Project description:Microarray comparative genome hybridization (mCGH) data was collected from one Neisseria cinerea, two Neisseria lactamica, two Neisseria gonorrhoeae, and 48 Neisseria meningitidis isolates. For N. meningitidis, these isolates are from diverse clonal complexes, invasive and carriage strains, and all major serogroups. The microarray platform represented N. meningitidis strains MC58, Z2491, and FAM18 and N. gonorrhoeae FA1090.
Project description:Whole genome DNA microarray of Neisseria meningitidis serogroup B strain MC58 and the isogenic mutant strain deficient of the transcriptional regulator FarR, MC58 ∆farR.
Project description:Baart2007 - Genome-scale metabolic network of
Neisseria meningitidis (iGB555)
This model is described in the article:
Modeling Neisseria
meningitidis metabolism: from genome to metabolic fluxes.
Baart GJ, Zomer B, de Haan A, van
der Pol LA, Beuvery EC, Tramper J, Martens DE.
Genome Biol. 2007; 8(7): R136
Abstract:
BACKGROUND: Neisseria meningitidis is a human pathogen that
can infect diverse sites within the human host. The major
diseases caused by N. meningitidis are responsible for death
and disability, especially in young infants. In general, most
of the recent work on N. meningitidis focuses on potential
antigens and their functions, immunogenicity, and pathogenicity
mechanisms. Very little work has been carried out on Neisseria
primary metabolism over the past 25 years. RESULTS: Using the
genomic database of N. meningitidis serogroup B together with
biochemical and physiological information in the literature we
constructed a genome-scale flux model for the primary
metabolism of N. meningitidis. The validity of a simplified
metabolic network derived from the genome-scale metabolic
network was checked using flux-balance analysis in chemostat
cultures. Several useful predictions were obtained from in
silico experiments, including substrate preference. A minimal
medium for growth of N. meningitidis was designed and tested
successfully in batch and chemostat cultures. CONCLUSION: The
verified metabolic model describes the primary metabolism of N.
meningitidis in a chemostat in steady state. The genome-scale
model is valuable because it offers a framework to study N.
meningitidis metabolism as a whole, or certain aspects of it,
and it can also be used for the purpose of vaccine process
development (for example, the design of growth media). The flux
distribution of the main metabolic pathways (that is, the
pentose phosphate pathway and the Entner-Douderoff pathway)
indicates that the major part of pyruvate (69%) is synthesized
through the ED-cleavage, a finding that is in good agreement
with literature.
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Project description:Neisseria meningitidis is the leading cause of bacterial meningitis and septicemia worldwide. The novel ST-4821 clonal complex caused several serogroup C meningococcal outbreaks unexpectedly during 2003–2005 in China. We fabricated a whole-genome microarray of Chinese N. meningitidis serogroup C representative isolate 053442 and characterized 27 ST-4821 complex isolates which were isolated from different serogroups using comparative genomic hybridization (CGH) analysis. This paper provides important clues which are helpful to understand the genome composition and genetic background of different serogroups isolates, and possess significant meaning to the study of the newly emerged hyperinvasive lineage. Keywords: comparative genomic hybridization
Project description:Species of the Neisseria genus harbor close relationships with their mamallian hosts, including humans. The outcome of these interactions can result in commensalism, asymptomatic carriage, or acute inflammatory responses. Little is known of the mechanisms Neisseria use to maintain and shape their host niche in the context of asymptomatic infection or long term commensal colonization and persistence. To identify novel host interaction factors contributing to host persistence, a Tn5 transposon library was created in Neisseria musculi, and inoculated into a permissive strain of laboratory mice (CAST/EiJ). At various time points post inoculation, transposon mutants were recovered from fecal and oral samples, and analyzed to identifiy mutants incapable of maintaining a host niche at either site.