Leishmania major
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ABSTRACT:
PROVIDER: PRJNA168505 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiling of Leishmania major parasites overexpressing LmSir2rp3 protein compared with wild-type cell line transfected with empty vector in normal growth conditions. Goal of this experiment was to evaluate the possible effect of LmSir2rp3 in the control of gene expression in this protozoan parasite that has a polycistronic transcription. Two-condition experiment, LmSir2rp3 overexpressor vs. Wild-type cell line bearing empty vector. Biological replicates, 3 LmSir2rp3 overexpressor replicates and 3 wild-type cell line bearing empty-vector
2012-09-10 | E-GEOD-38731 | biostudies-arrayexpress
Project description:Comparative Genomic Hybridization of Leishmania major methotrexate resistant strains vs wild-type LV39
| PRJNA106135 | ENA
Project description:Transcriptional profiling of Leishmania major parasites overexpressing LmSir2rp3 protein compared with wild-type cell line transfected with empty vector in normal growth conditions. Goal of this experiment was to evaluate the possible effect of LmSir2rp3 in the control of gene expression in this protozoan parasite that has a polycistronic transcription.
2012-09-10 | GSE38731 | GEO
Project description:Leishmania major selfing analysis
| PRJNA900217 | ENA
Project description:Leishmania major promastigote ChIP-chip: TBP, SNAP50, acetylH3
| PRJNA110061 | ENA
Project description:Comparative Genomic Hybridization of Leishmania major SbIII resistant mutants and L. major WT
| PRJNA178109 | ENA
Project description:The genomic DNAs of strains JPCM5 and 263 of L. infantum, strains LV39 and Friedlin of L. major and strains Parrot-TarII and S125 of L. tarentolae were used in comparative genomic hybridizations to reveal the intra-species and inter-species gene content, and to validate L. tarentolae Parrot-TarII genome sequencing results. Leishmania (Sauroleishmania) tarentolae was first isolated in the lizard Tarentola mauritanica. This species is not known to be pathogenic to humans but is often used as a model organism for molecular analyses or protein overproduction. The Leishmania tarentolae Parrot-TarII strain genome sequence was resolved by high-throughput sequencing technologies. The L. tarentolae genome was first assembled de novo and then aligned against the reference L. major Friedlin genome to facilitate contig positioning and annotation, providing a 23-fold coverage of the genome. This is the first non-pathogenic to humans kinetoplastid protozoan genome to be described, and it provides an opportunity for comparison with the completed genomes of the pathogenic Leishmania species. A high synteny was observed in de novo assembled contigs between all sequenced Leishmania species. A number of limited chromosomal regions diverged between L. tarentolae and L. infantum, while remaining syntenic with L. major. Globally, over 90% of the L. tarentolae gene content was shared with the other Leishmania species. There were 250 L. major genes absent from L. tarentolae, and interestingly these missing genes were primarily expressed in the intracellular amastigote stage of the pathogenic parasites. This implies that L. tarentolae may have impaired ability to survive as an intracellular parasite. In contrast to other Leishmania genomes, two gene families were expanded in L. tarentolae, namely the leishmanolysin (GP63) and a gene related to the promastigote surface antigen (PSA31C). Overall, L. tarentolae appears to have a gene content more adapted to the insect stage rather than the mammalian one. This may partly explain its inability to replicate within mammalian macrophages and its suspected preferred life style as promastigote in the lizards.
2011-10-21 | GSE27184 | GEO
Project description:Leishmaniasis is a disease caused by the protozoan parasite Leishmania known to affect millions of individuals worldwide. In recent years, we have established the critical role played by Leishmania zinc-metalloprotease GP63 in the modulation of host macrophage signaling and functions, favouring its survival and progression within its host. Leishmania major lacking GP63 was reported to cause limited infection in mice, however it is still unclear how GP63 may influence the innate inflammatory response and parasite survival in an in vivo context. Therefore, we were interested in analyzing the early innate inflammatory events upon Leishmania inoculation within mice and establish whether Leishmania GP63 influences this initial inflammatory response. Experimentally, L. major WT, L. major GP63 KO or L. major GP63 rescue were intraperitoneally inoculated in mice and inflammatory cells recruited were characterized microscopically and by flow cytometry (number and cell type), and their infection determined. Pro-inflammatory markers such as cytokines, chemokines and extracellular vesicles (EVs, e.g. exosomes) were monitored and proteomic analysis was performed on exosome contents. Data obtained from this study suggest that Leishmania GP63 does not significantly influence the pathogen-induced inflammatory cell recruitment, but rather their activation status and effector function. Concordantly, internalization of promastigotes during early infection could be influenced by GP63 as less L. major KO amastigotes were found within host cells and appear to maintain in host cells over time. Collectively this study provides a clear analysis of innate inflammatory events occurring during L. major infection and further establish the prominent role of the virulence factor GP63 to provide favorable conditions for host cell infection.
2022-01-01 | GSE189385 | GEO