AM055943
Toxoplasma gondii, strain RH, genomic DNA chromosome Ib
gi95007251embAM055943.1[95007251][95007251]
Thursday, November 30, 2006
Wednesday, November 29, 2006
Wednesday, November 15, 2006
ASM: 107th General Meeting May21-25, 2007
The American Society for Microbiology will hold its 107th General Meeting in the Metro Toronto Convention Centre in Toronto, Canada from Monday, May 21 to noon on Friday, May 25, 2007.
Call for Abstracts
The Call for Abstracts is now available for your review and planning. The Abstract Submission Site on the OASIS system for the 107th General Meeting will open on November 14, 2006.
Scientific Program
Key information on the Scientific program may be viewed through this page.
Full details:
http://gm.asm.org/7200.shtm
Call for Abstracts
The Call for Abstracts is now available for your review and planning. The Abstract Submission Site on the OASIS system for the 107th General Meeting will open on November 14, 2006.
Scientific Program
Key information on the Scientific program may be viewed through this page.
Full details:
http://gm.asm.org/7200.shtm
Tuesday, November 14, 2006
Ocular toxoplasmosis
Parasite Immunol. 2006 Dec;28(12):635-42.
Ocular toxoplasmosis: in the storm of the eye.
Jones LA, Alexander J, Roberts CW.
Department of Immunology, Strathclyde Institute for Biomedical Sciences, University of Strathclyde, Glasgow, UK.
Ocular toxoplasmosis (OT) can occur in the children of mothers infected with Toxoplasma gondii during pregnancy. It is not limited to the congenitally infected, but can also occur following adult-acquired infection or as a result of disease reactivation in immune-compromised and pregnant individuals. Many aspects of immune privilege in the eye, including constitutive TGF-beta expression and reduced MHC class 1 expression, would appear at first to favour parasite survival. Conversely, many of the mechanisms that control parasite multiplication in other anatomical sites, such as nitric oxide expression, IFN-gamma and TNF-alpha, are known to disrupt immune privilege and are associated with ocular damage. Taking into account the opposing needs of limiting parasite multiplication and minimizing tissue destruction we review the pathogenesis of OT in the murine model.
Ocular toxoplasmosis: in the storm of the eye.
Jones LA, Alexander J, Roberts CW.
Department of Immunology, Strathclyde Institute for Biomedical Sciences, University of Strathclyde, Glasgow, UK.
Ocular toxoplasmosis (OT) can occur in the children of mothers infected with Toxoplasma gondii during pregnancy. It is not limited to the congenitally infected, but can also occur following adult-acquired infection or as a result of disease reactivation in immune-compromised and pregnant individuals. Many aspects of immune privilege in the eye, including constitutive TGF-beta expression and reduced MHC class 1 expression, would appear at first to favour parasite survival. Conversely, many of the mechanisms that control parasite multiplication in other anatomical sites, such as nitric oxide expression, IFN-gamma and TNF-alpha, are known to disrupt immune privilege and are associated with ocular damage. Taking into account the opposing needs of limiting parasite multiplication and minimizing tissue destruction we review the pathogenesis of OT in the murine model.
ApiDB facilitates apicomplexan bioinformatics
Nucleic Acids Res. 2006 Nov 10; [Epub ahead of print]
ApiDB: integrated resources for the apicomplexan bioinformatics resource center.
Aurrecoechea C, Heiges M, Wang H, Wang Z, Fischer S, Rhodes P, Miller J, Kraemer E, Stoeckert CJ Jr, Roos DS, Kissinger JC.
Center for Tropical and Emerging Global Diseases Athens GA, USA.
ApiDB (http://ApiDB.org) represents a unified entry point for the NIH-funded Apicomplexan Bioinformatics Resource Center (BRC) that integrates numerous database resources and multiple data types. The phylum Apicomplexa comprises numerous veterinary and medically important parasitic protozoa including human pathogenic species of the genera Cryptosporidium, Plasmodium and Toxoplasma. ApiDB serves not only as a database in its own right, but as a single web-based point of entry that unifies access to three major existing individual organism databases (PlasmoDB.org, ToxoDB.org and CryptoDB.org), and integrates these databases with data available from additional sources. Through the ApiDB site, users may pose queries and search all available apicomplexan data and tools, or they may visit individual component organism databases.
[Abstract] [Full Text] [Print PDF] [Screen PDF] [Request Permissions]
ApiDB: integrated resources for the apicomplexan bioinformatics resource center.
