Early colonization pattern of maize (Zea mays L. Poales, Poaceae) roots by Herbaspirillum seropedicae (Burkholderiales, Oxalobacteraceae)

The bacterium Herbaspirillum seropedicae is an endophytic diazotroph found in several plants, including economically important poaceous species. However, the mechanisms involved in the interaction between H. seropedicae and these plants are not completely characterized. We investigated the attachment of Herbaspirillum to maize roots and the invasion of the roots by this bacterium using H. seropedicae strain SMR1 transformed with the suicide plasmid pUTKandsRed, which carries a mini-Tn5 transposon containing the gene for the Discosoma red fluorescent protein (Dsred) constitutively expressed together with the kanamycin resistance gene. Integration of the mini-Tn5 into the bacterial chromosome yielded the mutant H. seropedicae strain RAM4 which was capable of expressing Dsred and could be observed on and inside fresh maize root samples. Confocal microscopy of maize roots inoculated with H. seropedicae three days after germination showed that H. seropedicae cell were attached to the root surface 30 min after inoculation, were visible in the internal tissues after twenty-four hours and in the endodermis, the central cylinder and xylem after three days

Genome of Herbaspirillum seropedicae Strain SmR1, a Specialized Diazotrophic Endophyte of Tropical Grasses

The molecular mechanisms of plant recognition, colonization, and nutrient exchange between diazotrophic endophytes and plants are scarcely known. Herbaspirillum seropedicae is an endophytic bacterium capable of colonizing intercellular spaces of grasses such as rice and sugar cane. The genome of H. seropedicae strain SmR1 was sequenced and annotated by The Paraná State Genome Programme—GENOPAR. The genome is composed of a circular chromosome of 5,513,887 bp and contains a total of 4,804 genes. The genome sequence revealed that H. seropedicae is a highly versatile microorganism with capacity to metabolize a wide range of carbon and nitrogen sources and with possession of four distinct terminal oxidases. The genome contains a multitude of protein secretion systems, including type I, type II, type III, type V, and type VI secretion systems, and type IV pili, suggesting a high potential to interact with host plants. H. seropedicae is able to synthesize indole acetic acid as reflected by the four IAA biosynthetic pathways present. A gene coding for ACC deaminase, which may be involved in modulating the associated plant ethylene-signaling pathway, is also present. Genes for hemagglutinins/hemolysins/adhesins were found and may play a role in plant cell surface adhesion. These features may endow H. seropedicae with the ability to establish an endophytic life-style in a large number of plant species

Dissemination of NDM-producing bacteria in Southern Brazil

Background: The dissemination of NDM-1 carbapenemases (New Delhi Metallo-β-lactamase) is a global public health problem, mainly in developing countries. The aim of this study was to characterize the spread of NDM-producing bacteria in the Southern Brazilian states analyzing epidemiological, molecular, and antimicrobial susceptibility aspects. Methods: A total of 10,684 carbapenem-resistant isolates of Enterobacterales, Pseudomonas spp. and Acinetobacter spp. obtained from several hospitals in eight cities in Southern Brazil were screened, and 486 NDM-producing bacteria were selected. Results: The incidence varied from 0.5 to 77 cases/100.000 habitants. ST11, ST15, ST340 and ST674 were the most common in K. pneumoniae. A total of five plasmids were identified in one K. pneumoniae strain: Col440I, Col440II, IncFIA(HI1), IncFIB(K), IncFIB(pQil)/ IncFII(K), and IncR. Conclusions: The number of patients with NDM-producing bacteria has increased in Southern Brazil, whose gene is present in different plasmids, explaining the expansion of this enzyme

The type III secretion system is necessary for the development of a pathogenic and endophytic interaction between <it>Herbaspirillum rubrisubalbicans</it> and Poaceae

Abstract Background Herbaspirillum rubrisubalbicans was first identified as a bacterial plant pathogen, causing the mottled stripe disease in sugarcane. H. rubrisubalbicans can also associate with various plants of economic interest in a non pathogenic manner. Results A 21 kb DNA region of the H. rubrisubalbicans genome contains a cluster of 26 hrp/hrc genes encoding for the type three secretion system (T3SS) proteins. To investigate the contribution of T3SS to the plant-bacterial interaction process we generated mutant strains of H. rubrisubalbicans M1 carrying a Tn5 insertion in both the hrcN and hrpE genes. H. rubrisulbalbicans hrpE and hrcN mutant strains of the T3SS system failed to cause the mottled stripe disease in the sugarcane susceptible variety B-4362. These mutant strains also did not produce lesions on Vigna unguiculata leaves. Oryza sativa and Zea mays colonization experiments showed that mutations in hrpE and hrcN genes reduced the capacity of H. rubrisulbalbicans to colonize these plants, suggesting that hrpE and hrcN genes are involved in the endophytic colonization. Conclusions Our results indicate that the T3SS of H. rubrisubalbicans is necessary for the development of the mottled stripe disease and endophytic colonization of rice.</p

Comparative Genomics of Sibling Species of Fonsecaea Associated with Human Chromoblastomycosis

