not well understood. RNA sequencing data analysis was employed to demonstrate that PACC transcription factor binding sites (TFBS) are significantly overrepresented in the promoter of PACC-upregulated, alkaline-expressed genes. In contrast, they are not overrepresented in the PACC-downregulated, acid-expressed genes. Instead, acid-expressed genes showed overrepresentation of AREB GATA TFBS in C. gloeosporioides and in homologs of five other ascomycetes genomes. The areB promoter contains PACC TFBS; its transcript was upregulated at pH 7 and repressed in ΔpacC. Furthermore, acid-expressed genes were found to be constitutively upregulated in ΔareB during alkalizing conditions. The areB mutants showed significantly reduced ammonia secretion and pathogenicity on tomato fruit. Present results indicate that PACC activates areB expression, thereby conditionally repressing acid-expressed genes and contributing critically to C. gloeosporioides pathogenicity.

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Gupta, Goutam, Paige Pardington, Anu Chaudhary, Ahmet Zeytun, Jennifer Harris, and Ruy Ribeiro. "Host innate immune responses are different for high and low pathogenicity influenza A virus subtypes (INM8P.443)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 124.9. http://dx.doi.org/10.4049/jimmunol.192.supp.124.9.

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Abstract Different influenza A virus subtypes display different pathogenicity during host infection. It is our hypothesis that the host innate immune defense inversely correlates with the viral pathogenicity, i.e., the higher the viral pathogenicity the lower is the host innate immune defense and vice versa. In order to test our hypothesis, we monitored infection of normal human bronchial epithelial cells due to high pathogenicity H1N1 and low pathogenicity H3N2 subtypes during the early stages (0 to 24 hours) of infection. Specifically, we performed whole genome microarray analysis of the infected cells, identified the genes significantly altered in their expression, and validated the expression patterns of these genes by real-time qPCR. Of particular importance were the inducer and effector genes in the IFN-α/β pathway, a prominent innate immune response against viral infection. The prominent inducers include: (i) the OAS genes involved in the production of small viral RNA, (ii) the viral RNA sensors RIG-I, MDA-5, and TLR3, and (iii) the IRF transcription factors involved in the expression of IFN-α/β. The prominent effectors include: (i) ISG15, which activates RIG-I by ubiquitination, (ii) RSAD2 which inhibit the budding of influenza A virus, and (iii) GBPs, which inhibit viral replication. We validate our hypothesis by demonstrating that the release and expression of inducers and effectors of IFN-α/β are lower in high pathogenicity H1N1 than those in low pathogenicity H3N2. .

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Tu, Jian, Ting Xue, Kezong Qi, Ying Shao, Boyan Huang, Xueyan Wang, and Xiuhong Zhou. "The irp2 and fyuA genes in High Pathogenicity Islands are involved in the pathogenesis of infections caused by avian pathogenic Escherichia coli (APEC)." Polish Journal of Veterinary Sciences 19, no. 1 (March 1, 2016): 21–29. http://dx.doi.org/10.1515/pjvs-2016-0004.

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Abstract Avian pathogenic Escherichia coli (APEC) is a major bacterial infectious disease that may lead to local or systemic infections in chickens with clinical manifestations. The irp2-fyuA gene cluster has been confirmed to be the main genes involved in the synthesis of HPI. The objective of this study was to determine the influence of the irp2 and fyuA genes in the high pathogenicity island (HPI) of avian pathogenic Escherichia coli (APEC) on its pathogenicity by knocking out these genes. The ΔAE17 (lacking irp2) and ΔΔAE17 (lacking irp2 and fyuA) strains of APEC were constructed. The ΔAE17 and ΔΔAE17 strains showed significantly impaired capacity to adhere onto DF-1 cells. The LD50 results indicated that the virulence of the ΔAE17 and ΔΔAE17 strains was decreased in comparison with that of the AE17 strain. We concluded that the knock-out of the core HPI genes weakened APEC adhesion onto DF-1 cells, inhibited transcription of virulence genes, and reduced pathogenicity in chicks. The effects of genetic deletion of irp2 and fyuA on APEC were more severe than those produced by deletion of irp2 only, indicating that irp2 and fyuA co-regulate APEC pathogenicity.

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Dufresne, Marie, Theo Lee, Sarrah M’Barek, X. Xu, X. Zhang, Taiguo Liu, Wenwei Zhang, Gert Kema, Marie-Josée Daboussi, and Cees Waalwijk. "Tagging pathogenicity genes inFusarium graminearumusing the transposon systemmimp/impala." Cereal Research Communications 36, Supplement 6 (September 2008): 415–19. http://dx.doi.org/10.1556/crc.36.2008.suppl.b.34.

