RNA sequencing analysis of HEK293T cells infected with a lentivirus coding the BRCT domain from Leishmania major Pes protein
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA674644 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12982730_1.fastq.gz | Fastqsanger.gz | |||
| SRR12982730_2.fastq.gz | Fastqsanger.gz | |||
| SRR12982731_1.fastq.gz | Fastqsanger.gz | |||
| SRR12982731_2.fastq.gz | Fastqsanger.gz | |||
| SRR12982732_1.fastq.gz | Fastqsanger.gz |
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Project description:Given the prevalence of leishmaniasis and cancer, the co-existence of these two diseases may be merely coincidental. However, a number of epidemiological studies suggest that an association between these two entities does exist. Mammalian PES protein has been reported to be involved in different cellular processes such as cell cycle regulation. Its BRCT domain has been identified as a key factor in DNA damage-responsive checkpoints. We aimed to elucidate the hypothetical oncogenic character of this BRCT domain from Leishmania major PES protein (LmPES) on the host cells. For this purpose, we generated a lentivirus carrying this BRCT domain sequence (lentiBRCT) and a lentivirus expressing the lucifarese protein (lentiLuc), as control. Then, HEK293T mammal cells were infected with these lentivirus. Gene expression profiling analysis revealed that BRCT domain from LmPES protein altered the expression of proliferation, survival and chemoresistance related genes. In addition, RNA sequencing study showed a down-regulation of mitochondrial genes in the BRCT domain expressing cells triggering a mitochondrial dysfunction. Altogether, our results reinforce the idea that in eukaryotes, horizontal gene transfer may be also achieved by parasitism like Leishmania infection driving therefore to some crucial biological changes such as proliferation and drug resistance.
2022-11-16 | GSE160853 | GEO
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:Murine bone marrow derived macrophages were infected with Leishmania major or Leishmania donovania promastigotes, allowed to phagocytose latex beads or not treated. Gene expression profiles were compared to identify i) the effect of Leishmania infection; ii) the differences in effects between L. major and L. donovani; and iii) the effect of pahgocytosis of latex beads.
2008-02-05 | E-MEXP-1254 | biostudies-arrayexpress
Project description:Leishmania major: Sir2rp3 overexpressor vs wild-type
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Project description:Origins of genetic exchange in Leishmania parasites
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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. Six strains of three Leishmania species were hybridizated to 12 microarrays, each with four biological replicates (independent cultures). Supplementary file: Represents final results obtained after statistical analysis of all replicates.
2011-10-20 | E-GEOD-27184 | biostudies-arrayexpress
Project description:Leishmania major promastigote ChIP-chip: TBP, SNAP50, acetylH3
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