Submitted by Manoel Barata ([email protected]) on 2018-02-09T13:19:12Z No. of bitstreams: 1 FaoroComparativ.pdf: 5399928 bytes, checksum: af51deed6d3e60618950577e576e6aad (MD5)Approved for entry into archive by Manoel Barata ([email protected]) on 2018-05-03T19:30:23Z (GMT) No. of bitstreams: 1 FaoroComparativ.pdf: 5399928 bytes, checksum: af51deed6d3e60618950577e576e6aad (MD5)Made available in DSpace on 2018-05-03T19:30:23Z (GMT). No. of bitstreams: 1 FaoroComparativ.pdf: 5399928 bytes, checksum: af51deed6d3e60618950577e576e6aad (MD5) Previous issue date: 2017Universidade Federal do Paraná. Departamento de Patologia Básica. Laboratório de Imunogenética e Histocompatibilidade. Curitiba, PR, Brasil / Universidade Federal do Paraná. Engenharia de Bioprocessos e Biotecnologia. Curitiba, PR, Brasil.Universidade Federal do Paraná. Setor de Educação Profissional e Tecnológica. Laboratório de Bioinformática. Curitiba, PR, Brasil / Universidade Federal do Paraná. Departamento de Bioquímica. Curitiba, PR, Brasil.Universidade Federal do Paraná. Departamento de Patologia Básica. Laboratório de Imunogenética e Histocompatibilidade. Curitiba, PR, Brasil.Universidade Federal do Paraná. Departamento de Patologia Básica. Laboratório de Imunogenética e Histocompatibilidade. Curitiba, PR, Brasil / CBS-KNAW Fungal Biodiversity Centre. Utrecht, Netherlands / University of Amsterdam. Institute for Biodiversity and Ecosystem Dynamics. Amsterdam, Netherlands.Universidade Federal do Paraná. Engenharia de Bioprocessos e Biotecnologia. Curitiba, PR, Brasil.Universidade Federal do Paraná. Setor de Educação Profissional e Tecnológica. Laboratório de Bioinformática. Curitiba, PR, Brasil.Universidade Federal do Paraná. Engenharia de Bioprocessos e Biotecnologia. Curitiba, PR, Brasil / Universidade Federal do Paraná. Setor de Educação Profissional e Tecnológica. Laboratório de Bioinformática. Curitiba, PR, Brasil / Universidade Federal do Paraná. Departamento de Bioquímica. Curitiba, PR, Brasil.Universidade Federal do Paraná. Departamento de Patologia Básica. Laboratório de Imunogenética e Histocompatibilidade. Curitiba, PR, Brasil.Universidade de Brasília. Departamento de Biologia Celular. Brasilia, Brasil.Universidade Federal do Paraná. Departamento de Patologia Básica. Laboratório de Imunogenética e Histocompatibilidade. Curitiba, PR, Brasil.Universidade de Brasília. Departamento de Biologia Celular. Brasilia, Brasil.Guangdong Provincial Center for Disease Control and Prevention. Guangdong Provincial Institute of Public Health, Guangzhou, China.Universidade Federal do Paraná. Departamento de Bioquímica. Curitiba, PR, Brasil / Fundação Oswaldo Cruz. Instituto Carlos Chagas. Curitiba, PR, Brasil.Universidade Federal do Paraná. Departamento de Bioquímica. Curitiba, PR, Brasil.Universidade Federal do Paraná. Departamento de Bioquímica. Curitiba, PR, Brasil.Universidade Federal do Paraná. Departamento de Bioquímica. Curitiba, PR, Brasil.Universidade de São Paulo. Faculdade de Ciências Farmacêuticas. Departamento de Análises Clínicas e Toxicológicas. São Paulo, SP, Brasil.Universidade de São Paulo. Faculdade de Ciências Farmacêuticas. Departamento de Análises Clínicas e Toxicológicas. São Paulo, SP, Brasil.Universidade de Brasília. Departamento de Biologia Celular. Brasilia, Brasil / Northern Arizona University. Pathogen and Microbiome Institute. Flagstaff, United States.Universidade Católica de Brasília. Departamento de Ciências Genômicas e Biotecnologia. Brasília, DF, Brasil.Universidade Federal do Paraná. Departamento de Patologia Básica. Laboratório de Imunogenética e Histocompatibilidade. Curitiba, PR, Brasil.Universidade Federal do Paraná. Departamento de Bioquímica. Curitiba, PR, Brasil.Universidade Federal do Paraná. Setor de Educação Profissional e Tecnológica. Laboratório de Bioinformática. Curitiba, PR, Brasil / Universidade Federal do Paraná. Departamento de Bioquímica. Curitiba, PR, Brasil.Universidade de Campinas. Divisão de Recursos Microbianos. Campinas, SP, Brasil.Mashhad University of Medical Sciences. School of Medicine. Department of Parasitology and Mycology. Mashhad, Iran.Universidade Federal do Paraná. Departamento de Patologia Básica. Laboratório de Imunogenética e Histocompatibilidade. Curitiba, PR, Brasil / Universidade Federal do Paraná. Hospital das Clínicas. Curitiba, PR, Brasil.Universidade Federal do Paraná. Setor de Educação Profissional e Tecnológica. Laboratório de Bioinformática. Curitiba, PR, Brasil / Universidade Federal do Paraná. Departamento de Bioquímica. Curitiba, PR, Brasil.Universidade Federal do Paraná. Departamento de Patologia Básica. Laboratório de Imunogenética e Histocompatibilidade. Curitiba, PR, Brasil / CBS-KNAW Fungal Biodiversity Centre. Utrecht, Netherlands / University of Amsterdam. Institute for Biodiversity and Ecosystem Dynamics. Amsterdam, Netherlands.Fonsecaea and Cladophialophora are genera of black yeast-like fungi harboring agents of a mutilating implantation disease in humans, along with strictly environmental species. The current hypothesis suggests that those species reside in somewhat adverse microhabitats, and pathogenic siblings share virulence factors enabling survival in mammal tissue after coincidental inoculation driven by pathogenic adaptation. A comparative genomic analysis of environmental and pathogenic siblings of Fonsecaea and Cladophialophora was undertaken, including de novo assembly of F. erecta from plant material. The genome size of Fonsecaea species varied between 33.39 and 35.23 Mb, and the core genomes of those species comprises almost 70% of the genes. Expansions of protein domains such as glyoxalases and peptidases suggested ability for pathogenicity in clinical agents, while the use of nitrogen and degradation of phenolic compounds was enriched in environmental species. The similarity of carbohydrate-active vs. protein-degrading enzymes associated with the occurrence of virulence factors suggested a general tolerance to extreme conditions, which might explain the opportunistic tendency of Fonsecaea sibling species. Virulence was tested in the Galleria mellonella model and immunological assays were performed in order to support this hypothesis. Larvae infected by environmental F. erecta had a lower survival. Fungal macrophage murine co-culture showed that F. erecta induced high levels of TNF-α contributing to macrophage activation that could increase the ability to control intracellular fungal growth although hyphal death were not observed, suggesting a higher level of extremotolerance of environmental species

