Chapter 17 : Neisseria

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Neisseria, Page 1 of 2

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The genus consists of two human pathogens, (gonococcus) and (meningococcus), as well as several commensal species, including . Although the pathogenic species are considered classical extracellular pathogens, intraepithelial cell growth was documented recently, and it is possible that invasion of and growth within host cells plays an important role in pathogenesis. The pathogenic species express a wide array of iron acquisition systems. Although the species are not known to synthesize or secrete detectable siderophores, they are capable of iron acquisition from host transferrin, lactoferrin, and hemoglobin without the synthesis of a siderophore intermediate. Iron acquisition from these host proteins occurs via a process that is dependent on the expression of specific outer membrane receptors. In addition to these sources of iron, the pathogenic species are capable of using heme, siderophores made by other microorganisms (xenosiderophores), and a variety of keto acid-iron complexes as sole iron sources.

Citation: Nau Cornelissen C, Sparling P. 2004. Neisseria, p 256-272. In Crosa J, Mey A, Payne S, Iron Transport in Bacteria. ASM Press, Washington, DC. doi: 10.1128/9781555816544.ch17

Key Concept Ranking

Outer Membrane Proteins
Sodium Dodecyl Sulfate
Pelvic Inflammatory Disease
Integral Membrane Proteins
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Image of FIGURE 1

Model of iron acquisition systems expressed by the species. TbpA and TbpB are outer membrane (OM) proteins that bind to transferrin and subsequently facilitate iron removal and internalization. LbpA and LbpB are similar proteins that function as the lactoferrin receptor. HpuA and HpuB are homologous to the Tbp and Lbp receptor proteins and facilitate the utilization of hemoglobin as a heme and iron source. Another hemoglobin receptor, HmbR (not shown), is expressed by and does not conform to this two-protein receptor paradigm, as discussed in the text. FbpA is a periplasmic (PP), protein and FbpB and FbpC are shown as integral cytoplasmic membrane (CM) proteins. This group of proteins facilitates the periplasmic and cytoplasmic transport of iron, donated by transferrin or lactoferrin. The TonB, ExbB, and ExbD energy transduction system is shown within or tethered to the cytoplasmic membrane. This group of proteins is required for energization of all three iron acquisition systems shown. See the text for details.

Citation: Nau Cornelissen C, Sparling P. 2004. Neisseria, p 256-272. In Crosa J, Mey A, Payne S, Iron Transport in Bacteria. ASM Press, Washington, DC. doi: 10.1128/9781555816544.ch17
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Image of FIGURE 2

Genetic arrangement of genes. By comparison with the genes, encoding the lactoferrin receptor, and with the genes, encoding the hemoglobin receptor, only the genes are separated by an intergenic region. This region consists of 86 bp and includes a region of dyad symmetry (arrows) capable of forming a stem-loop structure in mRNA. The promoter region that precedes is also shown; it includes canonical promoter, overlapped by a putative Fur binding site (Fur box). The transcriptional start site, ribosome start site (RBS), and start codon are also shown.

Citation: Nau Cornelissen C, Sparling P. 2004. Neisseria, p 256-272. In Crosa J, Mey A, Payne S, Iron Transport in Bacteria. ASM Press, Washington, DC. doi: 10.1128/9781555816544.ch17
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Image of FIGURE 3

Naturally occurring mutations in . Two major classes of mutants have been characterized that result in no expression of the LbpB protein. (A) A polypyrimidine tract consisting of 10 C residues results in expression of the LbpB protein, while a decrease in the number of C residues to 8 or 9 shifts the gene out of frame and prevents LbpB expression. Expression is found with C strings of 7 or 13 residues as well. (B) A deletion of 2.7 kb with a concomitant insertion of 41 residues of a repeated element (black box) results in a gene fusion between the upstream gene, which encodes a GTP-binding protein, and the gene. This fusion event results in no expression of either LbpB or LbpA. Not shown are various point mutations in or , which also result in loss of expression in some isolates. P indicates the approximate position of the iron-regulated promoter that drives the expression of .

Citation: Nau Cornelissen C, Sparling P. 2004. Neisseria, p 256-272. In Crosa J, Mey A, Payne S, Iron Transport in Bacteria. ASM Press, Washington, DC. doi: 10.1128/9781555816544.ch17
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