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22

Rakhashiya, Purvi M., Pooja P. Patel, Bhavisha P. Sheth, Jigna G. Tank, and Vrinda S. Thaker. "Detection of virulence and pathogenicity genes in selected phytopathovars." Archives of Phytopathology and Plant Protection 49, no. 1-4 (February 25, 2016): 64–73. http://dx.doi.org/10.1080/03235408.2016.1157378.

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23

Dobrindt, U., B. Janke, K. Piechaczek, G. Nagy, W. Ziebuhr, G. Fischer, A. Schierhorn, M. Hecker, G. Blum-Oehler, and J. Hacker. "Toxin genes on pathogenicity islands: impact for microbial evolution." International Journal of Medical Microbiology 290, no. 4-5 (October 2000): 307–11. http://dx.doi.org/10.1016/s1438-4221(00)80028-4.

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Sweigard, J. "Functional analysis of pathogenicity genes in a genomics world." Current Opinion in Microbiology 4, no. 4 (August 1, 2001): 387–92. http://dx.doi.org/10.1016/s1369-5274(00)00222-8.

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Chen, John, Geeta Ram, José R. Penadés, Stuart Brown, and Richard P. Novick. "Pathogenicity Island-Directed Transfer of Unlinked Chromosomal Virulence Genes." Molecular Cell 57, no. 1 (January 2015): 138–49. http://dx.doi.org/10.1016/j.molcel.2014.11.011.

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Dufresne, Marie, Theo van der Lee, Sarrah Ben M’Barek, Xiude Xu, Xu Zhang, Taiguo Liu, Cees Waalwijk, Wenwei Zhang, Gert H. J. Kema, and Marie-Josée Daboussi. "Transposon-tagging identifies novel pathogenicity genes in Fusarium graminearum." Fungal Genetics and Biology 45, no. 12 (December 2008): 1552–61. http://dx.doi.org/10.1016/j.fgb.2008.09.004.

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Piedra-Quintero, Zayda L., Shouvonik Sengupta, Lindsay M. Webb, Stephanie A. Amici, Georgios Laliotis, Philip N. Tsichlis, and Mireia Guerau-de-Arellano. "PRMT5 controls pathogenicity and metabolic genes during Th17 polarization." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 230.1. http://dx.doi.org/10.4049/jimmunol.204.supp.230.1.

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Abstract PRMT5 catalyzes symmetric dimethylation (SDM) on arginine residues. PRMT5 methylates histone H3 and H4 producing remodeling of chromatin and regulation of gene transcription. PRMT5 is induced after T cell activation. Furthermore, both PRMT5 inhibitors and PRMT5 knockdown impair T cell proliferation and activation. However, the role of PRMT5 in T cell differentiation has not been analyzed. T cells undergo metabolic reprograming during activation which is critical for polarization. Differentiating T cells increase bioenergetics and anabolic pathways enhancing glycolysis, catabolism, uptake of fatty acids and oxidative phosphorylation. Whether PRMT5 has an impact on Th17 differentiation and metabolic reprograming is unknown. To address this question, we performed Th17 differentiation and RNA sequencing analyses in T cells from PRMT5fl/fl and iCD4-PRMT5Δ/Δ mice. Th17 differentiation was sharply suppressed in PRMT5 KO T cells, in which 25–30% of genes in the glycolysis, lactate or TCA pathways were reduced. To evaluate the functional effects of PRMT5 on energy metabolism, extracellular acidification rate (ECAR) and Oxygen consumption rate (OCR) were analyzed in Jurkat T cells transduced with control or PRMT5 shRNA and lactate secretion was measured on supernatants of Th1 and Th17 cells from PRMT5fl/fl and iCD4-PRMT5Δ/Δ mice. Knock down of PRMT5 decreased ECAR in Jurkat cells and lactate production in Th1 and Th17 cells in absence of PRMT5. In conclusion, PRMT5 promotes glycolytic energy metabolism and Th17 differentiation in T cells.

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An, Se-Hee, Seung-Min Hong, Seung-Eun Son, Jin-Ha Song, Chung-Young Lee, Jun-Gu Choi, Youn-Jeong Lee, et al. "Improvement of PR8-Derived Recombinant Clade 2.3.4.4c H5N6 Vaccine Strains by Optimization of Internal Genes and H103Y Mutation of Hemagglutinin." Vaccines 8, no. 4 (December 20, 2020): 781. http://dx.doi.org/10.3390/vaccines8040781.

