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==Cell Biology== | ==Cell Biology== | ||
*''Mycoplasma'' is the smallest [[self-replicating]] organism. They are bacteria that lack a cell wall and [[periplasmic space]], have reduced [[genome]]s, and limited [[metabolic]] activity. | *''Mycoplasma'' is the smallest [[self-replicating]] organism. They are bacteria that lack a cell wall and [[periplasmic space]], have reduced [[genome]]s, and limited [[metabolic]] activity.<ref name=Romero-Arroyo>{{cite journal | last1 = Romero-Arroyo | first1 = C. E. | last2 = Jordan | first2 = J. | last3 = Peacock | first3 = S. J. | last4 = Willby | first4 = M. J. | last5 = Farmer | first5 = M. A. | last6 = Krause | first6 = D. C. | year = 1994 | title = ''Mycoplasma pneumoniae'' protein P30 is required for cytadherence and associated with proper cell development | url = | journal = J. Bacteriol | volume = 181 | issue = | pages = 1079–1087 | doi = 10.1128/CMR.17.4.697-728.2004 }}</ref><ref name=Dallo>S. Dallo, and J. Baseman "Intracellular DNA replication and long-term survival of pathogenic mycoplasmas" ''Microb. Pathog.'' 2000; 29, 301–309. {{10.1006/mpat.2000.0395}}</ref> | ||
*''Mycoplasma pneumoniae'' cells have an elongated shape that is approximately 1-2 µm in length and 0.1–0.2 µm in width. | *''Mycoplasma pneumoniae'' cells have an elongated shape that is approximately 1-2 µm in length and 0.1–0.2 µm in width. | ||
*The extremely small cell size means they are incapable of being examined by [[light microscopy]]; a [[stereomicroscope]] is required for viewing the [[Morphology (biology)|morphology]] of ''M. pneumoniae'' [[Colony (biology)|colonies]], which are usually less than 100 µm in length. | *The extremely small cell size means they are incapable of being examined by [[light microscopy]]; a [[stereomicroscope]] is required for viewing the [[Morphology (biology)|morphology]] of ''M. pneumoniae'' [[Colony (biology)|colonies]], which are usually less than 100 µm in length. The inability to synthesize a [[peptidoglycan cell wall]] is due to the absence of [[gene]]s encoding its formation and results in an increased importance in maintenance of [[osmotic]] stability to avoid [[desiccation]]. The lack of a cell wall also calls for increased support of the [[cell membrane]], which includes a rigid [[cytoskeleton]] composed of an intricate [[protein]] network and, potentially, an [[extracellular]] [[Capsule (microbiology)|capsule]] to facilitate [[adhesion (medicine)|adherence]] to the [[host cell]].<ref name=Waites>{{cite journal | last1 = Ken | first1 = | last2 = Waites | first2 = B | last3 = Deborah | first3 = F. Talkington | year = 2004 | title = ''Mycoplasma pneumoniae'' and Its Role as a Human Pathogen | url = | journal = Clin. Microbiol. Rev | volume = 17 | issue = 4| pages = 697–728 | doi = 10.1128/CMR.17.4.697-728.2004 }}</ref> | ||
*''M. pneumoniae'' are the only [[bacteria]]l cells that possess [[cholesterol]] in their cell membrane (obtained from the host) and possess more genes that encode for membrane [[lipoprotein]] variations than other mycoplasmas, which are thought to be associated with its parasitic lifestyle. ''M. pneumoniae'' cells also possess an attachment [[organelle]], which is used in the [[Bacterial gliding|gliding motility]] of the organism by an unknown mechanism.