What's new for 'Trypanosomatids' in PubMed

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Sent on Saturday, 2011 Oct 08
Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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PubMed Results

Items 1 - 3 of 3

1.	PLoS Negl Trop Dis. 2011 Sep;5(9):e1227. Epub 2011 Sep 27. Visceral leishmaniasis and arsenic: an ancient poison contributing to antimonial treatment failure in the Indian subcontinent? Perry MR, Wyllie S, Prajapati VK, Feldmann J, Sundar S, Boelaert M, Fairlamb AH. Source Division of Biological Chemistry and Drug Discovery, College of Life Sciences, University of Dundee, Dundee, Scotland, United Kingdom.
	PMID: 21980542 [PubMed - in process]

2.	PLoS One. 2011;6(9):e25313. Epub 2011 Sep 28. Identification of Trypanosoma brucei RMI1/BLAP75 Homologue and Its Roles in Antigenic Variation. Kim HS, Cross GA. Source Laboratory of Molecular Parasitology, The Rockefeller University, New York, New York, United States of America. Abstract At any time, each cell of the protozoan parasite Trypanosoma brucei expresses a single species of its major antigenic protein, the variant surface glycoprotein (VSG), from a repertoire of >2,000 VSG genes and pseudogenes. The potential to express different VSGs by transcription and recombination allows the parasite to escape the antibody-mediated host immune response, a mechanism known as antigenic variation. The active VSG is transcribed from a sub-telomeric polycistronic unit called the expression site (ES), whose promoter is 40-60 kb upstream of the VSG. While the mechanisms that initiate recombination remain unclear, the resolution phase of these reactions results in the recombinational replacement of the expressed VSG with a donor from one of three distinct chromosomal locations; sub-telomeric loci on the 11 essential chromosomes, on minichromosomes, or at telomere-distal loci. Depending on the type of recombinational replacement (single or double crossover, duplicative gene conversion, etc), several DNA-repair pathways have been thought to play a role. Here we show that VSG recombination relies on at least two distinct DNA-repair pathways, one of which requires RMI1-TOPO3α to suppress recombination and one that is dependent on RAD51 and RMI1. These genetic interactions suggest that both RAD51-dependent and RAD51-independent recombination pathways operate in antigenic switching and that trypanosomes differentially utilize recombination factors for VSG switching, depending on currently unknown parameters within the ES.
	PMID: 21980422 [PubMed - in process]

3.	Exp Parasitol. 2011 Sep 29. [Epub ahead of print] Expression of a Leishmaniadonovani nucleotide sugar transporter in Leishmaniamajor enhances survival in visceral organs. Zhang WW, Chan KF, Song Z, Matlashewski G. Source Department of Microbiology and Immunology, McGill University, 3775 University Street, Montreal, Canada H3A 2B4. Abstract Leishmania donovani and Leishmaniainfantum infections cause fatal visceral leishmaniasis, and Leishmaniamajor causes self healing cutaneous lesions. It is poorly understood what genetic differences between these Leishmania species are responsible for the different pathologies of infection. To investigate whether L.donovani species-specific genes are involved in visceral Leishmania infection, we have examined a L.donovani species-specific gene Ld1590 (ortholog of LinJ15_V3.0900) that is a pseudogene in L.major. We have previously shown that transgenic expression of L.donovani Ld1590 in L.major significantly increased the liver and spleen parasite burdens in infected BALB/c mice. In this study we report that Ld1590 potentially encodes a nucleotide sugar transporter (NST) which localizes in the L.donovani Golgi apparatus. Surprisingly, although transgenic expression of the Ld1590 NST increased L.major survival in visceral organs, deletion of Ld1590 NST in L.donovani had no significant effect on L.donovani survival in mice. These observations suggest that loss of the functional Ld1590 gene in L.major may have been associated with reduced virulence in visceral organs in its animal reservoir and could have contributed to L.major's tropism for cutaneous infections. Copyright © 2011. Published by Elsevier Inc.
	PMID: 21978449 [PubMed - as supplied by publisher]