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Clade 2.3.4.4c H5N6 avian influenza A viruses (AIVs) may have originally adapted to infect chickens and have caused highly pathogenic avian influenza (HPAI) in poultry and human fatalities. Although A/Puerto Rico/8/1934 (H1N1) (PR8)-derived recombinant clade 2.3.4.4c H5N6 vaccine strains have been effective in embryonated chicken eggs-based vaccine production system, they need to be improved in terms of immunogenicity and potential mammalian pathogenicity. We replaced the PB2 gene alone or the PB2 (polymerase basic protein 2), NP (nucleoprotein), M (matrix protein) and NS (non-structural protein) genes together in the PR8 strain with corresponding genes from AIVs with low pathogenicity to remove mammalian pathogenicity and to match CD8+ T cell epitopes with contemporary HPAI viruses, respectively, without loss of viral fitness. Additionally, we tested the effect of the H103Y mutation of hemagglutinin (HA) on antigen productivity, mammalian pathogenicity and heat/acid stability. The replacement of PB2 genes and the H103Y mutation reduced the mammalian pathogenicity but increased the antigen productivity of the recombinant vaccine strains. The H103Y mutation increased heat stability but unexpectedly decreased acid stability, probably resulting in increased activation pH for HA. Interestingly, vaccination with inactivated recombinant virus with replaced NP, M and NS genes halted challenge virus shedding earlier than the recombinant vaccine without internal genes replacement. In conclusion, we successfully generated recombinant clade 2.3.4.4c H5N6 vaccine strains that were less pathogenic to mammals and more productive and heat stable than conventional PR8-derived recombinant strains by optimization of internal genes and the H103Y mutation of HA.

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Miyara, I., C. Shnaiderman, X. Meng, W. A. Vargas, J. M. Diaz-Minguez, A. Sherman, M. Thon, and D. Prusky. "Role of Nitrogen-Metabolism Genes Expressed During Pathogenicity of the Alkalinizing Colletotrichum gloeosporioides and Their Differential Expression in Acidifying Pathogens." Molecular Plant-Microbe Interactions® 25, no. 9 (September 2012): 1251–63. http://dx.doi.org/10.1094/mpmi-01-12-0017-r.

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Pathogens can actively alter fruit pH around the infection site, signaling modulation of pathogenicity-factor expression, as found for alkalinizing (Colletotrichum and Alternaria spp.) and acidifying (Penicillium, Botrytis, and Sclerotinia spp.) fungi. The nitrogen-metabolism genes GDH2, GS1, GLT, and MEP genes are differentially expressed during colonization by Colletotrichum gloeosporioides, and a Δgdh2 strain reduces ammonia accumulation and pathogenicity. We analyzed the contribution of transporters GLT and MEPB to C. gloeosporiodes pathogenicity. Germinating spores of Δglt strains showed reduced appressorium formation; those of ΔmepB mutants showed rapid ammonia uptake and accumulation inside the hyphae, indicating deregulated uptake. Both mutants reduced pathogenicity, indicating that these transporters function during alkalinizing species pathogenicity. We compared the expressions of these genes in C. gloeosporioides and Sclerotinia sclerotiorum, and found five to 10-fold higher expression at the transcript level in the former. Interestingly, GLT and MEPB in the alkalinizing species showed no and very low sequence identity, respectively, with their counterparts in the acidifying species. Knockout analysis of GLT and MEPB and their differential transcript regulation in the alkalinizing and acidifying species suggest that the ammonia accumulation contributing to pathogenicity in the former is modulated by factors at the gene-regulation levels that are lacking in the acidifying species.

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Kuleshevich, Evgenia V., Yury Y. Ilyasov, Dmitry S. Linnik, Anastasia A. Malchenkova, Olga N. Arzhanova, Nikolay I. Briko, Ekaterina V. Glushkova, Tatyana V. Priputnevich, and Alexander N. Suvorov. "Russian strains of group B streptococci are different in the content and organization of the PAI-A and PAI-A1 pathogenicity islands." Journal of obstetrics and women's diseases 70, no. 4 (October 5, 2021): 65–72. http://dx.doi.org/10.17816/jowd61875.

