Neisseria gonorrhoeae
A Microbial Biorealm page on the genus Neisseria gonorrhoeae
Classification
Higher order taxa
Domain; Phylum; Class; Order; family [Others may be used. Use NCBI link to find]
Species
|
NCBI: Taxonomy |
Genus species
Description and significance
Neisseria gonorrhoeae is a gram- negative coccus, or bacteria whose overall shape is spherical. It is usually seen in pairs with adjacent sides flattened. The organism is usually find interacellulary in polymorphonuclear leukocytes, or a specific category of white blood cells which varying shapes of nuclei, of the gonorrhea pustular exudates [8] with humans as its only natural host. [10] N. gonorrhoeae is highly efficient in using transferrin-bound iron for in vitro growth. Many strains can also utilize lactoferrin-bound iron. The bacteria bind only human transferrin and lactoferrin. This specificity is thought to be the reason these bacteria are exclusively human pathogens. [8] The bacterium was first discovered in 1879 by a German physician Albert Ludwig Sigesmund. [1] This organism is relatively fragile and is susceptible to temperature changes, drying, uv light, and some other environmental conditions. [8] The recommended procedure for isolating Neisseria gonorrhoeae involves the inoculation of a specimen directly onto a nutritive growth medium that is at room temperature and immediate incubation at 35-37ºC in an atmosphere of 3 – 10% added CO2. [6] Strains are inconsistent in their cultural requirements so the media needed for growth and isolation of the organism contain hemoglobin, NAD, yeast extract and other supplements.
Genome structure
Neisseria gonorrhoeae has a circular DNA genome. [7] N. gonorrheeae strain 1090 genome was sequenced by the University of Oklahoma. [11] The genome length is 2,153,922 nt and contains 2069 genes and 67 structural RNAs. It also has 2002 protein genes. This includes the opacity (Opa) proteins which are responsible for the opaque colony phenotyle caused by tight junctions between adjacent Neisseria, and are also responsible for tight adherence to host cells. This organism is also naturally competent for the update of DNA. [1] Neisseria gonorrhoeae can produce one or several Opa proteins. These proteins are subject to phase variation and are usually found on cells from colonies possessing a unique opaque phenotype called O+. At any particular time, the bacterium can express zero, one, or several different Opa proteins, and each strain has 10 or more genes for different Opas. [8] More specifically, during infection, N. gonorrhoeae is like to encounter hydrogen peroxide, which inhibits growth. Since it is an obligate human pathogen, it would not be exposed to typical environmental stress such as UV light, ionizing radiation, or chemical mutagens. The type of DNA damage N. gonorrhoeae would come across is oxidative. [12]
N. gonorrhoeae genome contains many genes that are predicted to be involved severeal DNA repair pathyways. Recombinational DNA repair has been studied in N. gonorrhoeae and requires the recA and recX genes, which act with either the RecBCD pathway (recB, recC, and recD genes) or the RecF-like pathway (recO, recQ, recR, and recJ genes). Also, contributing to the recombinational DNA repair pathway is the Holliday junction processing enzymes encoded by recG, ruvA, ruvB, and ruvC. N. gonorrhoeae seems to use both DNA recombinational repair pathways simultaneously. This is in contrast to Escherichia coli, where mutants in the RecF pathway generally show phenotypes only in the context of recBC sbcBC mutations. This leads to the conclusion that recombinational DNA repair is especially important for the repair of damaged DNA in N.gonorrhoeae. [12]
During repair of oxidatively damage in E.coli, recA and other reocombinational rpair genes have been shown to be important. E. coli RecA is important for both functions in DNA repair and its role in the induction of the SOS response of DNA repair. But because N. gonorrhoeae does not have SOS response, it does not use RecA for the repair of oxidatively damaged DNA. [12]
Microarray analysis has shown that only recN, a single known DNA repair and recombination gene is upregulated after hydrogen peroxide treatment. It is unclear as to what the exact role of this gene is, but it seems to function in the repair of DNA double strand breaks. In addition, an N. gonorrhoeae recN mutant displays decreased survival to nalidixic acid and hydrogen peroxide, both of which can result in DNA double-strand breaks. [12]
Although several gonococcal genes have been identified that protect against oxidative damage, few of them are predicted to function in the repair of DNA. To date, only two genes that are involved in DNA repair and recombination have been found to protect against oxidative damage in N. gonorrhoeae. Both the N. gonorrhoeae recN mutant and a mutant inactivated in priA, which is involved in replication restart, show decreased resistance to oxidative damaging agents. In contrast to E. coli recA, N. gonorrhoeae recA was reported to not protect against oxidative damage caused by H2O2. This suggests that DNA repair and recombination enzymes may differ between N. gonorrhoeae and E. coli in their importance to the repair of oxidatively damaged DNA. [12]
To test the importance of gonococcal DNA recombination and repair genes in conferring resistance to oxidative damage, the resistance was measured of a recA mutant and of several mutants with defects in recombinational DNA repair enzymes RecA, in addition to the RecBCD and RecF-like recombinational repair pathways and Holliday junction processing enzymes, contribute to the survival of N. gonorrhoeae to oxidative damage. [12]
RecA, genes of the RecBCD and RecF-like recombination pathways, and genes whose products are involved in Holliday junction processing are all important for mediating repair of oxidative damage. Moreover, data suggest that these genes are expressed at basal levels sufficient to mediate repair and do not need to be upregulated upon encountering DNA damage in order to function in N. gonorrhoeae.
