The role of BRCT domain from LmjPES in Leishmania major biology
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PROVIDER: PRJNA979236 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the implications of LmjPES BRCT domain overexpression in Leishmania major. We generated a strain of L. major constitutively overexpressing LmjPES BRC domain and we compared its gene expression with other L. major strain no-overexpressing this domain.The data showed a role of LmjPES BRC domain in genes related mainly to metabolic patways
2025-09-03 | GSE234048 | GEO
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: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
Project description:Leishmania major: Sir2rp3 overexpressor vs wild-type
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Project description:RNA sequencing analysis of HEK293T cells infected with a lentivirus coding the BRCT domain from Leishmania major Pes protein
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