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Group B streptococci, or Streptococcus agalactiae, are the major cause of severe diseases in newborns and adults. The PAI-A and PAI-A1 pathogenicity islands containing the sspB1 and sspB1a genes, respectively, were found among group B streptococci mobile genetic elements. The presence of sspB genes correlates with urogenital tract infections. The aim of this study was to determine the frequency of group B streptococci strains with the PAI-A and PAI-A1 pathogenicity islands, circulating in Moscow, in comparison with strains from St. Petersburg. The sspB1 gene, and hence the PAI-A pathogenicity island, was not found in the genomes of strains from Moscow. The frequency of the sspB1a gene and the PAI-A1 pathogenicity island in the genomes of clinical strains was three times higher than in the genomes of colonizing strains. Thus, it can be assumed that the genes of the sspB family are more specific of group B streptococci colonizing pregnant women and newborns.

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Kuleshevich, Evgenia V., Yury Y. Ilyasov, Dmitry S. Linnik, Anastasia A. Malchenkova, Olga N. Arzhanova, Nikolay I. Briko, Ekaterina V. Glushkova, Tatyana V. Priputnevich, and Alexander N. Suvorov. "Russian strains of group B streptococci are different in the content and organization of the PAI-A and PAI-A1 pathogenicity islands." Journal of obstetrics and women's diseases 70, no. 4 (October 5, 2021): 65–72. http://dx.doi.org/10.17816/jowd61875.

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Group B streptococci, or Streptococcus agalactiae, are the major cause of severe diseases in newborns and adults. The PAI-A and PAI-A1 pathogenicity islands containing the sspB1 and sspB1a genes, respectively, were found among group B streptococci mobile genetic elements. The presence of sspB genes correlates with urogenital tract infections. The aim of this study was to determine the frequency of group B streptococci strains with the PAI-A and PAI-A1 pathogenicity islands, circulating in Moscow, in comparison with strains from St. Petersburg. The sspB1 gene, and hence the PAI-A pathogenicity island, was not found in the genomes of strains from Moscow. The frequency of the sspB1a gene and the PAI-A1 pathogenicity island in the genomes of clinical strains was three times higher than in the genomes of colonizing strains. Thus, it can be assumed that the genes of the sspB family are more specific of group B streptococci colonizing pregnant women and newborns.

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Paudel, Atmika, Hiroshi Hamamoto, Suresh Panthee, Yasuhiko Matsumoto, and Kazuhisa Sekimizu. "Large-Scale Screening and Identification of Novel Pathogenic Staphylococcus aureus Genes Using a Silkworm Infection Model." Journal of Infectious Diseases 221, no. 11 (January 8, 2020): 1795–804. http://dx.doi.org/10.1093/infdis/jiaa004.

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Abstract The regulatory network of virulence factors produced by the opportunistic pathogen Staphylococcus aureus is unclear and the functions of many uncharacterized genes in its genome remain to be elucidated. In this study, we screened 380 genes whose function was unassigned, utilizing gene-disrupted transposon mutants of the community-acquired methicillin-resistant S. aureus USA300 for pathogenicity in silkworms. We identified 10 strains with reduced silkworm killing ability. Among them, 8 displayed reduced virulence in a mouse model as evidenced by reduced colony-forming units in organs of infected mice. The role of each gene in pathogenicity was further confirmed by complementation and pathogenicity tests in silkworms, where we found that the phenotype was not restored in 1 strain. Additionally, some of the mutants displayed reduced hemolysis, proteolysis, pigment production, and survival in murine RAW 264.7 monocyte-macrophage cells. These newly identified genes involved in virulence will enhance our understanding of the pathogenicity of S. aureus.

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Banaszkiewicz, Sylwia, Jessica K. Calland, Evangelos Mourkas, Samuel K. Sheppard, Ben Pascoe, and Jacek Bania. "Genetic Diversity of Composite Enterotoxigenic Staphylococcus epidermidis Pathogenicity Islands." Genome Biology and Evolution 11, no. 12 (November 26, 2019): 3498–509. http://dx.doi.org/10.1093/gbe/evz259.

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Abstract The only known elements encoding enterotoxins in coagulase-negative staphylococci are composite Staphylococcus epidermidis pathogenicity islands (SePIs), including SePI and S. epidermidis composite insertion (SeCI) regions. We investigated 1545 Staphylococcus spp. genomes using whole-genome MLST, and queried them for genes of staphylococcal enterotoxin family and for 29 ORFs identified in prototype SePI from S. epidermidis FRI909. Enterotoxin-encoding genes were identified in 97% of Staphylococcus aureus genomes, in one Staphylococcus argenteus genome and in nine S. epidermidis genomes. All enterotoxigenic S. epidermidis strains carried composite SePI, encoding sec and sel enterotoxin genes, and were assigned to a discrete wgMLST cluster also containing genomes with incomplete islands located in the same region as complete SePI in enterotoxigenic strains. Staphylococcus epidermidis strains without SeCI and SePI genes, and strains with complete SeCI and no SePI genes were identified but no strains were found to carry only SePI and not SeCI genes. The systematic differences between SePI and SeCI regions imply a lineage-specific pattern of inheritance and support independent acquisition of the two elements in S. epidermidis. We provided evidence of reticulate evolution of mobile elements that contain elements with different putative ancestry, including composite SePI that contains genes found in other coagulase-negative staphylococci (SeCI), as well as in S. aureus (SePI-like elements). We conclude that SePI-associated elements present in nonenterotoxigenic S. epidermidis represent a scaffold associated with acquisition of virulence-associated genes. Gene exchange between S. aureus and S. epidermidis may promote emergence of new pathogenic S. epidermidis clones.