<ref name=Romero-Arroyo>{{cite journal | last1 = Romero-Arroyo | first1 = C. E. | last2 = Jordan | first2 = J. | last3 = Peacock | first3 = S. J. | last4 = Willby | first4 = M. J. | last5 = Farmer | first5 = M. A. | last6 = Krause | first6 = D. C. | year = 1994 | title = ''Mycoplasma pneumoniae'' protein P30 is required for cytadherence and associated with proper cell development | url = | journal = J. Bacteriol | volume = 181 | issue = | pages = 1079–1087 | doi = 10.1128/CMR.17.4.697-728.2004 }}</ref | *''M. pneumoniae'' are the only [[bacteria]]l cells that possess [[cholesterol]] in their cell membrane (obtained from the host) and possess more genes that encode for membrane [[lipoprotein]] variations than other mycoplasmas, which are thought to be associated with its parasitic lifestyle. ''M. pneumoniae'' cells also possess an attachment [[organelle]], which is used in the [[Bacterial gliding|gliding motility]] of the organism by an unknown mechanism.<ref name=Romero-Arroyo>{{cite journal | last1 = Romero-Arroyo | first1 = C. E. | last2 = Jordan | first2 = J. | last3 = Peacock | first3 = S. J. | last4 = Willby | first4 = M. J. | last5 = Farmer | first5 = M. A. | last6 = Krause | first6 = D. C. | year = 1994 | title = ''Mycoplasma pneumoniae'' protein P30 is required for cytadherence and associated with proper cell development | url = | journal = J. Bacteriol | volume = 181 | issue = | pages = 1079–1087 | doi = 10.1128/CMR.17.4.697-728.2004 }}</ref> | ||
*The absence of a [[peptidoglycan cell wall]] results in resistance to many [[Antibacterial|antibacterial agents]]. The persistence of ''M. pneumoniae'' infections even after treatment is associated with its ability to mimic [[host cell]] surface composition. | *The absence of a [[peptidoglycan cell wall]] results in resistance to many [[Antibacterial|antibacterial agents]]. The persistence of ''M. pneumoniae'' infections even after treatment is associated with its ability to mimic [[host cell]] surface composition. | ||
*On Gram-stain, ''Mycoplasma'' stains pink, i.e. it is Gram-negative by staining. However, it is structurally different from other Gram-negative organisms because it lacks a cell wall. | *On Gram-stain, ''Mycoplasma'' stains pink, i.e. it is Gram-negative by staining. However, it is structurally different from other Gram-negative organisms because it lacks a cell wall. | ||
== Genomics== | == Genomics== | ||
*[[Sequencing]] of the ''M. pneumoniae'' genome in 1996 revealed it is 816,394 bp (approximately 800 kb) in size. | *[[Sequencing]] of the ''M. pneumoniae'' genome in 1996 revealed it is 816,394 bp (approximately 800 kb) in size. The genome contains 687 genes that encode for proteins, of which about 56.6% code for essential metabolic [[enzymes]]; notably those involved in [[glycolysis]] and [[organic acid]] [[fermentation]].<ref name="Romero-Arroyo">{{cite journal | last1 = Romero-Arroyo | first1 = C. E. | last2 = Jordan | first2 = J. | last3 = Peacock | first3 = S. J. | last4 = Willby | first4 = M. J. | last5 = Farmer | first5 = M. A. | last6 = Krause | first6 = D. C. | year = 1994 | title = ''Mycoplasma pneumoniae'' protein P30 is required for cytadherence and associated with proper cell development | url = | journal = J. Bacteriol | volume = 181 | issue = | pages = 1079–1087 | doi = 10.1128/CMR.17.4.697-728.2004 }}</ref><ref name="Wodke">{{cite journal | last1 = Wodke | first1 = J. A. H. | last2 = Puchałka | first2 = J. | last3 = Lluch-Senar | first3 = M. | last4 = Marcos | first4 = J. | last5 = Yus | first5 = E. | last6 = Godinho | first6 = M. | last7 = Gutiérrez-Gallego | first7 = R. | last8 = Serrano | first8 = L. | last9 = Klipp | first9 = E. | last10 = Maier | first10 = T. | title = Dissecting the energy metabolism in ''Mycoplasma pneumoniae'' through genome-scale metabolic modeling | url = | journal = Mol. Syst. Biol | volume = 2010 | issue = | page = 9 | doi = 10.1038/msb.2013.6 }}</ref> | ||