Aurrecoechea C, Heiges M, Wang H, Wang Z, Fischer S, Rhodes P, Miller J, Kraemer E, Stoeckert CJ Jr, Roos DS, Kissinger JC.
Center for Tropical and Emerging Global Diseases Athens GA, USA.
ApiDB (http://ApiDB.org) represents a unified entry point for the NIH-funded Apicomplexan Bioinformatics Resource Center (BRC) that integrates numerous database resources and multiple data types. The phylum Apicomplexa comprises numerous veterinary and medically important parasitic protozoa including human pathogenic species of the genera Cryptosporidium, Plasmodium and Toxoplasma. ApiDB serves not only as a database in its own right, but as a single web-based point of entry that unifies access to three major existing individual organism databases (PlasmoDB.org, ToxoDB.org and CryptoDB.org), and integrates these databases with data available from additional sources. Through the ApiDB site, users may pose queries and search all available apicomplexan data and tools, or they may visit individual component organism databases.
[Abstract] [Full Text] [Print PDF] [Screen PDF] [Request Permissions]
Sunday, November 12, 2006
Friday, November 10, 2006
Seeking postdoc position
I am slated to graduate in Spring 07 with a Ph.D in Genetics and am looking for labs that work on gene-regulation in a multi-cellular system, especially host-response to pathogens in terms of modifying gene-regulation in the host.
For more information, please contact...
***************************************************
Nandita Mullapudi
Graduate student
Kissinger lab, Dept. of Genetics, Coverdell Building.
Lab phone: 706-542-6563 Cell phone: 706-254-2444
** we have moved, again!** please note new
Mailing address:
Paul D. Coverdell Center, 500 D.W. Brooks Drive
University of Georgia,
Athens, Georgia 30602
****************************************************
For more information, please contact...
***************************************************
Nandita Mullapudi
Graduate student
Kissinger lab, Dept. of Genetics, Coverdell Building.
Lab phone: 706-542-6563 Cell phone: 706-254-2444
** we have moved, again!** please note new
Mailing address:
Paul D. Coverdell Center, 500 D.W. Brooks Drive
University of Georgia,
Athens, Georgia 30602
****************************************************
The MIC formerly known as H4
Y09782
Toxoplasma gondii MIC5 gene (formerly know as H4) for microneme protein
gi1806540embY09782.1[1806540][1806540]
Toxoplasma gondii MIC5 gene (formerly know as H4) for microneme protein
gi1806540embY09782.1[1806540][1806540]
Thursday, November 09, 2006
Common infection strategies of pathogenic eukaryotes
Nat Rev Microbiol. 2006 Nov 6; [Epub ahead of print]
Common infection strategies of pathogenic eukaryotes.
Haldar K, Kamoun S, Hiller NL, Bhattacharje S, van Ooij C.Departments of Pathology and Microbiology-Immunology, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611, USA.
Pathogenic eukaryotes belong to several distinct phylogenetic lineages and have evolved the ability to colonize a range of hosts, including animals and plants. Pathogenic lifestyles have evolved repeatedly in eukaryotes, indicating that unique molecular processes are involved in host infection. However, evidence is now emerging that divergent eukaryotic pathogens might share common mechanisms of pathogenicity. The results from recent studies demonstrate that Plasmodium falciparum and Phytophthora infestans use equivalent host-targeting signals to deliver virulence adhesins and avirulence gene products into human and plant cells, respectively. Remodelling of host cells by different eukaryotic pathogens might therefore share some common features.
Common infection strategies of pathogenic eukaryotes.
Haldar K, Kamoun S, Hiller NL, Bhattacharje S, van Ooij C.Departments of Pathology and Microbiology-Immunology, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611, USA.
Pathogenic eukaryotes belong to several distinct phylogenetic lineages and have evolved the ability to colonize a range of hosts, including animals and plants. Pathogenic lifestyles have evolved repeatedly in eukaryotes, indicating that unique molecular processes are involved in host infection. However, evidence is now emerging that divergent eukaryotic pathogens might share common mechanisms of pathogenicity. The results from recent studies demonstrate that Plasmodium falciparum and Phytophthora infestans use equivalent host-targeting signals to deliver virulence adhesins and avirulence gene products into human and plant cells, respectively. Remodelling of host cells by different eukaryotic pathogens might therefore share some common features.
Bradyzoites: a stealthy existence in the host cell
Infect Immun. 2006 Nov 6; [Epub ahead of print]
Infection with Toxoplasma bradyzoites has a diminished impact on host transcript levels relative to tachyzoite-infection.