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Wang, Yi, Qi Wu, Lina Liu, Xiaoling Li, Aijia Lin, and Chengyun Li. "MoMCP1, a Cytochrome P450 Gene, Is Required for Alleviating Manganese Toxin Revealed by Transcriptomics Analysis in Magnaporthe oryzae." International Journal of Molecular Sciences 20, no. 7 (March 29, 2019): 1590. http://dx.doi.org/10.3390/ijms20071590.

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Manganese, as an essential trace element, participates in many physiological reactions by regulating Mn associated enzymes. Magnaporthe oryzae is a serious pathogen and causes destructive losses for rice production. We identified a cytochrome P450 gene, MoMCP1, involving the alleviation of manganese toxin and pathogenicity. To identify the underlying mechanisms, transcriptomics were performed. The results indicated that many pathogenicity related genes were regulated, especially hydrophobin related genes in ∆Momcp1. Furthermore, the Mn2+ toxicity decreased the expressions of genes involved in the oxidative phosphorylation and energy production, and increased the reactive oxygen species (ROS) levels, which might impair the functions of mitochondrion and vacuole, compromising the pathogenicity and development in ∆Momcp1. Additionally, our results provided further information about Mn associated the gene network for Mn metabolism in cells.

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Kalashnikova, Viktoriya. "Pathogenic potential of Staphylococcus aureus colonizing the nasal cavity and lungs of monkeys." Russian veterinary journal 2020, no. 5 (November 25, 2020): 21–26. http://dx.doi.org/10.32416/2500-4379-2020-5-21-26.

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In this paper, data are presented on the study of genetic determinants of pathogenicity in S. aureus isolated from the respiratory tract of monkeys (nasal cavity and lungs) collected during 2017‒2019. The aim of this work is to determine some genes of pathogenicity and their combinations in S. aureus isolated from the nasal cavity of clinically healthy monkeys and from the lungs of monkeys that died from pneumonia. There was a high frequency of detection of adhesion genes (fnBpA ― 74.4 %, fnBpB ― 79.1 %, clfA ― 95.4 %, clfB ― 95.4 %), hemolysins (hla ― 83.7 %, hlb ― 81.4 %), Panton-Valentine leukocidin (pvl ― 48.1 %), which are regarded as markers of the increased pathogenicity of the microbe, as well as combinations of various genovariants. The hemolysin α gene was detected more often in S. aureus isolated from the lungs of monkeys with pneumonia (87.4 %), and the hemolysin β gene was found in almost all S. aureus isolated from the nasal cavity (96.2 %). Genes for fibronectin-binding proteins (fnBpA/B) were found with a high frequency in isolates detected from the nasal cavity, while the clumping factor gene (clfA/B) were isolated in 100 % of S. aureus studied. The genovariant hla-hlb-fnBpA-fnBpB-clfA-clfB was detected in almost half of the isolates (48.1%), the presence of all studied pathogenicity determinants (pvl-hla-hlb-fnBpA-fnBpB-clfA-clfB) was noted in 24.8 % S. aureus. Analysis of the high frequency of prevalence of genes responsible for the expression of pathogenicity factors confirms the pathogenicity of studied S. aureus isolates, detected in monkeys. Most of the isolates belonged to group IV of the regulatory gene (55.8%) and agr I takes second place (40.8 %). PCR detection of pvl, hla, hlb, fnBpA, fnBpB, clfA, clfB genes can be used to demonstrate the pathogenicity of S. aureus isolates from various animal biomaterials and serve as a criterion for epidemiological assessment in studying the S. aureus circulation in monkeys kept in captivity.

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Wang, Xiaoguang, Garry B. Coulson, Aleksandra A. Miranda-CasoLuengo, Raúl Miranda-CasoLuengo, Mary K. Hondalus, and Wim G. Meijer. "IcgA Is a Virulence Factor of Rhodococcus equi That Modulates Intracellular Growth." Infection and Immunity 82, no. 5 (February 18, 2014): 1793–800. http://dx.doi.org/10.1128/iai.01670-13.

