Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Jan 22;12:530. doi: 10.1038/s41467-020-20805-w

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 6 — K13 mutations are associated with an up-regulation of protein folding as well as proteasome-linked protein turnover that may provide a growth advantage via a greater capacity of the mutant parasite to target and eliminate damaged proteins caused by the proteotoxic ART drug. K13 also appears to be involved in other novel pathways including intracellular signaling, pyruvate metabolism, purine salvage, and the mitochondrial electron transport chain (ETC). These functions suggest an altered central carbon metabolism and represent a quiescent state maintained by the parasite that allows for a recovery advantage following DHA exposure. DHA inhibits hemoglobin uptake or degradation and induces stalling in both K13 mutant (MUT) and wild-type (WT) rings. Recovery in K13 mutants may occur through enhanced mitochondrial ATP metabolic function and remodeling of the parasite’s secretory and vesicular transport processes. Inhibition of mitochondrial ETC activity lowers the survival of K13 mutant parasites to DHA treatment.