Fouts AE, Boothroyd JC.
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5124, USA.
Toxoplasma gondii, an intracellular pathogen, has the potential to infect nearly every warm-blooded animal but rarely causes morbidity. The ability for the parasite to convert to the bradyzoite stage and live inside slow growing cysts that can go unnoticed by the host immune system allows for parasite persistence for the life of the infected host. This intracellular survival likely necessitates host cell modulation and tachyzoites are known to modify a number of signaling cascades within the host to promote parasite survival. Little is known, however, about how bradyzoites manipulate their host cell. Microarrays were used to profile the host transcriptional changes caused by bradyzoite-infection and compared with those of tachyzoite-infected and uninfected host cells 2 days post-infection in vitro. Infection resulted in chemokine, cytokine, extracellular matrix, and growth factor transcript level changes. A small group of genes were specifically induced by tachyzoite-infection, including CSF2, BCL2A1 and IL24, whereas bradyzoite-infection yielded only about half the changes seen with tachyzoite-infection and those changes that did occur were almost all of lower magnitude than those induced by tachyzoites. These results suggest that bradyzoites lead a more stealthy existence within the infected host cell.
Infection with Toxoplasma bradyzoites has a diminished impact on host transcript levels relative to tachyzoite-infection.
Fouts AE, Boothroyd JC.
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5124, USA.
Toxoplasma gondii, an intracellular pathogen, has the potential to infect nearly every warm-blooded animal but rarely causes morbidity. The ability for the parasite to convert to the bradyzoite stage and live inside slow growing cysts that can go unnoticed by the host immune system allows for parasite persistence for the life of the infected host. This intracellular survival likely necessitates host cell modulation and tachyzoites are known to modify a number of signaling cascades within the host to promote parasite survival. Little is known, however, about how bradyzoites manipulate their host cell. Microarrays were used to profile the host transcriptional changes caused by bradyzoite-infection and compared with those of tachyzoite-infected and uninfected host cells 2 days post-infection in vitro. Infection resulted in chemokine, cytokine, extracellular matrix, and growth factor transcript level changes. A small group of genes were specifically induced by tachyzoite-infection, including CSF2, BCL2A1 and IL24, whereas bradyzoite-infection yielded only about half the changes seen with tachyzoite-infection and those changes that did occur were almost all of lower magnitude than those induced by tachyzoites. These results suggest that bradyzoites lead a more stealthy existence within the infected host cell.
Toxo secretory serine-threonine kinase ROP18
DQ875878
Toxoplasma gondii secretory serine-threonine protein kinase ROP18-III (ROP18) gene, ROP18-III allele, complete cds
gi113473052gbDQ875878.1[113473052][113473052]
Toxoplasma gondii secretory serine-threonine protein kinase ROP18-III (ROP18) gene, ROP18-III allele, complete cds
gi113473052gbDQ875878.1[113473052][113473052]
Wednesday, November 08, 2006
Toxo PP2C targets host cell nucleus
Eukaryot Cell. 2006 Nov 3; [Epub ahead of print]
Toxoplasma gondii Targets a Protein Phosphatase 2C to the Nucleus of Infected Host Cells.
Gilbert LA, Ravindran S, Turetzky JM, Boothroyd JC, Bradley PJ.
Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles CA 90095-1489 USA; Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5124 USA.
Intracellular pathogens have evolved a wide array of mechanisms to invade and co-opt their host cells for intracellular survival. Apicomplexan parasites such as Toxoplasma gondii employ the action of unique secretory organelles named rhoptries for internalization of the parasite and formation of a specialized niche within the host cell. We demonstrate that Toxoplasma gondii also uses secretion from the rhoptries during invasion to deliver a parasite-derived protein phosphatase 2C (PP2C-hn) into the host cell and direct it to the host nucleus. Delivery to the host nucleus does not require completion of invasion as parasites blocked in the initial stages of invasion with cytochalasin D are able to target PP2C-hn to the host nucleus. We have disrupted the gene encoding PP2C-hn and shown that PP2C-hn knockout parasites exhibit a mild growth defect that can be rescued by complementation with the wild-type gene. Delivery of parasite effector proteins via the rhoptries provides a novel mechanism for Toxoplasma to directly access the command center of its host cell during infection by the parasite.
Toxoplasma gondii Targets a Protein Phosphatase 2C to the Nucleus of Infected Host Cells.
Gilbert LA, Ravindran S, Turetzky JM, Boothroyd JC, Bradley PJ.
Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles CA 90095-1489 USA; Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5124 USA.
