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Molecular Characterisation and Functions of Fis1 and PDCD6 Genes from Echinococcus granulosus
Cystic echinococcosis, a parasitic zoonosis that causes significant economic losses and poses a threat to public health, is caused by larvae of the tapeworm Echinococcus granulosus. Infection causes infertile cysts in intermediate hosts that cannot produce protoscoleces (PSCs) or complete the life c...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6165261/ https://www.ncbi.nlm.nih.gov/pubmed/30205566 http://dx.doi.org/10.3390/ijms19092669 |
Sumario: | Cystic echinococcosis, a parasitic zoonosis that causes significant economic losses and poses a threat to public health, is caused by larvae of the tapeworm Echinococcus granulosus. Infection causes infertile cysts in intermediate hosts that cannot produce protoscoleces (PSCs) or complete the life cycle. Herein, we cloned, expressed, and characterised mitochondrial fission protein 1 (Eg-Fis1) and programmed cell death protein 6 (Eg-PDCD6) from E. granulosus, and explored their functions related to infertile cysts. Eg-Fis1 and Eg-PDCD6 encode putative 157 and 174 residue proteins, respectively, and Western blotting indicated good reactogenicity for both. Eg-Fis1 and Eg-PDCD6 were ubiquitously distributed in all stages of E. granulosus. Furthermore, mRNAs of Eg-Fis1 and Eg-PDCD6 were upregulated following H(2)O(2) treatment which induced apoptosis in PSCs. To investigate the regulation of apoptosis in response to oxidative stress, RNA interference (RNAi) and terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) assays were performed. The apoptotic rate of the Eg-Fis1 RNAi group was significantly lower than non-interference group, but there was no such difference for Eg-PDCD6. In conclusion, Eg-Fis1 promotes apoptosis induced by oxidative stress, whereas Eg-PDCD6 does not appear to be a key regulator of apoptosis. |
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