*''M. pneumoniae'' is consequently very susceptible to loss of [[Enzymatic activity|enzymatic function]] by [[gene mutation]]s, as the only buffering systems against functional loss by point mutations are for maintenance of the [[pentose phosphate pathway]] and [[nucleotide]] metabolism.<ref name="Wodke">{{cite journal | last1 = Wodke | first1 = J. A. H. | last2 = Puchałka | first2 = J. | last3 = Lluch-Senar | first3 = M. | last4 = Marcos | first4 = J. | last5 = Yus | first5 = E. | last6 = Godinho | first6 = M. | last7 = Gutiérrez-Gallego | first7 = R. | last8 = Serrano | first8 = L. | last9 = Klipp | first9 = E. | last10 = Maier | first10 = T. | title = Dissecting the energy metabolism in ''Mycoplasma pneumoniae'' through genome-scale metabolic modeling | url = | journal = Mol. Syst. Biol | volume = 2010 | issue = | page = 9 | doi = 10.1038/msb.2013.6 }}</ref> | *''M. pneumoniae'' is consequently very susceptible to loss of [[Enzymatic activity|enzymatic function]] by [[gene mutation]]s, as the only buffering systems against functional loss by point mutations are for maintenance of the [[pentose phosphate pathway]] and [[nucleotide]] metabolism.<ref name="Wodke">{{cite journal | last1 = Wodke | first1 = J. A. H. | last2 = Puchałka | first2 = J. | last3 = Lluch-Senar | first3 = M. | last4 = Marcos | first4 = J. | last5 = Yus | first5 = E. | last6 = Godinho | first6 = M. | last7 = Gutiérrez-Gallego | first7 = R. | last8 = Serrano | first8 = L. | last9 = Klipp | first9 = E. | last10 = Maier | first10 = T. | title = Dissecting the energy metabolism in ''Mycoplasma pneumoniae'' through genome-scale metabolic modeling | url = | journal = Mol. Syst. Biol | volume = 2010 | issue = | page = 9 | doi = 10.1038/msb.2013.6 }}</ref> | ||
*Loss of function in other pathways is suggested to be compensated by host cell metabolism.<ref name="Wodke">{{cite journal | last1 = Wodke | first1 = J. A. H. | last2 = Puchałka | first2 = J. | last3 = Lluch-Senar | first3 = M. | last4 = Marcos | first4 = J. | last5 = Yus | first5 = E. | last6 = Godinho | first6 = M. | last7 = Gutiérrez-Gallego | first7 = R. | last8 = Serrano | first8 = L. | last9 = Klipp | first9 = E. | last10 = Maier | first10 = T. | title = Dissecting the energy metabolism in ''Mycoplasma pneumoniae'' through genome-scale metabolic modeling | url = | journal = Mol. Syst. Biol | volume = 2010 | issue = | page = 9 | doi = 10.1038/msb.2013.6 }}</ref> | *Loss of function in other pathways is suggested to be compensated by host cell metabolism.<ref name="Wodke">{{cite journal | last1 = Wodke | first1 = J. A. H. | last2 = Puchałka | first2 = J. | last3 = Lluch-Senar | first3 = M. | last4 = Marcos | first4 = J. | last5 = Yus | first5 = E. | last6 = Godinho | first6 = M. | last7 = Gutiérrez-Gallego | first7 = R. | last8 = Serrano | first8 = L. | last9 = Klipp | first9 = E. | last10 = Maier | first10 = T. | title = Dissecting the energy metabolism in ''Mycoplasma pneumoniae'' through genome-scale metabolic modeling | url = | journal = Mol. Syst. Biol | volume = 2010 | issue = | page = 9 | doi = 10.1038/msb.2013.6 }}</ref> | ||
