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Toxoplasma's Taste for Exotic Fat.

Roberts RG - PLoS Biol. (2015)

Bottom Line: A new study reveals that an exotic lipid, phosphatidylthreonine, makes up a substantial proportion of the membrane of a widespread human parasite and is essential for its virulence.Read the Research Article.

View Article: PubMed Central - PubMed

Affiliation: Public Library of Science, Cambridge, United Kingdom.

ABSTRACT
A new study reveals that an exotic lipid, phosphatidylthreonine, makes up a substantial proportion of the membrane of a widespread human parasite and is essential for its virulence. Read the Research Article.

Show MeSH

Related in: MedlinePlus

Phosphatidylthreonine-mediated control of lytic cycle and virulence in T. gondii.The parental strain of T. gondii expresses PTS, which produces PtdThr. Genetic disruption of PTS results in parasites that are unable to make PtdThr. Lack of PtdThr in the mutant compromises its gliding motility, which blights the sequential events of exit from parasitized cells, and entry into new host cells. Consequently, the PtdThr-deficient strain displays a severely impaired lytic cycle in human cells. Moreover, the mutant is highly attenuated in mice and confers potent immunity against hypervirulent and cyst-forming strains of T. gondii. Image credit: Nishith Gupta.
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pbio.1002289.g001: Phosphatidylthreonine-mediated control of lytic cycle and virulence in T. gondii.The parental strain of T. gondii expresses PTS, which produces PtdThr. Genetic disruption of PTS results in parasites that are unable to make PtdThr. Lack of PtdThr in the mutant compromises its gliding motility, which blights the sequential events of exit from parasitized cells, and entry into new host cells. Consequently, the PtdThr-deficient strain displays a severely impaired lytic cycle in human cells. Moreover, the mutant is highly attenuated in mice and confers potent immunity against hypervirulent and cyst-forming strains of T. gondii. Image credit: Nishith Gupta.

Mentions: But does PtdThr matter for Toxo? The authors compared how the PTS mutant and the rescued strain fared in cultured human fibroblast host cells. Normally, the Toxo infection results in clear patches of host cell destruction called plaques, which in essence represent successive lytic cycles. Mutating the PTS gene dramatically reduced the size and number of plaques, while reinstating the functional enzyme rescued this effect. To find out why Toxo needed the exotic lipid, the authors dissected the mutant’s poor growth phenotype. Unexpectedly, the authors discovered that the parasite replication was normal; however, the exit from host cells was impaired, and invasion of new host cells was also compromised (Fig 1). Consistently, calcium-regulated gliding movement of the parasite that is needed for both entry and exit was halved. Because PtdThr’s close cousin PtdSer has been described to regulate calcium storage and signaling, the authors speculate that Toxo may have evolved PtdThr as a specialized variant of PtdSer to modulate calcium during its entry and exit to and from host cells.


Toxoplasma's Taste for Exotic Fat.

Roberts RG - PLoS Biol. (2015)

Phosphatidylthreonine-mediated control of lytic cycle and virulence in T. gondii.The parental strain of T. gondii expresses PTS, which produces PtdThr. Genetic disruption of PTS results in parasites that are unable to make PtdThr. Lack of PtdThr in the mutant compromises its gliding motility, which blights the sequential events of exit from parasitized cells, and entry into new host cells. Consequently, the PtdThr-deficient strain displays a severely impaired lytic cycle in human cells. Moreover, the mutant is highly attenuated in mice and confers potent immunity against hypervirulent and cyst-forming strains of T. gondii. Image credit: Nishith Gupta.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4643891&req=5

pbio.1002289.g001: Phosphatidylthreonine-mediated control of lytic cycle and virulence in T. gondii.The parental strain of T. gondii expresses PTS, which produces PtdThr. Genetic disruption of PTS results in parasites that are unable to make PtdThr. Lack of PtdThr in the mutant compromises its gliding motility, which blights the sequential events of exit from parasitized cells, and entry into new host cells. Consequently, the PtdThr-deficient strain displays a severely impaired lytic cycle in human cells. Moreover, the mutant is highly attenuated in mice and confers potent immunity against hypervirulent and cyst-forming strains of T. gondii. Image credit: Nishith Gupta.
Mentions: But does PtdThr matter for Toxo? The authors compared how the PTS mutant and the rescued strain fared in cultured human fibroblast host cells. Normally, the Toxo infection results in clear patches of host cell destruction called plaques, which in essence represent successive lytic cycles. Mutating the PTS gene dramatically reduced the size and number of plaques, while reinstating the functional enzyme rescued this effect. To find out why Toxo needed the exotic lipid, the authors dissected the mutant’s poor growth phenotype. Unexpectedly, the authors discovered that the parasite replication was normal; however, the exit from host cells was impaired, and invasion of new host cells was also compromised (Fig 1). Consistently, calcium-regulated gliding movement of the parasite that is needed for both entry and exit was halved. Because PtdThr’s close cousin PtdSer has been described to regulate calcium storage and signaling, the authors speculate that Toxo may have evolved PtdThr as a specialized variant of PtdSer to modulate calcium during its entry and exit to and from host cells.

Bottom Line: A new study reveals that an exotic lipid, phosphatidylthreonine, makes up a substantial proportion of the membrane of a widespread human parasite and is essential for its virulence.Read the Research Article.

View Article: PubMed Central - PubMed

Affiliation: Public Library of Science, Cambridge, United Kingdom.

ABSTRACT
A new study reveals that an exotic lipid, phosphatidylthreonine, makes up a substantial proportion of the membrane of a widespread human parasite and is essential for its virulence. Read the Research Article.

Show MeSH
Related in: MedlinePlus