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ABSTRACTVirulence of the intracellular pathogenRhodococcus equidepends on a 21.3-kb pathogenicity island located on a conjugative plasmid. To date, the only nonregulatory pathogenicity island-encoded virulence factor identified is the cell envelope-associated VapA protein. Although the pathogenicity islands from porcine and equineR. equiisolates have undergone major rearrangements, thevirRoperon (virR-icgA-vapH-orf7-virS) is highly conserved in both, suggesting these genes play an important role in pathogenicity. VirR and VirS are transcriptional regulators controlling expression of pathogenicity island genes, includingvapA. Here, we show that whilevapHandorf7are dispensable for intracellular growth ofR. equi, deletion oficgA, formerly known asorf5, encoding a major facilitator superfamily transport protein, elicited an enhanced growth phenotype in macrophages and a significant reduction in macrophage viability, while extracellular growth in broth remained unaffected. Transcription ofvirS, located downstream oficgA, andvapAwas not affected by theicgAdeletion during growth in broth or in macrophages, showing that the enhanced growth phenotype caused by deletion oficgAwas not mediated through abnormal transcription of these genes. Transcription oficgAincreased 6-fold within 2 h following infection of macrophages and remained significantly higher 48 h postinfection compared to levels at the start of the infection. The major facilitator superfamily transport protein IcgA is the first factor identified inR. equithat negatively affects intracellular replication. Aside from VapA, it is only the second pathogenicity island-encoded structural protein shown to play a direct role in intracellular growth of this pathogenic actinomycete.

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BAYOUMI, MOHAMED A., and MANSEL W. GRIFFITHS. "Probiotics Down-Regulate Genes in Salmonella enterica Serovar Typhimurium Pathogenicity Islands 1 and 2." Journal of Food Protection 73, no. 3 (March 1, 2010): 452–60. http://dx.doi.org/10.4315/0362-028x-73.3.452.

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Salmonella Typhimurium pathogenesis relies mainly on the expression of genes of two pathogenicity islands, Salmonella pathogenicity islands 1 and 2 (SPI1 and SPI2). Each island has its own pattern of expression and regulation. Success in suppression of the responsible key activator of each island would be an effective way of controlling Salmonella, especially with the emerging problem of antibiotic-resistant strains. Probiotics have been shown to inhibit several foodborne pathogens, and their mode of action may partly involve down-regulation of virulence genes. To investigate whether probiotics played a role in the regulation of the pathogenicity islands SPI1 and SPI2 in Salmonella, two reporter strains were constructed in which the general regulator of SPI1, hilA, and the response regulator of SPI2, ssrB, were fused with luxCDABE genes. These constructs were used to screen the effect of probiotics on the expression of each gene. Molecules secreted by Bifidobacterium bifidum were able to down-regulate both genes.

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Huser, Aurélie, Hiroyuki Takahara, Wolfgang Schmalenbach, and Richard O'Connell. "Discovery of Pathogenicity Genes in the Crucifer Anthracnose Fungus Colletotrichum higginsianum, Using Random Insertional Mutagenesis." Molecular Plant-Microbe Interactions® 22, no. 2 (February 2009): 143–56. http://dx.doi.org/10.1094/mpmi-22-2-0143.

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Agrobacterium tumefaciens–mediated transformation (ATMT) was used for random insertional mutagenesis to identify pathogenicity genes in the hemibiotrophic fungus Colletotrichum higginsianum. A high-throughput primary infection assay on Arabidopsis thaliana seedlings allowed the rapid screening of 8,850 transformants. Forty mutants showing reproducible pathogenicity defects on Arabidopsis and Brassica plants were obtained, and their infection phenotypes were characterized microscopically. Six mutants were impaired in appressorial melanization, fifteen had reduced penetration ability, 14 induced host papillae or hypersensitive cell death, and five were affected in the transition from biotrophy to necrotrophy. Southern blot analysis showed 58% of the transformants had single-site T-DNA integrations. Right-border flanking sequences were recovered from 12 mutants by inverse polymerase chain reaction (PCR) or thermal asymmetric interlaced PCR and were used to isolate the tagged genes from a genomic library. The putative pathogenicity genes encoded homologs of a major facilitator superfamily phosphate transporter, importin-β2, ornithine decarboxylase, β-1,3(4)-glucanase, ATP-binding endoribonuclease, carbamoyl-phosphate synthetase, and the polyprotein precursor of N-acetylglutamate kinase and N-acetylglutamyl-phosphate reductase. Six further loci were homologous to proteins of unknown function. None of these genes were previously implicated in the pathogenicity of any Colletotrichum species. The results demonstrate that ATMT is an effective tool for gene discovery in this model pathogen.