*In addition to the potential for loss of pathway function, the reduced genome of ''M. pneumoniae'' outright lacks a number of pathways, including the [[TCA cycle]], [[Electron transport chain|respiratory electron transport chain]], and [[biosynthesis]] pathways for [[amino acids]], [[fatty acids]], [[cholesterol]] and [[purines]] and [[pyrimidines]]. | *In addition to the potential for loss of pathway function, the reduced genome of ''M. pneumoniae'' outright lacks a number of pathways, including the [[TCA cycle]], [[Electron transport chain|respiratory electron transport chain]], and [[biosynthesis]] pathways for [[amino acids]], [[fatty acids]], [[cholesterol]] and [[purines]] and [[pyrimidines]].<ref name="Romero-Arroyo">{{cite journal | last1 = Romero-Arroyo | first1 = C. E. | last2 = Jordan | first2 = J. | last3 = Peacock | first3 = S. J. | last4 = Willby | first4 = M. J. | last5 = Farmer | first5 = M. A. | last6 = Krause | first6 = D. C. | year = 1994 | title = ''Mycoplasma pneumoniae'' protein P30 is required for cytadherence and associated with proper cell development | url = | journal = J. Bacteriol | volume = 181 | issue = | pages = 1079–1087 | doi = 10.1128/CMR.17.4.697-728.2004 }}</ref><ref name="Wodke">{{cite journal | last1 = Wodke | first1 = J. A. H. | last2 = Puchałka | first2 = J. | last3 = Lluch-Senar | first3 = M. | last4 = Marcos | first4 = J. | last5 = Yus | first5 = E. | last6 = Godinho | first6 = M. | last7 = Gutiérrez-Gallego | first7 = R. | last8 = Serrano | first8 = L. | last9 = Klipp | first9 = E. | last10 = Maier | first10 = T. | title = Dissecting the energy metabolism in ''Mycoplasma pneumoniae'' through genome-scale metabolic modeling | url = | journal = Mol. Syst. Biol | volume = 2010 | issue = | page = 9 | doi = 10.1038/msb.2013.6 }}</ref> | ||
*These limitations make ''M. pneumoniae'' dependent upon import systems to acquire essential building blocks from their host or the environment that cannot be obtained through [[Glycolytic Pathways|glycolytic pathways]].<ref name="Romero-Arroyo">{{cite journal | last1 = Romero-Arroyo | first1 = C. E. | last2 = Jordan | first2 = J. | last3 = Peacock | first3 = S. J. | last4 = Willby | first4 = M. J. | last5 = Farmer | first5 = M. A. | last6 = Krause | first6 = D. C. | year = 1994 | title = ''Mycoplasma pneumoniae'' protein P30 is required for cytadherence and associated with proper cell development | url = | journal = J. Bacteriol | volume = 181 | issue = | pages = 1079–1087 | doi = 10.1128/CMR.17.4.697-728.2004 }}</ref><ref name="Wodke">{{cite journal | last1 = Wodke | first1 = J. A. H. | last2 = Puchałka | first2 = J. | last3 = Lluch-Senar | first3 = M. | last4 = Marcos | first4 = J. | last5 = Yus | first5 = E. | last6 = Godinho | first6 = M. | last7 = Gutiérrez-Gallego | first7 = R. | last8 = Serrano | first8 = L. | last9 = Klipp | first9 = E. | last10 = Maier | first10 = T. | title = Dissecting the energy metabolism in ''Mycoplasma pneumoniae'' through genome-scale metabolic modeling | url = | journal = Mol. Syst. Biol | volume = 2010 | issue = | page = 9 | doi = 10.1038/msb.2013.6 }}</ref> | *These limitations make ''M. pneumoniae'' dependent upon import systems to acquire essential building blocks from their host or the environment that cannot be obtained through [[Glycolytic Pathways|glycolytic pathways]].