The recent demonstration that N. gonorrhoeae is polyploid suggests that, in the event of chromosomal damage, these additional copies of the chromosome could provide the genetic information present on the damaged copy, perhaps anticipating the necessity of recombinational repair. Therefore, of the many mechanisms of resistance used by N. gonorrhoeae to combat oxidative insult, recombinational DNA repair appears to be one layer of resistance. [12]
Cell structure and metabolism
Neisseria gonorrhoeae posses a typical gram negative our membrane that is composed of proteins, phospholipids, and lipopolysaccharide (LPS). Neisserial LPS is unique in that it has highly-branched basal oligosaccharide structure and the absence of repeating O-antigen subunits. Thus, they are referred to as lipooligosaccharide (LOS). During growth, the bacterium releases outer membrane fragments called "blebs". These contain LOS and may have a role in the pathogenesis if hey are distributed during the course of an infection. [8] The bacterium have Fimbriae, whichn is a proteinaceous appendage that is thinner than a flagellum. They play a major role in adherence to extend several micrometers from its cell surface. [8] There are four types of N. gonorrhoeae based on the presences of fimbriae and they are called T1, T2, T3, and T4. [4]. In vitro studies show that these piliated cells bind more efficiently to eukaryotic cells than non piliated cells, which suggests that the pilus structure plays an important role in this interaction [3] N. gonorrhoeae also can move in a jerky fashion across solid surfaces. This type of motility is called twitching, which depends on type IV pili and takes place by a “grappling hook” mechanism, which is the extension of the pilus, its attachment, and its retraction back into the cell. Twitching motility also contributes to the formation of biofilms and a kind of aggregation that causes differentiation in the myxobacteria. [9]. During growth, Neisseria gonorrhoeae releases soluble fragments of peptidoglycan. These molecules are implicated in the pathogenesis of different forms of gonococcal infection. A major peptidoglycan fragment released by N. gonorrhoeae is identical to the tracheal cytotoxin of Bordetella pertussis and has been shown to kill ciliated fallopian tube cells in organ culture. In the examination of the role of other putative lytic transglycosylases in PGCT production, results suggest that this gonococcal gene (ltgA) encodes a lytic peptidoglycan transglycosylase and that it is responsible for a significant proportion of the PGCT released by N. gonorrhoeae .[2] N. gonorrhoeae genome contains homologues of enzymes involved in PG recycling, and the levels of turnover are consistent with a certain level of recycling occurring in gonococci. [2] It is unknown N. gonorrhoeae has cytoplasmic proteins for sensing PG fragments; but, this would be an attractive mechanism for controlling cell processes, including autolysis. The presence of two (and possibly more) enzymes with potentially redundant functions either indicates that gonococci have an elaborate backup system for cell wall processes or may suggest that the enzymes have different functions or are differently regulated or localized. AtlA is encoded in a group of type IV secretion genes in the gonococcal genetic island, and recent evidence suggests that AtlA may have a dedicated role in assembly of the type IV secretion system. [2] PGCT is expected to be released during infection, due to the extensive turnover and release of PG fragments in vitro. [2] Although many lytic transglycosylases were characterized in E. coli, the genes for PGCT production have not been previously characterized in bacteria in which PGCT is thought to act in infection. Characterization of lytic transglycosylases in gonococci increases understanding of how PGCT is generated and released during infection, and creation of mutant strains deficient in these enzymes should aid investigation of the role of PG in gonococcal virulence-related processes. These organisms are aerobic, strongly oxidase-positive, have an oxidative metabolism, are susceptible to drying and are fastidious (growth is inhibited by free fatty acids). [4]
Ecology
Describe any interactions with other organisms (included eukaryotes), contributions to the environment, effect on environment, etc.
Pathology
How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.
Application to Biotechnology
Does this organism produce any useful compounds or enzymes? What are they and how are they used?
Current Research
Enter summaries of the most recent research here--at least three required
References
Edited by student of Rachel Larsen
