What's new for 'Trypanosomatids' in PubMed

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Sent on Thursday, 2012 May 31
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 - 6 of 6

1.	Open Biol. 2012 Feb;2(2):110037. A modular and optimized single marker system for generating Trypanosoma brucei cell lines expressing T7 RNA polymerase and the tetracycline repressor. Poon SK, Peacock L, Gibson W, Gull K, Kelly S. Source Sir William Dunn School of Pathology , University of Oxford , South Parks Road, Oxford OX1 3RE , UK. Abstract Here, we present a simple modular extendable vector system for introducing the T7 RNA polymerase and tetracycline repressor genes into Trypanosoma brucei. This novel system exploits developments in our understanding of gene expression and genome organization to produce a streamlined plasmid optimized for high levels of expression of the introduced transgenes. We demonstrate the utility of this novel system in bloodstream and procyclic forms of Trypanosoma brucei, including the genome strain TREU927/4. We validate these cell lines using a variety of inducible experiments that recapture previously published lethal and non-lethal phenotypes. We further demonstrate the utility of the single marker (SmOx) TREU927/4 cell line for in vivo experiments in the tsetse fly and provide a set of plasmids that enable both whole-fly and salivary gland-specific inducible expression of transgenes.
	PMID: 22645659 [PubMed - in process]

2.	Front Plant Sci. 2012;3:26. Epub 2012 Feb 7. Biochemical and Molecular-Genetic Characterization of SFD1's Involvement in Lipid Metabolism and Defense Signaling. Lorenc-Kukula K, Chaturvedi R, Roth M, Welti R, Shah J. Source Department of Biological Sciences and Center for Plant Lipid Research, University of North Texas Denton, TX, USA. Abstract The Arabidopsis thaliana SFD1 (suppressor of fatty acid desaturase deficiency1) gene (also known as GLY1) is required for accumulation of 34:6 (i.e., 18:3-16:3) monogalactosyldiacylglycerol (MGDG) and for the activation of systemic acquired resistance (SAR), an inducible defense mechanism that confers resistance against a broad spectrum of pathogens. SFD1, which has been suggested to be involved in lipid-based signaling in SAR, contains a putative chloroplast transit peptide and has glycerol-3-phosphate synthesizing dihydroxyacetone phosphate (DHAP) reductase (also referred as glycerol-3-phosphate dehydrogenase) activity. The goals of this study were to determine if the DHAP reductase activity and chloroplast localization are required for SFD1's involvement in galactolipid metabolism and SAR signaling. The crystal structure of a Leishmania mexicana glycerol-3-phosphate dehydrogenase was used to model SFD1 structure and identify Lys194, Lys279, and Asp332 as potential catalytic site residues in SFD1. Mutational analysis of SFD1 confirmed that Lys194, Lys279, and Asp332 are critical for SFD1's DHAP reductase activity, and its involvement in SAR. SFD1 proteins with these residues individually substituted by Ala lacked DHAP reductase activity and were unable to complement the SAR defect of the sfd1 mutant. The SFD1-Ala279 protein was also unable to restore 34:6-MGDG content when expressed in the sfd1 mutant. In vivo imaging of a green fluorescent protein-tagged SFD1 protein demonstrated that SFD1 is targeted to the chloroplast. The N-terminal 43 amino acids, which are required for proper targeting of SFD1 to the chloroplast, are also required for SFD1's function in lipid metabolism and SAR. Taken together, these results demonstrate that SFD1's DHAP reductase activity is required in the chloroplast for lipid metabolism and defense signaling.
	PMID: 22645576 [PubMed - in process]

3.	J Biol Chem. 2012 May 29. [Epub ahead of print] Reactive oxygen species-mediated immunity against Leishmania mexicana and Serratia marcescens in the phlebotomine sand fly Lutzomyia longipalpis. Diaz-Albiter H, Sant' Anna MR, Genta FA, Dillon RJ. Source Liverpool School of Tropical Medicine, United Kingdom; Abstract Phlebotomine sand flies are the vectors of medically important Leishmania. The Leishmania protozoa reside in the sand fly gut but the nature of the immune response to the presence of Leishmania is unknown. Reactive Oxygen Species (ROS) are a major component of insect innate immune pathways regulating gut-microbe homeostasis. Here we show that the concentration of ROS increased in sand fly midguts after they fed on the insect pathogen Serratia marcescens but not after feeding on the Leishmania that uses the sand fly as a vector. Moreover the Leishmania is sensitive to ROS either by oral administration of ROS to the infected fly or by silencing a gene that expresses a sand fly ROSscavenging enzyme. Finally the treatment of sand flies with an exogenous ROS-scavenger (uric acid) altered the gut microbial homeostasis, led to an increased commensal gut microbiota and reduced insect survival after oral infection with S. marcescens. Our study demonstrates a differential response of the sand fly ROS system to gut microbiota, an insect pathogen and the Leishmania that utilise the sand fly as a vehicle for transmission between mammalian hosts.
	PMID: 22645126 [PubMed - as supplied by publisher]