<ref name="Romero-Arroyo">{{cite journal | last1 = Romero-Arroyo | first1 = C. E. | last2 = Jordan | first2 = J. | last3 = Peacock | first3 = S. J. | last4 = Willby | first4 = M. J. | last5 = Farmer | first5 = M. A. | last6 = Krause | first6 = D. C. | year = 1994 | title = ''Mycoplasma pneumoniae'' protein P30 is required for cytadherence and associated with proper cell development | url = | journal = J. Bacteriol | volume = 181 | issue = | pages = 1079–1087 | doi = 10.1128/CMR.17.4.697-728.2004 }}</ref><ref name="Wodke">{{cite journal | last1 = Wodke | first1 = J. A. H. | last2 = Puchałka | first2 = J. | last3 = Lluch-Senar | first3 = M. | last4 = Marcos | first4 = J. | last5 = Yus | first5 = E. | last6 = Godinho | first6 = M. | last7 = Gutiérrez-Gallego | first7 = R. | last8 = Serrano | first8 = L. | last9 = Klipp | first9 = E. | last10 = Maier | first10 = T. | title = Dissecting the energy metabolism in ''Mycoplasma pneumoniae'' through genome-scale metabolic modeling | url = | journal = Mol. Syst. Biol | volume = 2010 | issue = | page = 9 | doi = 10.1038/msb.2013.6 }}</ref> | ||
*Along with energy costly protein and [[RNA]] production, a large portion of energy metabolism is exerted to maintain [[proton gradient]]s (up to 80%) due to the high [[Surface-area-to-volume ratio|surface area to volume ratio]] of ''M. pneumoniae'' cells. Only 12 – 29% of energy metabolism is directed at [[cell growth]], which is unusually low for bacterial cells, and is thought to be an [[adaptation]] of its parasitic lifestyle.<ref name="Wodke" /> Unlike other bacteria, ''M. pneumoniae'' uses the [[codon]] UGA to code for [[tryptophan]] rather than using it as a stop codon. | *Along with energy costly protein and [[RNA]] production, a large portion of energy metabolism is exerted to maintain [[proton gradient]]s (up to 80%) due to the high [[Surface-area-to-volume ratio|surface area to volume ratio]] of ''M. pneumoniae'' cells. Only 12 – 29% of energy metabolism is directed at [[cell growth]], which is unusually low for bacterial cells, and is thought to be an [[adaptation]] of its parasitic lifestyle.<ref name="Wodke" /> Unlike other bacteria, ''M. pneumoniae'' uses the [[codon]] UGA to code for [[tryptophan]] rather than using it as a stop codon. | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Latest revision as of 01:25, 8 February 2016
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| Mycoplasma pneumoniae Somerson et al., 1963 |
This page is about microbiologic aspects of the organism(s). For clinical aspects of the disease, see Mycoplasma pneumonia.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Mycoplasma pneumonia is caused by Mycoplasma pneumoniae, a very small bacterium that lacks cell wall and periplasmic space. On Gram-stain, Mycoplasma stains pink, i.e. it is Gram-negative by staining. However, it is structurally different from other Gram-negative organisms because it lacks a cell wall.
Clinical Significance
M. pneumoniae is the bacterium responsible for Mycoplasma pneumonia, an atypical pneumonia common in children and young adults.
Taxonomy
- Bacteria; Firmicutes; Mollicutes; Mycoplasmatales; Mycoplasmataceae; Mycoplasma pneumoniae
- The term Mycoplasma (“mykes”, meaning fungus and “plasma”, meaning formed) is derived from the fungal-like growth of some mycoplasma species.[1]
Cell Biology
- Mycoplasma is the smallest self-replicating organism. They are bacteria that lack a cell wall and periplasmic space, have reduced genomes, and limited metabolic activity.[2][3]
- Mycoplasma pneumoniae cells have an elongated shape that is approximately 1-2 µm in length and 0.1–0.2 µm in width.