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Mat Razali, Nurhani, Boon Huat Cheah, and Kalaivani Nadarajah. "Transposable Elements Adaptive Role in Genome Plasticity, Pathogenicity and Evolution in Fungal Phytopathogens." International Journal of Molecular Sciences 20, no. 14 (July 23, 2019): 3597. http://dx.doi.org/10.3390/ijms20143597.

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Transposable elements (TEs) are agents of genetic variability in phytopathogens as they are a source of adaptive evolution through genome diversification. Although many studies have uncovered information on TEs, the exact mechanism behind TE-induced changes within the genome remains poorly understood. Furthermore, convergent trends towards bigger genomes, emergence of novel genes and gain or loss of genes implicate a TE-regulated genome plasticity of fungal phytopathogens. TEs are able to alter gene expression by revamping the cis-regulatory elements or recruiting epigenetic control. Recent findings show that TEs recruit epigenetic control on the expression of effector genes as part of the coordinated infection strategy. In addition to genome plasticity and diversity, fungal pathogenicity is an area of economic concern. A survey of TE distribution suggests that their proximity to pathogenicity genes TEs may act as sites for emergence of novel pathogenicity factors via nucleotide changes and expansion or reduction of the gene family. Through a systematic survey of literature, we were able to conclude that the role of TEs in fungi is wide: ranging from genome plasticity, pathogenicity to adaptive behavior in evolution. This review also identifies the gaps in knowledge that requires further elucidation for a better understanding of TEs’ contribution to genome architecture and versatility.

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Dow, J. M., and M. J. Daniels. "XylellaGenomics and Bacterial Pathogenicity to Plants." Yeast 1, no. 4 (2000): 263–71. http://dx.doi.org/10.1002/1097-0061(200012)17:4<263::aid-yea44>3.0.co;2-g.

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Xylella fastidiosa, a pathogen of citrus, is the first plant pathogenic bacterium for which the complete genome sequence has been published. Inspection of the sequence reveals high relatedness to many genes of other pathogens, notablyXanthomonas campestris. Based on this, we suggest thatXylellapossesses certain easily testable properties that contribute to pathogenicity. We also present some general considerations for deriving information on pathogenicity from bacterial genomics.

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Guo, Huimin, Benzheng Zhang, Xin Zheng, Juan Sun, Huiduo Guo, Gang Li, Guodong Zhao, Anying Xu, and Heying Qian. "Pathogenicity Detection and Genome Analysis of Two Different Geographic Strains of BmNPV." Insects 12, no. 10 (September 30, 2021): 890. http://dx.doi.org/10.3390/insects12100890.

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The pathogenicity of different concentrations of Bombyx mori nuclear polyhedrosis virus- Zhenjiang strain (BmNPV ZJ) and Yunnan strain (BmNPV YN) was assessed in Baiyu larvae. The structures of the two viral strains were observed by negative-staining electron microscopy, and their proliferation was examined by quantitative polymerase chain reaction (qPCR). The genomic sequences of these two viruses were obtained to investigate the differences in their pathogenicity. The lethal concentration 50 (LC50) of BmNPV ZJ against Baiyu larvae was higher than that of BmNPV YN, indicating a relatively more robust pathogenicity in BmNPV YN. Electron microscopic images showed that the edges of BmNPV YN were clearer than those of BmNPV ZJ. The qPCR analysis demonstrated significantly higher relative expressions of immediately early 1 gene (ie-1), p143, vp39, and polyhedrin genes (polh) in BmNPV ZJ than in BmNPV YN at 12–96 h. The complete genomes of BmNPV ZJ and BmNPV YN were, respectively, 135,895 bp and 143,180 bp long, with 141 and 145 coding sequences and 40.93% and 39.71% GC content. Considering the BmNPV ZJ genome as a reference, 893 SNP loci and 132 InDel mutations were observed in the BmNPV YN genome, resulting in 106 differential gene sequences. Among these differential genes, 76 (including 22 hub genes and 35 non-hub genes) possessed amino acid mutations. Thirty genes may have been related to viral genome replication and transcription and five genes may have been associated with the viral oral infection. These results can help in understanding the mechanisms of pathogenicity of different strains of BmNPV in silkworms.

