Structural and antigenic differences between two types of meningococcal pili

Diaz, J-L.; Virji, Mumtaz; Heckels, John E.

doi:10.1111/j.1574-6968.1984.tb00207.x

Cited by 33 publications

(5 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These include three large related proteins that contain homologies to adhesins, as well as toxin motifs and an additional type IV pilin protein (NMB0547) that is unrelated to the pilElpilS.system. This protein is distinct from the neisserial type I1 pilus protein previously recognized as an alternative pilus system in N meningitidis (45).…”

Section: Iht-amentioning

confidence: 69%

See 1 more Smart Citation

Complete Genome Sequence of Neisseria meningitidis Serogroup B Strain MC58

Tettelin¹,

Saunders

Heidelberg³

et al. 2000

Science

1,043

893

View full text Add to dashboard Cite

The 2,272,351-base pair genome of Neisseria meningitidis strain MC58 (serogroup B), a causative agent of meningitis and septicemia, contains 2158 predicted coding regions, 1158 (53.7%) of which were assigned a biological role. Three major islands of horizontal DNA transfer were identified; two of these contain genes encoding proteins involved in pathogenicity, and the third island contains coding sequences only for hypothetical proteins. Insights into the commensal and virulence behavior of N. meningitidis can be gleaned from the genome, in which sequences for structural proteins of the pilus are clustered and several coding regions unique to serogroup B capsular polysaccharide synthesis can be identified. Finally, N. meningitidis contains more genes that undergo phase variation than any pathogen studied to date, a mechanism that controls their expression and contributes to the evasion of the host immune system.

show abstract

Section: Iht-amentioning

confidence: 69%

“…Estrategy (7). N. meningitidis strain MC58 has mail: tettelin@tigr.org 'ypresent address: Celera Genomics, 45 with an average G+C content of 51.5%. Base pair 1 of the chromosome was assigned within the putative origin of replication that was determined by the presence of a cluster of DnaA boxes, oligomer-skew (8), and G-C skew (9) analyses.…”

mentioning

confidence: 99%

Complete Genome Sequence of Neisseria meningitidis Serogroup B Strain MC58

Tettelin¹,

Saunders

Heidelberg³

et al. 2000

Science

1,043

893

View full text Add to dashboard Cite

show abstract

“…N. meningitidis strain FAM18, which lacks a well-defined G-4 quartet and encodes class II pilin (6,18), undergoes pilin Av at a rate not detectable by the assay described here and is unlikely to undergo antigenic variation at all. These data clearly show that major differences in strain-to-strain pilin Av rates exist, an observation previously made for N. gonorrhoeae (10).…”

Section: ϫ3mentioning

confidence: 82%

Frequency and Rate of Pilin Antigenic Variation of Neisseria meningitidis

Helm

Seifert

2010

J Bacteriol

View full text Add to dashboard Cite

The rates of pilin antigenic variation (Av) of two strains of Neisseria meningitidis were determined using an unbiased DNA sequencing assay. Strain MC58 underwent pilin Av at a rate similar to that of N. gonorrhoeae strain MS11 but lower than that of N. gonorrhoeae strain FA1090. Pilin Av was undetectable in strain FAM18.Neisseria meningitidis is a Gram-negative diplococcus that colonizes the nasopharynx of approximately 5 to 10% of the population and is usually nonpathogenic but can occasionally enter the bloodstream to cause septicemia and can eventually spread to the meninges, causing meningitis (15). Approximately 500,000 cases of meningococcal meningitis occur every year, with nearly 10% resulting in fatality (2).Type IV pili (TFP) are long filamentous structures protruding from the bacterial surface and are required for adherence of N. meningitidis to host cells (7). As with the TFP of the closely related pathogen Neisseria gonorrhoeae, the pili are able to undergo antigenic variation (Av). In N. gonorrhoeae, pilin Av occurs as a result of recombination between one of the multiple silent pilS copies and the expressed pilin gene (pilE). The pilS copies share significant regions of homology with pilE yet lack a promoter or ribosome-binding site and the initial 5Ј coding sequence. Pilin Av relies on RecA and the RecF-like recombination pathway to catalyze gene conversion, resulting in an altered pilE sequence, carrying part of the pilS donor, and the original unaltered pilS sequence (8, 9).While the frequency of pilin Av has been measured in N. gonorrhoeae (5,10,12), this process has never been quantified in N. meningitidis. Two sequenced strains were picked to measure pilin Av: serogroup B strain MC58 (sequence type complex), isolated from an invasive infection (14), and serogroup C strain FAM18 (ST-11 complex), which was isolated from a patient with septicemia (1). In both strains, the native recA gene was replaced with the very highly conserved N. gonorrhoeae recA6 construct, which allows regulation of expression with IPTG (isopropyl-␤-D-thiogalactopyranoside) (17). recA6 strains are RecA ϩ when grown with IPTG but are RecA Ϫ when grown without IPTG (17). These phenotypes were confirmed by measuring the UV sensitivities and DNA transformation competence levels of both strains with or without IPTG, and both strains were shown to be piliated by transmission electron microscopy (data not shown). Bacteria were grown at 37°C with 5% CO 2 on gonococcal medium base (GCB; Difco) plus Kellogg supplements I and II (11).The pilin Av sequencing assay was performed as described previously (5, 10, 12) with slight modifications. Briefly, FAM18 and MC58 were grown on solid GCB with 1 mM IPTG, allowing for the expression of RecA, for 22 h and 12.5 h, respectively, which was estimated to produce 20 generations. For FAM18, little or no pilin Av was expected since the G-quartetforming sequence required for pilin Av is degenerate in this strain (3). Therefore, two random progenitor colonies were picked from IPTG-enriched medi...

show abstract

“…A large proportion failed to react with both antibodies but were nevertheless shown by electron microscopy to be piliated (9). These strains also failed to react on Western immunoblots with polyclonal antisera raised against gonococcal pili, but did react with the same sera on immune precipitation under nondenaturing conditions, to reveal pilins with Mr in the range 13,000 to 16,000.…”

Section: Pilus Structure Subunit Structurementioning

confidence: 97%

“…Nevertheless, pili do mediate adhesion of meningococci to nasopharyngeal cells and may therefore be important factors in establishing the carrier state (48). Isolates cultured from the blood and cerebrospinal fluid of patients with meningococcal disease are also piliated (9,48,49), and pili have been directly demonstrated in the cerebrospinal fluid of a child with meningococcal meningitis (47). Whether pili play any role in the ability of meningococci to transgress the blood-brain barrier or interact with meningeal tissues remains unclear.…”

Section: Role Of Pili In Pathogenesismentioning

confidence: 99%

Structure and function of pili of pathogenic Neisseria species

Heckels

1989

Clin Microbiol Rev

View full text Add to dashboard Cite

Structural and antigenic differences between two types of meningococcal pili

Cited by 33 publications

References 7 publications

Complete Genome Sequence of Neisseria meningitidis Serogroup B Strain MC58

Complete Genome Sequence of Neisseria meningitidis Serogroup B Strain MC58

Frequency and Rate of Pilin Antigenic Variation of Neisseria meningitidis

Structure and function of pili of pathogenic Neisseria species

Contact Info

Product

Resources

About