- The extremely small cell size means they are incapable of being examined by light microscopy; a stereomicroscope is required for viewing the morphology of M. pneumoniae colonies, which are usually less than 100 µm in length. The inability to synthesize a peptidoglycan cell wall is due to the absence of genes encoding its formation and results in an increased importance in maintenance of osmotic stability to avoid desiccation. The lack of a cell wall also calls for increased support of the cell membrane, which includes a rigid cytoskeleton composed of an intricate protein network and, potentially, an extracellular capsule to facilitate adherence to the host cell.[1]
- M. pneumoniae are the only bacterial cells that possess cholesterol in their cell membrane (obtained from the host) and possess more genes that encode for membrane lipoprotein variations than other mycoplasmas, which are thought to be associated with its parasitic lifestyle. M. pneumoniae cells also possess an attachment organelle, which is used in the gliding motility of the organism by an unknown mechanism.[2]
- The absence of a peptidoglycan cell wall results in resistance to many antibacterial agents. The persistence of M. pneumoniae infections even after treatment is associated with its ability to mimic host cell surface composition.
- On Gram-stain, Mycoplasma stains pink, i.e. it is Gram-negative by staining. However, it is structurally different from other Gram-negative organisms because it lacks a cell wall.
Genomics
- Sequencing of the M. pneumoniae genome in 1996 revealed it is 816,394 bp (approximately 800 kb) in size. The genome contains 687 genes that encode for proteins, of which about 56.6% code for essential metabolic enzymes; notably those involved in glycolysis and organic acid fermentation.[2][4]
- M. pneumoniae is consequently very susceptible to loss of enzymatic function by gene mutations, as the only buffering systems against functional loss by point mutations are for maintenance of the pentose phosphate pathway and nucleotide metabolism.[4]
- Loss of function in other pathways is suggested to be compensated by host cell metabolism.[4]
- In addition to the potential for loss of pathway function, the reduced genome of M. pneumoniae outright lacks a number of pathways, including the TCA cycle, respiratory electron transport chain, and biosynthesis pathways for amino acids, fatty acids, cholesterol and purines and pyrimidines.[2][4]
- These limitations make M. pneumoniae dependent upon import systems to acquire essential building blocks from their host or the environment that cannot be obtained through glycolytic pathways.[2][4]
- Along with energy costly protein and RNA production, a large portion of energy metabolism is exerted to maintain proton gradients (up to 80%) due to the high surface area to volume ratio of M. pneumoniae cells. Only 12 – 29% of energy metabolism is directed at cell growth, which is unusually low for bacterial cells, and is thought to be an adaptation of its parasitic lifestyle.[4] Unlike other bacteria, M. pneumoniae uses the codon UGA to code for tryptophan rather than using it as a stop codon.
References
- ↑ 1.0 1.1 Ken; Waites, B; Deborah, F. Talkington (2004). "Mycoplasma pneumoniae and Its Role as a Human Pathogen". Clin. Microbiol. Rev. 17 (4): 697–728. doi:10.1128/CMR.17.4.697-728.2004.
- ↑ 2.0 2.1 2.2 2.3 2.4 Romero-Arroyo, C. E.; Jordan, J.; Peacock, S. J.; Willby, M. J.; Farmer, M. A.; Krause, D. C. (1994). "Mycoplasma pneumoniae protein P30 is required for cytadherence and associated with proper cell development". J. Bacteriol. 181: 1079–1087. doi:10.1128/CMR.17.4.697-728.2004.
- ↑ S. Dallo, and J. Baseman "Intracellular DNA replication and long-term survival of pathogenic mycoplasmas" Microb. Pathog. 2000; 29, 301–309. Template:10.1006/mpat.2000.0395
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 Wodke, J. A. H.; Puchałka, J.; Lluch-Senar, M.; Marcos, J.; Yus, E.; Godinho, M.; Gutiérrez-Gallego, R.; Serrano, L.; Klipp, E.; Maier, T. "Dissecting the energy metabolism in Mycoplasma pneumoniae through genome-scale metabolic modeling". Mol. Syst. Biol. 2010: 9. doi:10.1038/msb.2013.6.