Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/80806
Title: DNA damage regulation and its role in drug-related phenotypes in the malaria parasites
Authors: Gupta, Devendra Kumar
Patra, Alok Tanala
Zhu, Lei
Gupta, Archana Patkar
Bozdech, Zbynek
Keywords: DNA Repair
DRNTU::Science::Biological sciences
DNA Damage
Issue Date: 2016
Source: Gupta, D. K., Patra, A. T., Zhu, L., Gupta, A. P., & Bozdech, Z. (2016). DNA damage regulation and its role in drug-related phenotypes in the malaria parasites. Scientific Reports, 6, 23603-. doi:10.1038/srep23603
Series/Report no.: Scientific Reports
Abstract: DNA of malaria parasites, Plasmodium falciparum, is subjected to extraordinary high levels of genotoxic insults during its complex life cycle within both the mosquito and human host. Accordingly, most of the components of DNA repair machinery are conserved in the parasite genome. Here, we investigated the genome-wide responses of P. falciparum to DNA damaging agents and provided transcriptional evidence of the existence of the double strand break and excision repair system. We also showed that acetylation at H3K9, H4K8, and H3K56 play a role in the direct and indirect response to DNA damage induced by an alkylating agent, methyl methanesulphonate (MMS). Artemisinin, the first line antimalarial chemotherapeutics elicits a similar response compared to MMS which suggests its activity as a DNA damaging agent. Moreover, in contrast to the wild-type P. falciparum, two strains (Dd2 and W2) previously shown to exhibit a mutator phenotype, fail to induce their DNA repair upon MMS-induced DNA damage. Genome sequencing of the two mutator strains identified point mutations in 18 DNA repair genes which may contribute to this phenomenon.
URI: https://hdl.handle.net/10356/80806
http://hdl.handle.net/10220/46602
DOI: 10.1038/srep23603
Rights: © 2016 The Authors (Nature Publishing Group). This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Journal Articles

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