Intracellular pathogens have evolved a wide array of mechanisms to invade and co-opt their host cells for intracellular survival. Apicomplexan parasites such as Toxoplasma gondii employ the action of unique secretory organelles named rhoptries for internalization of the parasite and formation of a specialized niche within the host cell. We demonstrate that Toxoplasma gondii also uses secretion from the rhoptries during invasion to deliver a parasite-derived protein phosphatase 2C (PP2C-hn) into the host cell and direct it to the host nucleus. Delivery to the host nucleus does not require completion of invasion as parasites blocked in the initial stages of invasion with cytochalasin D are able to target PP2C-hn to the host nucleus. We have disrupted the gene encoding PP2C-hn and shown that PP2C-hn knockout parasites exhibit a mild growth defect that can be rescued by complementation with the wild-type gene. Delivery of parasite effector proteins via the rhoptries provides a novel mechanism for Toxoplasma to directly access the command center of its host cell during infection by the parasite.
Tuesday, November 07, 2006
Toxo and schizophrenia
Torrey EF, Bartko JJ, Lun ZR, Yolken RH.
Antibodies to Toxoplasma gondii in Patients With Schizophrenia: A Meta-Analysis.
Schizophr Bull. 2006 Nov 3; [Epub ahead of print] PMID: 17085743
...Toxoplasma is in some way associated with a large number of cases of schizophrenia. If an etiological association can be proven, it would have implications for the design of measures for the prevention and treatment of this disease.
Antibodies to Toxoplasma gondii in Patients With Schizophrenia: A Meta-Analysis.
Schizophr Bull. 2006 Nov 3; [Epub ahead of print] PMID: 17085743
...Toxoplasma is in some way associated with a large number of cases of schizophrenia. If an etiological association can be proven, it would have implications for the design of measures for the prevention and treatment of this disease.
Monday, November 06, 2006
Toxo aspartic proteases - new in GenBank
1:
EF031151
Toxoplasma gondii aspartic protease 6 (ASP6) mRNA, complete cds
gi116878167gbEF031151.1[116878167][116878167]
2:
EF031152
Toxoplasma gondii aspartic protease 7 (ASP7) mRNA, complete cds
gi116878165gbEF031152.1[116878165][116878165]
3:
EF031150
Toxoplasma gondii aspartic protease 5 (ASP5) mRNA, complete cds
gi116878163gbEF031150.1[116878163][116878163]
4:
EF031149
Toxoplasma gondii aspartic protease 4 (ASP4) mRNA, complete cds
gi116878161gbEF031149.1[116878161][116878161]
Sunday, November 05, 2006
Welcome to the Anti-Toxo!
The Anti-Toxo is a blog dedicated to the nefarious protozoan pathogen Toxoplasma gondii. This single-celled microbe infects nucleated cells of warm-blooded vertebrates. In humans, infection may cause congenital birth defects or lead to serious disease (toxoplasmosis) in AIDS or other immunocompromised patients. Toxoplasma, or Toxo for short, is a permanent infection for which there is no known cure. While the acute phase of the infection is controlled by a normal healthy immune response, this does not eradicate the infection. Rather, Toxo stays in the bodily tissues (including the heart and brain) as a cyst that can be reactivated during times of immunological suppression. Consequently, tens of millions of people are unwittingly walking around with this parasite in their heads!
Toxo infection is acquired from handling cats (the definitive host), ingesting contaminated food/water products, or contaminated soil. For more info, go here.
The Anti-Toxo is designed to be a “one-stop” site where researchers can grab the latest news and reports concerning this and related parasites (such as Plasmodium (malaria) or Cryptosporidium). If you have news you wish to share, please contact us. In addition, we would encourage the posting of job opportunities or meeting announcements related to Toxo research.
The blog is moderated by Dr. Bill Sullivan at the Indiana University School of Medicine (IUSM). Contact: wjsulliv@iupui.edu.
www.sullivanlab.com
Toxo infection is acquired from handling cats (the definitive host), ingesting contaminated food/water products, or contaminated soil. For more info, go here.
The Anti-Toxo is designed to be a “one-stop” site where researchers can grab the latest news and reports concerning this and related parasites (such as Plasmodium (malaria) or Cryptosporidium). If you have news you wish to share, please contact us. In addition, we would encourage the posting of job opportunities or meeting announcements related to Toxo research.
The blog is moderated by Dr. Bill Sullivan at the Indiana University School of Medicine (IUSM). Contact: wjsulliv@iupui.edu.
www.sullivanlab.com
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