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Åhlund, Monika K., Patrik Rydén, Anders Sjöstedt, and Svenja Stöven. "Directed Screen of Francisella novicida Virulence Determinants Using Drosophila melanogaster." Infection and Immunity 78, no. 7 (May 17, 2010): 3118–28. http://dx.doi.org/10.1128/iai.00146-10.

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ABSTRACT Francisella tularensis is a highly virulent, facultative intracellular human pathogen whose virulence mechanisms are not well understood. Occasional outbreaks of tularemia and the potential use of F. tularensis as a bioterrorist agent warrant better knowledge about the pathogenicity of this bacterium. Thus far, genome-wide in vivo screens for virulence factors have been performed in mice, all however restricted by the necessity to apply competition-based, negative-selection assays. We wanted to individually evaluate putative virulence determinants suggested by such assays and performed directed screening of 249 F. novicida transposon insertion mutants by using survival of infected fruit flies as a measure of bacterial virulence. Some 20% of the genes tested were required for normal virulence in flies; most of these had not previously been investigated in detail in vitro or in vivo. We further characterized their involvement in bacterial proliferation and pathogenicity in flies and in mouse macrophages. Hierarchical cluster analysis of mutant phenotypes indicated a functional linkage between clustered genes. One cluster grouped all but four genes of the Francisella pathogenicity island and other loci required for intracellular survival. We also identified genes involved in adaptation to oxidative stress and genes which might induce host energy wasting. Several genes related to type IV pilus formation demonstrated hypervirulent mutant phenotypes. Collectively, the data demonstrate that the bacteria in part use similar virulence mechanisms in mammals as in Drosophila melanogaster but that a considerable proportion of the virulence factors active in mammals are dispensable for pathogenicity in the insect model.

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TSUYUMU, Shinji, Sachi KIMURA, and Hisae HIRATA. "Regulation of Pathogenicity-related Genes in Phytopathogenic Bacteria and Plant." Japan Agricultural Research Quarterly: JARQ 48, no. 2 (2014): 105–9. http://dx.doi.org/10.6090/jarq.48.105.

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Remya, P. A., M. Shanthi, and Uma Sekar. "Characterisation of Virulence Genes Associated with Pathogenicity in Klebsiella pneumoniae." Indian Journal of Medical Microbiology 37, no. 2 (April 2019): 210–18. http://dx.doi.org/10.4103/ijmm.ijmm_19_157.

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Gennari, Micol, Valentina Ghidini, Greta Caburlotto, and Maria M. Lleo. "Virulence genes and pathogenicity islands in environmentalVibriostrains nonpathogenic to humans." FEMS Microbiology Ecology 82, no. 3 (June 25, 2012): 563–73. http://dx.doi.org/10.1111/j.1574-6941.2012.01427.x.

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Wang, J. C., B. H. So, J. H. Kim, Y. J. Park, B. M. Lee, and H. W. Kang. "Genome-wide identification of pathogenicity genes inXanthomonas oryzaepv.oryzaeby transposon mutagenesis." Plant Pathology 57, no. 6 (December 2008): 1136–45. http://dx.doi.org/10.1111/j.1365-3059.2008.01884.x.

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VanEtten, Hans, Deanna Funnell-Baerg, Catherine Wasmann, and Kevin McCluskey. "Location of pathogenicity genes on dispensable chromosomes inNectria haematococca MPVI." Antonie van Leeuwenhoek 65, no. 3 (1994): 263–67. http://dx.doi.org/10.1007/bf00871955.

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MAZAREI, M., and A. KERR. "Plasmids in Pseudomonas syringae pv. pisi carry genes for pathogenicity." Plant Pathology 40, no. 3 (September 1991): 408–14. http://dx.doi.org/10.1111/j.1365-3059.1991.tb02398.x.

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Lieberman, Tami D., Jean-Baptiste Michel, Mythili Aingaran, Gail Potter-Bynoe, Damien Roux, Michael R. Davis, David Skurnik, et al. "Parallel bacterial evolution within multiple patients identifies candidate pathogenicity genes." Nature Genetics 43, no. 12 (November 13, 2011): 1275–80. http://dx.doi.org/10.1038/ng.997.

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El-Bahar, Helmy Mohamed, Nadia Gabr Ali, Ibrahim Mohamed Aboyadak, Samy Abd El Salam Khalil, and Madiha Salah Ibrahim. "Virulence genes contributing to Aeromonas hydrophila pathogenicity in Oreochromis niloticus." International Microbiology 22, no. 4 (April 15, 2019): 479–90. http://dx.doi.org/10.1007/s10123-019-00075-3.

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Journal articles on the topic 'Pathogenicity genes'

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