4.	Am J Trop Med Hyg. 2012 Apr;86(4):677-82. House infestation dynamics and feeding sources of Triatoma dimidiata in central Veracruz, Mexico. Torres-Montero J, López-Monteon A, Dumonteil E, Ramos-Ligonio A. Source LADISER Inmunología y Biología Molecular, Facultad de Ciencias Químicas, Universidad Veracruzana, Orizaba, Mexico. jetorres@uv.mx Abstract Chagas disease is endemic in the state of Veracruz, Mexico, and we investigated here the dynamics of house infestation by Chagas disease vectors to understand disease transmission and design effective control interventions. Bug collections in 42 rural villages confirmed the widespread distribution of Triatoma dimidiata in central Veracruz. Unexpectedly, collection data further indicated a clear pattern of seasonal infestation by mostly adult bugs. Analysis of feeding sources with a polymerase chain reaction-heteroduplex assay indicated a frequent feeding on humans, in agreement with the high seroprevalence previously observed. Feeding sources also confirmed a significant dispersal of bugs between habitats. High dispersal capabilities and seasonal infestation may thus be a shared characteristic of several of the T. dimidiata sibling species from this complex. It would thus be critical to adapt vector control interventions to this behavior to improve their efficacy and sustainability, as the control of T. dimidiata has been notoriously challenging.
	PMID: 22492153 [PubMed - indexed for MEDLINE]
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5.	Mol Biochem Parasitol. 2012 Mar-Apr;182(1-2):62-74. Epub 2011 Dec 30. Molecular and functional characterization of the ceramide synthase from Trypanosoma cruzi. Figueiredo JM, Rodrigues DC, Silva RC, Koeller CM, Jiang JC, Jazwinski SM, Previato JO, Mendonça-Previato L, Urményi TP, Heise N. Source Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Centro de Ciências da Saúde Bloco G-019, Av. Carlos Chagas Filho 373, Cidade Universitária, Ilha do Fundão, Rio de Janeiro, RJ 21941-902, Brazil. Abstract In this study, we characterized ceramide synthase (CerS) of the protozoan parasite Trypanosoma cruzi at the molecular and functional levels. TcCerS activity was detected initially in a cell-free system using the microsomal fraction of epimastigote forms of T. cruzi, [(3)H]dihydrosphingosine or [(3)H]sphingosine, and fatty acids or acyl-CoA derivatives as acceptor or donor substrates, respectively. TcCerS utilizes both sphingoid long-chain bases, and its activity is exclusively dependent on acyl-CoAs, with palmitoyl-CoA being preferred. In addition, Fumonisin B(1), a broad and well-known acyl-CoA-dependent CerS inhibitor, blocked the parasite's CerS activity. However, unlike observations in fungi, the CerS inhibitors Australifungin and Fumonisin B(1) did not affect the proliferation of epimastigotes in culture, even after exposure to high concentrations or after extended periods of treatment. A search of the parasite genome with the conserved Lag1 motif from Lag1p, the yeast acyl-CoA-dependent CerS, identified a T. cruzi candidate gene (TcCERS1) that putatively encodes the parasite's CerS activity. The TcCERS1 gene was able to functionally complement the lethality of a lag1Δ lac1Δ double deletion yeast mutant in which the acyl-CoA-dependent CerS is not detectable. The complemented strain was capable of synthesizing normal inositol-containing sphingolipids and is 10 times more sensitive to Fumonisin B(1) than the parental strain. © 2011 Elsevier B.V. All rights reserved.
	PMID: 22226824 [PubMed - indexed for MEDLINE]
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6.	Mol Biochem Parasitol. 2012 Mar-Apr;182(1-2):83-7. Epub 2011 Dec 22. Kinetic analyses and inhibition studies reveal novel features in peptide deformylase 1 from Trypanosoma cruzi. Rodrígues-Poveda CA, Pérez-Moreno G, Vidal AE, Urbina JA, González-Pacanowska D, Ruiz-Pérez LM. Source Instituto de Parasitología y Biomedicina "López Neyra", Parque Tecnológico Ciencias de la Salud, Av. del Conocimiento, s/n, Consejo Superior de Investigaciones Científicas, 18100 Armilla, Granada, Spain. Abstract In eubacteria and eukaryotic organelles N-terminal methionine excision requires the sequential action of two activities, a peptide deformylase (PDF), which systematically removes the N-formyl group present on all nascent polypeptides and methionine aminopeptidase (MAP), which exscinds methionine specifically and depends on the previous removal of the N-formyl group. In Trypanosoma cruzi two genes encoding bacterial PDF homologues have been identified and referred to as TcPDF-1 and TcPDF-2. Here we report the biochemical characterization of a truncated soluble version of TcPDF-1 lacking the hydrophobic N-terminal domain that is active with the bacterial PDF substrate formyl-methionyl-alanyl-serine but, in contrast to other PDFs, is not inhibited by actinonin. The enzyme is strongly activated by Cu(2+) and inhibited by Ni(2+). Our results show that T. cruzi PDF exhibits unique features thus providing a new avenue for the design of potential inhibitors for use in the treatment of diseases caused by trypanosomatid parasites. © 2012 Elsevier B.V. All rights reserved.
	PMID: 22209909 [PubMed - indexed for MEDLINE]
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