Comparative genomics of sibling species of Fonsecaea associated with Human Chromoblastomycosis

Fonsecaea and Cladophialophora are genera of black yeast-like fungi harboring agents of a mutilating implantation disease in humans, along with strictly environmental species. The current hypothesis suggests that those species reside in somewhat adverse microhabitats, and pathogenic siblings share virulence factors enabling survival in mammal tissue after coincidental inoculation driven by pathogenic adaptation. A comparative genomic analysis of environmental and pathogenic siblings of Fonsecaea and Cladophialophora was undertaken, including de novo assembly of F. erecta from plant material. The genome size of Fonsecaea species varied between 33.39 and 35.23Mb, and the core genomes of those species comprises almost 70% of the genes. Expansions of protein domains such as glyoxalases and peptidases suggested ability for pathogenicity in clinical agents, while the use of nitrogen and degradation of phenolic compounds was enriched in environmental species. The similarity of carbohydrate-active vs. protein-degrading enzymes associated with the occurrence of virulence factors suggested a general tolerance to extreme conditions, which might explain the opportunistic tendency of Fonsecaea sibling species. Virulence was tested in the Galleria mellonella model and immunological assays were performed in order to support this hypothesis. Larvae infected by environmental F. erecta had a lower survival. Fungal macrophage murine co-culture showed that F. erecta induced high levels of TNF-alpha contributing to macrophage activation that could increase the ability to control intracellular fungal growth although hyphal death were not observed, suggesting a higher level of extremotolerance of environmental species8CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQCOORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPES573828/2008-3059201

Comparative Genomics of Sibling Species of Fonsecaea Associated with Human Chromoblastomycosis

Fonsecaea and Cladophialophora are genera of black yeast-like fungi harboring agents of a mutilating implantation disease in humans, along with strictly environmental species. The current hypothesis suggests that those species reside in somewhat adverse microhabitats, and pathogenic siblings share virulence factors enabling survival in mammal tissue after coincidental inoculation driven by pathogenic adaptation. A comparative genomic analysis of environmental and pathogenic siblings of Fonsecaea and Cladophialophora was undertaken, including de novo assembly of F. erecta from plant material. The genome size of Fonsecaea species varied between 33.39 and 35.23 Mb, and the core genomes of those species comprises almost 70% of the genes. Expansions of protein domains such as glyoxalases and peptidases suggested ability for pathogenicity in clinical agents, while the use of nitrogen and degradation of phenolic compounds was enriched in environmental species. The similarity of carbohydrate-active vs. protein-degrading enzymes associated with the occurrence of virulence factors suggested a general tolerance to extreme conditions, which might explain the opportunistic tendency of Fonsecaea sibling species. Virulence was tested in the Galleria mellonella model and immunological assays were performed in order to support this hypothesis. Larvae infected by environmental F. erecta had a lower survival. Fungal macrophage murine co-culture showed that F. erecta induced high levels of TNF-α contributing to macrophage activation that could increase the ability to control intracellular fungal growth although hyphal death were not observed, suggesting a higher level of extremotolerance of environmental species